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Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/textbookofmedici01str 


A  TEXT-BOOK  OF  MEDICINE 

FOR    STUDENTS    AND    PRACTITIONERS 


VOLUME   I 


Copyright,  1886,  1893,  1901,  1911, 
By  D.  APPLETON  AND  COMPANY 


**^L      1 


PRINTED   AT   THE   APPLETON   PRESS 
NEW   YORK,    TJ.   S.   A. 


PREFACE   TO   THE   AMERICAN   EDITION 


The  special  customs  and  habits  of  a  people  are  evidenced  even  in  it- 
medical  life.  The  facts  and  underlying  principles  of  science,  naturally,  arc 
common  to  all  nations.  In  addition,  however,  medical  science  and,  more 
particularly,  the  everyday  medical  practice  of  each  country  manifest  also 
special  characteristics.  Hence,  every  physician  may  learn  from  the  practi- 
tioners of  other  countries  something  new  to  broaden  and  better  his  own 
views.  This  is  due  not  only  to  the  fact  that  diseases  vary  in  different 
lands,  but  also  to  the  further  circumstance  that,  owing  to  the  diversity  of 
climate  and  other  factors,  identical  diseases  present  certain  distinct  varia- 
tions. The  individual  national  characteristics  of  the  physicians  themselves 
cannot  be  entirely  ignored. 

The  foregoing  considerations  have  convinced  me  of  the  utility  of  a  people 
supplementing  its  scientific  literature  by  translations  from  foreign  works, 
and  I  have  therefore  readily  given  my  consent  to  the  publication  of  an 
American  edition  of  my  "  Lehrbuch  der  speziellen  Pathologie  und  Therapie 
der  inneren  Krankheiten." 

In  both  the  United  States  and  England  there  is  no  lack  of  good  text- 
books of  medicine,  but,  nevertheless,,  the  American  students  and  physicians 
may  be  interested  to  learn  the  present  German  views  of  the  pathology  and 
therapy  of  medical  diseases.  My  text-book  has  found  wide  circulation  and 
recognition  in  Germany  as  well  as  in  other  countries,  and  I  may  therefore 
assume  that  it  has  not  altogether  failed  of  its  purpose  to  give  a  thorough 
and  reliable  survey  of  the  present  status  of  internal  medicine.  I  have  always 
been  happy  to  be  a  clinical  teacher,  for  teaching  was  ever  a  pleasure  to  me 
and  never  a  task.  This  accounts,  perhaps,  for  my  success  in  being  able 
clearly  and  distinctly  to  express  whatever  there  was  to  tell  about  indi- 
vidual diseases.  My  text-book  is  concerned  with  the  large  and  extensive 
domain  of  internal  medicine.  Nowadays  no  one  dares  profess  to  be  equally 
at  home  in  all  branches  of  this  study.  The  experienced  reader  will  observe 
that  some  sections,  as,  for  example,  Diseases  of  the  Nervous  System,  have 
been  more  fully  and  more  originally  presented  than  have  others.  Despite  this 
fact,  the  teacher  of  internal  medicine  should,  to  a  certain  extent,  command 
a  knowledge  of  all  the  branches  that  come  within  the  field  of  his  instruction, 


VI  PREFACE  TO  THE  AMERICAN  EDITION 

and  I  therefore  hope  that  my  book  will  he  found  throughout  to  present  at 
least  the  more  important  facts  and  views,  in  conformity  with  the  present 
status  of  medical  knowledge.  The  practical  end  has  not  been  my  main 
purpose  in  writing.  It  would  be  sad,  indeed,  if  the  physician  should  desire 
to  learn  and  know  only  that  which  he  could  use  in  his  practice.  Only  the 
physician  who  takes  a  scientific  theoretical  interest  in  his  work,  and  who 
remains  conscious  of  the  close  relations  that  always  exist  between  medical 
science  and  the  important  questions  of  general  biology,  can  find  happiness 
and  contentment  in  his  calling.  We  physicians  must  never  forget  that  many 
branches  of  human  physiology  can  be  marked  out  only  with  our  assistance. 
Therefore,  I  have  always  regarded  it  as  one  of  the  chief  duties  of  a  clinical 
teacher,  as  well  as  of  a  scientific  text-book,  in  addition  to  the  requirements 
of  practice,  also  to  bear  in  mind  the  connection  between  medical  science  and 
general  biology,  and  to  arouse  the  interest  of  the  coming  physicians  in  this 
subject.  A  scientific  pathology  is  possible  only  when  based  upon  physiological 
principles. 

I  trust  that  my  book,  in  its  new  form,  will  still  receive  a  friendly  wel- 
come from  its  American  and  English  readers.  May  it,  in  a  small  measure,  at 
least,  serve  to  unite  two  nations  in  a  domain  where,  after  all,  there  can  be 
nothing  that  estranges — the  promotion  of  knowledge  and  social  progress. 

Adolf  von  Strumpell. 

Vienna. 


AUTHORS  PREFACE   TO   THE   SEVENTEENTH 
GERMAN  EDITION 


The  extent  to  which  my  text-book  has  been  used,  both  in  Germany  and  in 

other  countries,1  justifies  me  in  the  assumption  that  it  has  exercised  some  little 
influence  upon  the  professional  thought  and  practice  of  numerous  medical  read- 
ers, and  imposes  upon  me  the  obligation  of  employing  every  opportunity  for 
the  improvement  and  perfection  of  my  work.  Yet  I  must  confess  that  this 
task  seems  more  difficult  to  me  with  every  new  edition  of  the  book,  for  scien- 
tific workers  are  making  deep  and  extensive  investigations  into  the  many 
subdivisions  of  internal  medicine,  with  such  zeal  and  skill  that  it  becomes 
difficult  for  any  one  man  to  keep  step  with  the  unceasing  progress  of  investi- 
gation in  this  wide  domain,  and  to  maintain  that,  complete  and  universal 
command  of  facts  and  theories  which  is  essential  for  a  presentation  of  the 
subject,  which  shall  be  at  once  brief  and  true  to  the  present  standpoint  of 
science.  The  author  has  often  been  painfully  sensible  of  these  limitations 
of  his  personal  knowledge  and  ability,  but  he  hopes  that  this  will  be  regarded 
not  merely  as  subject  for  criticism,  but  also  as  an  excuse  and  an  incentive  to 
clemency,  in  case  a  reader  who  is  expert  in  any  specialty  finds  here  and  there 
an  omission  or  an  error.  Above  all,  I  beg  the  reader  to  consider  that  no  text- 
book such  as  the  present  one  ought  to  replace,  or  could  replace,  the  vast  mate- 
rial of  the  larger  reference  books.  My  purpose  was  not  to  collect  all  the  facts 
of  pathology  which  have  been  discovered  up  to  date,  nor  all  the  methods  of 
treatment  which  may  have  been  recommended,  wisely  or  unwisely,  nor  all  the 
theories  or  views  which  have  been  propounded.  My  wish  was  to  give  a  com- 
plete presentation  of  the  essentials  of  our  present  knowledge  and  views  with 
regard  to  the  various  diseases,  from  a  scientific  and  individual  standpoint ;  and 
I  desired  particularly  to  impart  to  the  reader  an  insight  into  the  origin  and 
relation  of  the  various  morbid  phenomena.  To  this  end  I  have  brought  the 
facts  of  clinical  experience  into  the  closest  possible  relation  with  the  data  of 
pathological  anatomy  and  of  general  pathology,  and  have  endeavored,  also,  in 
discussing  therapeutics,  to  deduce  from  the  nature  of  the  symptoms  a  basis 
for  rational  medical  opinion  and  treatment,  although  I  have  not  undervalued 
the  importance  of  simple  experience.  A  text-book  intended  for  students  and 
a  larger  circle  of  graduate  readers  ought  not  to  incline  too  decidedly  toward 
any  one  of  the  prevailing  currents  of  scientific  opinion.  It  should,  however, 
acquaint  the  reader  to  such  an  extent  with  the  questions  at  present  under 

1  So  far  as  I  have  been  informed,  translations  of  my  text-book  have  appeared  in  the  following 
languages:  French,  English,  Italian,  Spanish,  Russian,  modern  Greek,  Turkish,  and  Japanese; 
and  some  of  these  translations  have  had  several  editions. 

vii 


Vlii     AUTHOR'S  PREFACE  TO  THE  SEVENTEENTH  GERMAN   EDITION 

discussion  relating  to  internal  medicine,  as  to  give  him  at  least  a  fair  start  in 
his  further  studies. 

The  completion  of  this,  the  seventeenth  edition  of  my  text-book,  has  un- 
fortunately been  delayed  by  my  transfer  of  residence  to  Vienna.  In  spite  of 
many  demands  made  on  my  time  by  my  new  activity,  I  have  endeavored,  to 
the  best  of  my  ability,  to  bring  the  book  to  the  level  of  contemporary  medical 
knowledge  by  making  numerous  changes  and  additions  in  all  parts  of  it.  I 
have  again  laid  greatest  stress  upon  the  presentation  of  clinical  phenomena 
as  they  appear  to  the  physician,  separately  and  in  combination,  in  the  course 
of  disease.  The  detailed  description  of  many  important  methods  of  exam- 
ination must  be  left  to  the  special  text-books.  We  cannot  emphasize  and 
recognize  too  often  how  much  our  diagnostic  knowledge  has  gained  in  cer- 
tainty and  precision  through  these  methods  of  examination,  and  how  much  we 
as  physicians  should  strive  to  give  all  patients  the  benefit  of  this  progress. 
The  only  disadvantage  resulting  from  this  is,  that  the  major  factor  of  the 
examination  shifts  more  and  more  from  the  bedside  to  the  laboratory,  with 
a  resulting  decrease  in  the  practice  of  and  interest  in  the  observation  of  the 
purely  clinical  phenomena.  I  have  repeatedly  noted  that  the  younger  gen- 
eration of  medical  men,  however  well  trained  in  bacteriological,  chemical, 
and  microscopic  methods  of  examination,  shows  a  remarkable  insecurity  and 
want  of  practice  in  clinical  observation  and  diagnosis.  Therefore,  I  believe 
that,  for  scientific  as  well  as  for  practical  reasons,  we  clinical  teachers  should 
not  lose  sight  of  the  purely  clinical  phase  of  instruction,  besides  the  modern 
achievements  in  the  field  of  diagnosis  and  pathological  physiology. 

The  accusation  is  often  made  that  "  what  the  text-books  tell  us  "  does  not 
fully  correspond  to  reality.  I  trust  that  my  text-book  does  not  deserve  this 
criticism.  It  is  the  outgrowth  of  an  unceasing,  broad,  clinical  activity,  and 
is  much  more  a  product  of  the  hospital  ward  than  of  the  study.  It  would, 
nevertheless,  be  unfair  to  expect  that  all  the  unlimited  and  numerous  possi- 
bilities and  differentiations  occurring  in  the  course  of  diseases  should  be 
mentioned.  The  presentation  of  a  text-book  can,  after  all,  in  a  certain  sense 
only  be  an  abstract  with  which  individual  cases  are  to  be  compared  in  order 
that  their  peculiarities  may  be  determined.  The  critical  examination  of  a 
case,  with  reference  to  average  medical  experience,  constitutes  one  of  the 
chief  attractions  of  clinical  observation.  However,  such  comparison  is  pos- 
sible only  when  the  essential  phases  of  the  common  course  of  diseases  are 
ever  present  in  the  physician's  mind.  It  is  the  aim  of  this  text-book  to 
present  these  essential  phases,  and  if  I  have  accomplished  this,  the  book  will 
be  of  help  to  the  physician  even  after  he  has  recognized  that  a  simple  rule 
rarely  embraces  all  the  variations  of  real  facts. 

A.  Strumpell. 

Vienna. 


EDITORS'   PREFACE 


It  is  just  a  quarter  of  a  century  since  the  first  edition  of  our  translation 
of  Professor  Strumpell's  Lehrbuch,  then  in  its  second  edition,  was  published 
■ — a  period  of  time  long  enough  to  have  seen  many  text-books  appear,  flourish, 
and  pass  into  oblivion — yet  each  of  the  fifteen  edit  ions  of  the  original  which 
have  appeared  since  that  date  has  shown  more  freshness  ami  vigor  than  most 
of  the  latest  candidates  for  medical  favor.  Our  study  of  the  successive  edi- 
tions, in  the  preparation  of  the  various  editions  of  our  translation  which  have 
been  called  for,  has  impressed  us  more  and  more  with  the  vast  clinical  expe- 
rience, the  wide  knowledge  and  sound  judgment  of  the  author,  his  familiarity 
with  the  great  progress  in  all  branches  of  internal  medicine,  his  clearness  of 
exposition,  and  his  admirable  critical  faculty  in  selecting  and  emphasizing 
the  facts  which  he  presents  to  the  student  in  the  moderate  compass  of  these 
volumes.  Long  familiarity  with  the  work  has  bred,  contrary  to  the  old  adage, 
a  greater  admiration  for  it  and  a  deeper  conviction  that  it  has,  during  this 
time,  kept  its  place  as  the  chief  text-book  of  internal  medicine. 

Of  the  present  edition  we  are  the  editors  and  not  the  translators,  but  an 
effort  has  been  made,  as  in  the  former  editions,  to  keep  as  close  to  the  orig- 
inal as  seemed  consistent  with  clearness.  Doses  and  temperatures  have  been 
given  in  apothecaries'  weight  and  the  Fahrenheit  scale,  corresponding  approxi- 
mately to  the  metric  values  of  the  original.  As  far  as  was  possible  we  have 
tried  to  follow  the  United  States  Pharmacopoeia  in  the  prescriptions  men- 
tioned, except  that  we  have  retained  certain  familiar  names  of  drugs  instead 
of  adopting  the  innovations  of  the  last  revision.  We  have  also  substituted 
specimens  of  handwriting  in  English  in  place  of  the  originals  in  German 
script.  We  have  retained  a  large  part  of  certain  chapters  and  some  of  the 
editorial  notes  contributed  to  the  first  edition  by  Dr.  F.  C.  Shattuck,  the 
former  editor;  but,  in  justice  to  him,  it  should  be  understood  that  he  is  in 
no  way  responsible  for  any  errors  or  shortcomings  in  the  present  edition, 
although  we  gladly  and  gratefully  acknowledge  our  indebtedness  to  him.  We 
have  ourselves  added  various  notes,  most  of  them  distinguished  by  our  respec- 
tive initials.  We  have  also  inserted  brief  chapters  on  The  Fourth  Disease, 
Malta  Fever,  Eocky  Mountain  Fever,  and  Pellagra. 

It  has  not  been  the  custom  to  include  a  section  on  mental  diseases  in  the 


X  EDITORS'   PREFACE 

ordinary  text-book  of  internal  medicine.  This  exclusion,  however,  seems  to 
us  wholly  unjustifiable  in  view  of  the  great  importance  of  the  subject  and  the 
necessity  for  some  knowledge  of  it  by  the  general  practitioner.  We  have 
therefore  added  such  a  section,  the  aim  of  which  is  to  give  a  brief  account 
of  the  commoner  forms  of  mental  disease  not  already  discussed  by  the  author. 
This  account  is,  of  course,  not  intended  to  be  exhaustive  or  to  consider  all  the 
forms  of  mental  disease.  For  such  considerations  the  student  must  refer  to 
the  special  treatises.  In  this  section  we  have  followed  in  the  main  the  classi- 
fication of  Ivraepelin,  now  so  much  in  vogue  in  this  country,  in  order  to  avoid 
confusing  the  beginner  by  any  less  familiar  nomenclature. 

H.    F.    VlCKERY, 

Philip  Coombs  Knapp. 


CONTENTS 


VOLUME    I 
I.     Acute  General  Infectious  Diseases 

CHAPTER 

I.     Typhoid   Fever 

Paratyphoid  Fever 
II.     Typhus  Fever 

III.  Relapsing   Fever 

IV.  Scarlet   Fever 
V.     Measles     . 

VI.  Rotheln     . 

VII.  Smallpox 

VIII.  Varicella 

IX.  Erysipelas 

X.  Diphtheria 

XI.  Influenza    (Grippe 

XII.  Dysentery 

XIII.  Cholera 

XIV.  Malarial  Diseases 

Intermittent  Fever 
Pernicious  Intermittent  Fever 
Chronic  Malarial  Cachexia 
Masked  Intermittent   Fever 
Typho-malarial  Fever 

XV.     Dengue 

XVI.     Yellow  Fever 

XVII.     Plague 

XVIII.     Epidemic  Cerebro-spinal  Meningitis 
XIX.     Septic    and    Pyemic    Diseases 

XX.     Tetanus 

XXI.     Hydrophobia    (Rabies  canina) 
XXII.     Glanders    (Farcy) 

XXIII.  Malignant  Pustule   (Anthrax.     Mycosis  intestinali 

XXIV.  Trichinosis        .... 
XXV.     The   "Fourth   Disease" 

XXVI.     Malta    Fever    .... 
XXVII.     Rocky  Mountain  Spotted  Fever 


PAGE 

1 

34 

:;i 

38 

43 

55 

(il 

Dl 

71 

72 

77 

88 

94 

99 

107 

111 

113 

114 

114 

115 

118 

119 

123 

126 

133 

141 

146 

150 

152 

157 

161 

161 

162 


II.     Diseases  of  the  Respiratory  Organs 
SECTION    I 

DISEASES   OP  THE  NOSE 

I.     Coryza 

Hay  Fever   (Hay  Asthma) 


164 
166 


Xli  CONTENTS 

CHAPTER  PAGE 

II.     Chronic  Rhinitis 166 

III.     Nosebleed 169 

SECTION    II 

DISEASES   OF   THE   LARYNX 

I.     Acute  Laryngeal  Catarrh 170 

II.     Chronic   Laryngitis 173 

III.  Laryngeal   Perichondritis          ....  - 175 

IV.  (Edema   of   the   Glottis 177 

V.     Tuberculosis  of  the  Larynx 178 

VI.     Paralyses   of   the   Laryngeal   Muscles 182 

VII.     Spasm  of  the  Glottis   (Laryngismus  Stridulus) 186 

VIII.     New  Growths  in  the  Larynx            187 

SECTION    III 

DISEASES   OF   THE   TRACHEA   AND   BRONCHI 

I.     Acute  Catarrh  of  the  Trachea  and  the  Bronchi 190 

II.     Chronic    Bronchitis 196 

III.  Foetid  Bronchitis        .        .        .        .        .        .        . 202 

IV.  Croupous  Bronchitis 206 

V.     Whooping  Cough   (Pertussis) 208 

VI.     Bronchiectasis 213 

VII.     Stenosis  of  the  Trachea  and  Bronchi 218 

VIII.     Bronchial   Asthma 220 

SECTION    IV 

DISEASES   OF   THE  LUNGS 

I.     Pulmonary   Emphysema 227 

II.     Pulmonary  Atelectasis   (Compression  of  the  Lungs.    Aplasia  of  the  Lungs)  238 

III.  Pulmonary   CEdema 241 

IV.  Catarrhal  Pneumonia    (Broncho-pneumonia.     Lobular   Pneumonia)      .        .  242 
V.     Croupous    Pneumonia 249 

VI.    Tuberculosis  of  the  Lungs  ( Pulmonary  Phthisis.    Pulmonary  Consumption)  274 

VII.    Acute    General   Miliary    Tuberculosis 318 

VIII.     Gangrene  of  the  Lungs      . ' 324 

IX.     Diseases  from  the  Inhalation  of  Dust    (Pneumonoconiosis)    ....  329 

X.     Embolic  Processes  in  the  Lungs   (Hemorrhagic  Infarction  of  the  Lungs)      .  332 

XL     Brown  Induration  of  the  Lungs    (Lungs  of  Heart  Disease)    ....  335 
XII.     Tumors  of  the  Lungs.     Cancer  of  the  Lungs.     Echinococcus  of  the  Lungs. 

Pulmonary  Syphilis 337 

SECTION    V 

DISEASES   OF   THE  PLEURA 

I.     Pleurisy 340 

II.     Peripleuritis 360 


CONTENTS  xni 

CHAPTER 

III.  Pneumothorax 360 

IV.  Ifydrothoiax.      Ileinatothorax 365 

V.    New  Growths  of  the  Pleura 366 

VI.    Mediastinal  Tumors '■'•<'<! 

VII.    Actinomycosis  of   the  Thoracic   Cavity 369 


III.     Diseases  of  the  Circulatory  Organs 
SECTION    I 

DISEASES   ill'  THE    HE  VBT 

T.    Acute  Endocarditis   (Endocarditis  verrucosa.  Endocarditis  ulcerosa)            .  371 

IT.     Valvular  Disease  of  the  Heart 37G 

ill.     Diseases  of  the  Myocardium 414 

Interstitial    Myocarditis     (Fibroid     Degeneration    of    the    Myocardium. 

Sclerosis  of  the  Coronary  Arteries) 414 

So-called  Idiopathic  Hypertrophy   of   the    Heart    (Functional   Strain   of 

the  Heart) 421 

Hypertrophy  of  the  Heart,  Associated  with  Congenital  Smallness  of  the 

Systemic  Arteries 428 

Primary   Weakness    of    the   Myocardium    (Congenital    Weakness    of   the 

Heart;   Weakened  Heart;   Acute  Muscular  Strain  of  the  Heart;   Toxic 

Weakness  of  the  Heart) 429 

The  So-called  Fatty  Heart 431 

IV.     Cardiac  Neuroses 434 

Purely  Psychogenetic  Heart  Disturbances 434 

Nervous  Heart  Disturbances  from  Endogenous  Toxic  Influences         .        .  434 

Nervous  Heart  Disturbance  Due  to  Exogenous  Toxic  Influences        .        .  435 

The  Nervous  "  Attacks  "  of  Patients  with  Heart  Diseases          .        .        .  435 

Nervous  Palpitation 438 

Paroxysmal  Tachycardia 439 

SECTION    II 

DISEASES    OF   THE   PERICARDIUM 

I.     Pericarditis    (Inflammation  of  the  Pericardium) 440 

II.     Hydropericardium,  Hemopericardium,  and  Pneumopericardium     .        .        .     452 

SECTION    III 

DISEASES   OF  THE  VESSELS 

I.     Arteriosclerosis     (Endarteritis    chronica    deformans.       Atheroma    of    the 

Vessels) 454 

II.     Aneurism  of  the  Thoracic  Aorta 459 

III.  Aneurisms  of  the  Other  Vessels 466 

IV.  Rupture  of  the  Aorta 467 

V.    Narrowing  of  the  Aorta 467 


XIV  CONTENTS 


IV.     Diseases  of  the  Digestive  Organs 
SECTION    I 

DISEASES   OF   THE   MOUTH,   TONGUE,   AND   SALIVARY   GLANDS 

CHAPTER  PAGE 

I.     Catarrhal  Stomatitis .        .        .        .        .  469 

II.     Ulcerative   Stomatitis .        .  471 

III.  Aphthous  Stomatitis 472 

IV.  Thrush 474 

V.     Diseases  of  the   Tongue    . 475 

Acute  Parenchymatous  Glossitis .  476 

Glossitis  Desiccans 476 

Lingual  Psoriasis.     Leucoplacia 476 

Black  Hair  Tongue   (Melanutrichia  linguae) 477 

VI.    Noma 477 

VII.     Parotitis    (Mumps) .479 

VIII.     Angina  Ludovici 481 

IX.     Anomalies  of  Dentition 482 


SECTON    II 

DISEASES    OF   THE    SOFT    PALATE,    TONSILS,    PHARYNX,    AND    NASOPHARYNX 

I.    Various  Forms  of  Sore  Throat    (Inflammation  of  the  Soft  Palate  and  of 

the  Tonsils) - 483 

Catarrhal  Sore  Throat 485 

Follicular   Tonsillitis     .        . 486 

Tonsillar  and  Peritonsillar  Abscess   (Parenchymatous  Sore  Throat)        .  486 

Necrotic  Tonsillitis   (Necrotic  Sore  Throat) 487 

II.     Chronic  Hypertrophy  of  the  Tonsils 489 

III.  Chronic   Pharyngitis 490 

IV.  Retropharyngeal   Abscess 494 

SECTION    III 

DISEASES   OF  THE   CESOPHAGUS 

I.     Inflammation  and  Ulcer  of  the  (Esophagus        .......  496 

II.     Dilatation  of  the  Oesophagus 497 

III.  Stenosis  of  the  Oesophagus 501 

IV.  Cancer  of  the  Oesophagus 505 

V.     Rupture  of  the  Oesophagus 507 

VI.     Neuroses  of  the  Oesophagus •        •  508 

Spasm  of  the  Oesophagus 508 

Paralysis  of  the  Oesophagus 508 

SECTION    IV 

DISEASES   OF   THE   STOMACH 

I.     Brief  Preliminary  Remarks  on  the  Examination  of  the  Gastric  Contents   .  508 

II.     Acute  Gastric  Catarrh    (Acute  Gastritis) 518 


CONTENTS  xv 

CHArTBK  PAOH 

III.  Chronic  Gastritis — Chronic  Catarrh  of  the  Stomach     ' 521 

IV.  Phlegmonous  Gastritis 

V.    Gastric    Ulcer 

VI.     Cancer  of   the   Stomach 

VII.     Anomalies  of  the  Secretion  of  Gastric  Juice 

Anacidity  of  the  Stomach    ( Achlorhydria ) .     Achylia  Gastrica    . 
Hypersecretion  and  Hyperacidity  of  the  Gastric  Juice   (Acid  Dyspepsia) 
VTII.     Abnormalities  in  the  Size  and  Position  of  the  Stomach.     Motor   Disturb- 
ances of  the  Stomach 563 

IX.    Nervous   Dyspepsia 567 


SECTION  V 

DISEASES   OF  THE  INTESTINES 

I.    Intestinal  Catarrh 573 

Membranous  Enteritis  and  Mucous  Colic  « 581 

II.     Cholera  Morbus 582 

III.  Intestinal  Catarrh  of  Children 584 

IV.  Typhlitis  and  Perityphlitis    (Appendicitis) 591 

V.     Perforating  Ulcer  of  the  Duodenum GOO 

VI.     Tuberculosis  of  the  Intestines 601 

VII.     Syphilis  of  the  Rectum 603 

VIII.     Cancer  of  the  Intestines 604 

IX.     Hemorrhoids 607 

X.     Habitual  Constipation 610 

XI.     Stricture  and  Obstruction  of  the  Intestines 615 

XII.     Intestinal  Parasites 628 

Tapeworms 628 

Roundworms 635 

Oxyuris  vermicularis 637 

Anchylostoma  duodenale 638 

Trichocephalus  dispar 640 

SECTION    VI 

DISEASES    OF   THE   PERITONEUM 

I.     Acute    Peritonitis 641 

II.     Chronic  and  Tuberculous  Peritonitis 652 

III.  Ascites 657 

IV.  Cancer  of  the  Peritoneum 660 


SECTION    VII 
i 

DISEASES    OF   THE   LIVER,    BILE    DUCTS,    AND    PORTAL   VEIN 

I.  Catarrhal  Jaundice 661 

II.  Biliary  Calculi 669 

III.  Suppurative  Hepatitis 681 

IV.  Cirrhosis  of  the. Liver 684 

1 


xvi  CONTENTS 

CHAPTER  PAGE 

V.     Biliary  Cirrhosis  and  Hypertrophic  Cirrhosis  of  the  Liver     ....  693 

VI.     Acute  Yellow  Atrophy  of  the  Liver 696 

Pernicious  Jaundice.     Cholsemia  and  Acholia 701 

VII.     Icterus  Neonatorum 702 

VIII.     Syphilis  of  the  Liver 703 

IX.     Cancer  of  the  Liver  and  Bile  Ducts .        .  705 

X.     Echinococcus  of  the  Liver 707 

XL     Circulatory  Disturbances  in  the  Liver          .        . 711 

Hepatic  Anaemia 711 

Passive  Congestion i.        .        .711 

Active  Hyperemia 712 

XII.     Atrophy,  Hypertrophy,  and  Degenerations  of  the  Liver   .        .        .        .        .  713 

XIII.  Anomalies  in  the  Shape  and  Position  of  the  Liver 714 

Corset  Liver     .                714 

Movable  Liver 715 

XIV.  Suppurative  Pylephlebitis 715 

XV.     Thrombosis  of  the  Portal  Vejn 717 

APPENDIX 

DISEASES   OF   THE  PANCEEAS 

Atrophy  of  the  Pancreas 720 

Hemorrhages  into  the  Pancreas 720 

Pancreatitis 721 

Cysts  of  the   Pancreas 721 

Cancer  of  the  Pancreas 722 

Pancreatic  Calculi 722 


V.     Diseases  of  the  Urinary  Organs 
SECTION  I 

DISEASES   OF  THE  KIDNEYS 

I.     General  Preliminary  Remarks  upon  the  Pathology  of  Renal  Disease         .  723 

II.     Acute  Nephritis 745 

III.  The  Subchronic  and  Chronic   Forms  of  Nephritis,  with  the  Exception  of 

the  Genuine  Contracted  Kidney .  763 

IV.  Contracted  Kidney 770 

V.     Amyloid  Kidney 782 

VI.     Purulent  Nephritis  and  Perinephritis 788 

VII.     Disturbances  of  Circulation  in  the  Kidneys 791 

The  Congested  Kidney .791 

Embolic  Infarction  in  the  Kidneys •        •  792 

VIII.     New  Growths  in  the  Kidneys 793 

IX.     Parasites  of  the  Kidneys  and  of  the  Urinary  Passages.     Chyluria     .        .  796 

Echinococcus  of  the  Kidney "...  796 

Distoma  Hematobium    (Bilharzia  Hematobia)    ' 797 

Strongylus  or  Eustrongylus  Gigas 797 

Filaria  Sanguinis.     Chyluria 797 


CONTENTS  xvii 

CHAPTER  PAGE 

X.    Movable  Kidney   (Floating  Kidney.     Ren  Mobilis) 798 

Appendix.     The  Discuses  of  the  Suprarenal   Capsules  and   Addison's    Di 

ease   (Bronzed  Skin) sul 


SECTION    II 

DISEASES    OF    THE    PELVIS    OF    Till;    KIDNEY    AND    OF    THE    BLADDEB 

I.     Inflammation  of  the  Pelvis  of  the  Kidney — Pyelitis 806 

II.    Nephrolithiasis 810 

III.  Tuberculosis  of  the  Genito-urinary  Apparatus KIT 

IV.  Hydronephrosis 820 

V.     Cystitis 822 

VI.     New  Growths  in  the  Bladder ". 829 

VII.     Enuresis  Nocturna 830 


LIST   OF   PLATKS 


VOLUME    I 

PLATB  ,A"N,: 

PAGE 

T.  Tertian,  Quartan,  and  Tropica i.  Forms  of  Malarial  Plasmodium  108 

II.  Rontgen  Photographs  of  Pulmonary  Tuiskkcii.osis 308 

III.  Rontgen  Photograph  of  a  Right-sided  Pneumothorax 360 

IV.  Radiogram  of  a  Stone  in  the  Right  Kidney 814 


LIST   OF  ILLUSTRATIONS   IN  TEXT 


VOLUME    I 

FIG.  page 

1.  Typhoid  bacilli.     Section  from  the  spleen 1 

2.  Typhoid  bacilli.     Pure  culture 2 

3.  Temperatures  in  typhoid  fever 7 

4.  Widal  reaction 25 

5.  Example  of  the  temperature  curve  in  relapsing  fever 40 

6.  Spirilli  of  relapsing  fever  in  the  blood 41 

7.  Example  of  a  normal  scarlet-fever  curve 45 

8.  Example  of  the  temperature  curve  in  measles 57 

9.  Example  of  the  temperature  curve  in  true  smallpox 65 

10.  The  cocci  of  erysipelas 72 

11.  Example  of  the  fever  curve  of  a  case  of  severe  facial  erysipelas  ....  75 

12.  Diphtheria  bacilli    (Loffler's  methylene  blue) 79 

13.  Diphtheria  bacilli    (Neisser's  polar  body  stain) 79 

14.  Diphtheria  bacilli.     Smear   from  the  tonsil 85 

15.  Influenza    bacilli 89 

16.  Example  of  a  double-pointed  fever  curve  in  influenza 91 

17.  Amoeba  dysenteriae 94 

18.  Comma    bacilli 100 

19.  Quotidian  intermittent  fever 112 

20.  Tertian  intermittent  fever 112 

21.  Plague  bacilli 124 

22.  Meningococcus  intracellulars  in  spinal  fluid 127 

23.  Severe  case  of  cerebro-spinal  meningitis 129 

24.  Fever  curve  in  pyemic  infection 136 

25.  Tetanus  bacilli 141 

26.  Facies  in  tetanus 143 

27.  Ganglion  cells  from  a  rabbit  showing  Negri  bodies 148 

28.  Anthrax  bacilli .153 

xix 


XX  LIST  OF  ILLUSTRATIONS  IN  TEXT 

FIG.  PAGE 

29.  Anthrax  bacilli;   spore  formation  and  spore  germination 153 

30.  Trichinae    . 157 

31.  Beginning    laryngeal    tuberculosis     .         .         .         .         .         .         .         .         .         .  179 

32.  Paralysis  of  left  vocal  cord 183 

33.  Bilateral  paralysis  of  the  posticus 184 

34.  Paralysis  of  both  internal  thyro-arytaenoid  muscles 184 

35.  Paralysis   of  the   arytsenoideus 185 

36.  Paralysis  of  the  thyro-arytsenoids  and  arytsenoideus 185 

37.  38.  Pediculated   fibromata 188 

39.  Turpentine    pipe 201 

40.  Crystals  of   fat   acids 203 

41.  Drumstick  fingers  in  a  case  of  bronchiectasis 217 

42.  Asthma  crystals  and   Curschmann's   spirals 224 

43.  Eosinophile  cells  in  the  sputum  in  bronchial  asthma 225 

44.  Advanced  pulmonary  emphysema 233 

45.  Pneumonia  diplococci  from  a  pneumonic  sputum   . 250 

46.  Bronchial  cast 255 

47.  Example  of  the  temperature  curve  in  croupous  pneumonia 263 

48.  Example  of  the  temperature  curve  in  "  intermitting "  pneumonia   .        .        .  263 

49.  Cholesterin   crystals 269 

50.  Influence  of  a  pulmonary  hemorrhage  upon  the  temperature    ....  290 

51.  Elastic  fibers  from  the  sputum  of  a  case  of  pulmonary  tuberculosis     .      .        .291 

52.  Tubercle  bacilli  in  the  sputum 291 

53.  Subfebrile  state  in  chronic  pulmonary  tuberculosis 298 

54.  Hectic  fever  in  chronic  pulmonary  tuberculosis 299 

55.  Pirquet  skin  reaction 307 

56.  Expectoration  of  a  man  who  worked  on  graphite 330 

57.  Sputum  containing  "  cells  of  heart  disease  " 336 

58.  Temperature  curve  in  pleurisy  before  and  after  tapping 358 

59.  Masses  of  actinomyces 369 

60.  Pulse  curve  in  marked  mitral  stenosis 382 

61.  Position  of  the  various  cardiac  segments  in  mitral  stenosis         ....  384 

62.  Pulse  curve  in  aortic  insufficiency 389 

63.  Pulse  curve  in  stenosis  of  the  aortic  orifice 391 

64.  Pulsus  bigeminus 399 

65.  Pseudodiepatic  cirrhosis  due  to  pericarditis   .        .        .        ...        •        •        •  449 

66.  Arteriosclerosis  of  the  ulnar  artery .-.."..  458 

67.  Radiogram  of  an  aneurism  of  the  arch  of  the  aorta       ......  462 

68.  Thrush  fungus  from  mouth 474 

69.  Plan  of  the  dentition            482 

70.  Method  of  washing  out  the  stomach 510 

71.  Hemin  crystals 517 

72.  Gastric  contents  in  cancer  of  the  pylorus 551 

73.  Gastric  contents  in  benign  stenosis •                 ■  552 

74.  Head  of  taenia  solium 628 

75.  Head   of   cysticercus   of   the   brain    ...-.....-■  628 

76.  Taenia   solium •        •  628 

77.  Eggs  of  the  commoner  intestinal  parasites 629 

78.  Head  of  taenia  mediocanellata 630 

79.  Taenia  mediocanellata 630 

80.  Head  of  bothriocephalus  latus 631 

81.  Bothriocephalus  latus •        •        •        .631 

82.  Embryo  of  bothriocephalus  latus 631 


LIST  OF   ILLUSTRATIONS   IN   TEXT 


xxi 


FIG. 

8.3.  Ascaris  Iumbricoidea     .... 

84.  Oxyuris   vermicularis    (natural   size) 

85.  Oxyuris  vermicularis,  male  ami  female  (enlarged) 
8(i.  Anchylostoma  duodenale   (natural  oize) 

87.  Anchylostoma  duodenale    (enlarged) 

88.  Egg  of  anchylostoma  duodenale  , 
8!).  Trichocephalus  dispar   .... 

90.  Leucin   and   tyrosin   crystals 

91.  Taenia  echinococcus   (enlarged) 
02,  93.   Echinococcus    scolicos 

94.  Echinococcus  hooklets    . 

95.  Different  forms  of  casts 
90.  Waxy   casts 

97.  Epithelial  cast 

98.  Simple  hot-air  apparatus  for  diaphoresis 

99.  Distoma  heniatobium 

100.  Embryos  of  filaria  .    •     . 

101.  Epithelium  from  the  pelvis  of  the  kidney 

102.  Crystals  of  triple  phosphate  and  amnionic  urate 


PAOH 

637 
637 

640 

tiin 
699 
Tiis 
70s 
709 
1-iu 
730 
73M 
700 
797 
798 
808 
825 


A   TEXT-BOOK    OF   .MEDH'LXE 


VOU'ME    I 


I.    ACUTE   GENERAL  INFECTIOUS  DISEASES 


CHAPTER    I 


TYPHOID    FEVER 

(Typhus  abdominalis.     Enteric  Fever.     Ileotyph.ua) 

.ZEtiology. — The  cause  of  typhoid  fever  is  an  infection  of  the  body  by  a 
definite  pathogenic  bacillus,  the  "  typhoid  bacillus "  discovered  by  Eberth 
and  Koch,  and  later  made  better  known  by  the  researches  of  Gaffky  and  others. 
Their  length  (see  Fig.  1)  is 
about  one  third  the  diameter 
of  a  red  blood  globule,  and 
their  breadth  equals  one  third 
their  length,  but  sometimes 
they  may  grow  out  in  long 
fibers.  It  is  not  yet  certain 
whether  spore  formation  takes 
place  in  their  interior  or  not. 
The  typhoid  bacilli  show  a 
very  active  spontaneous  move- 
ment in  water,  caused  by  very 
fine  filiform  threads  which 
Loftier  was  the  first  to  demon- 
strate on  the  surfaces  and 
the    ends    of   the    rods.      The 

typhoid  bacillus  is  closely  re- 
1/1  .        J  .pig.  1. — Typhoid  bacilli,     feection  from  the  spleen, 

lated    to    the    Bacterium    coli  800  :  l.    (From  Flugge.) 

communis     (Escherich),    but 

differs  from  the  latter  by  not  fermenting  grape  sugar  and  not  curdling  milk, 
though  acidulating  it.  Colon  bacilli,  in  contrast  to  typhoid  bacilli,  produce 
indol  in  meat  bouillon,  generating  a  foul  odor.  The  most  important  differen- 
tial method  depends,  however,  on  the  different  behavior  of  the  two  forms  of 
bacilli  toward  the  blood  serum  of  a  typhoid  patient  (see  under  serum  diag- 
nosis). The  special  characteristics  of  the  typhoid  bacillus,  in  its  growth  on 
various  nutritive  media,  cannot  be  here  detailed.  Attention  is,  however,  called 
to  the  fact  that  typhoid  bacilli  can  also  thrive  if  deprived  of  oxygen,  which 
fact  enables  us  to  understand  their  increase  within  the  intestine. 

The  typhoid  bacilli  have  thus  far  been  found  chiefly  in  the  typhoidal  infil- 
trations in  the  intestine,  where  they  lie  between  the  cells,  and  also  in  single 
foci  in  the  mesenteric  glands,  the  spleen,  the  liver,  the  kidneys,  the  pleura,  the 

1 


2  ACUTE  GENERAL  INFECTIOUS  DISEASES 

meninges,  in  typhoidal  foci  in  the  bones,  in  muscle  abscesses,  in  abscesses  of 
the  thyroid  gland,  in  the  inflamed  and  enlarged  testicle,  in  the  gall  bladder 
(where  the  bacilli  may  remain  alive  for  years  without  producing  symptoms), 
etc.  They  are  often  found  in  the  stools  of  typhoid  patients  and  also  in  the 
fluid  obtained  by  puncture  of  the  fresh  splenic  tumor  (in  one  quarter  to  one 
third  of  all  cases),  in  the  gall  bladder,  sometimes  in  the  urine,  also  in  the 
blood  taken  from  a  spot  of  roseola,  and  finally — a  fact  of  great  practical  im- 
portance— they  are  present  in  the  blood  of  typhoid  patients. 

Numerous  attempts  have  been  made  to  produce  typhoid  fever  artificially 
by  introducing  pure  cultures  of  the  typhoid  bacilli  into  the  bodies  of  animals, 
but  the  results  of  these  efforts  have  not  yet  proved 
^     /7iv'//    f /v*  perfectly   harmonious.      The   main   cause   of  the   dis- 

' '/i,,  f\"-V  /  ^/^.  crepancy  is  probably  that  animals  are  in  general  very 
slightly  susceptible  to  the  disease.  At  any  rate,  the 
attempts  at  artificial  infection  up  to  this  date  have 
proved  successful  only  in  cases  when  the  animals  sub- 
jected to  the  experiment  (rabbits,  guinea  pigs)  have 
received  large  amounts  of  the  typhoid  bacilli  directly 

pIG  2. Typhoid  bacilli.      ^o  a  vem  or  i11^0  the  abdominal  cavity  (E.  Frankel 

Pure  culture.  and  Simmonds ) ,  or  when  the  bacilli  have  been  intro- 

duced directly  into  the  duodenum  (A.  Frajikel). 
Even  here  we  have  to  do  rather  with  the  intoxication  of  the  animals  than  with 
an  actual  infection.  For  the  pathological  changes  of  typhoid  fever  are  but 
little  developed  in  the  animals,  and  the  injected  bacilli  themselves  appear  to 
be  for  the  most  part  destroyed  within  the  body  of  the  animal  experimented 
upon  (Fliigge  and  Sirotinin,  and  others).  Normal  body  fluids  have  the 
ability  to  destroy  a  certain  number  of  the  typhoid  bacilli  that  have  entered 
the  organism  ("bactericidal  power"),  and  to  dissolve  them.  This  solution 
of  the  bacteria  is  the  main  source  of  the  poisons  that  lead  to  the  intoxication 
in  typhoid  fever.  Attempts  to  produce  the  disease  by  mixing  the  dejecta  of 
typhoid  patients  with  animals'  food  have  thus  far  been  invariably  unsuccessful. 
Investigation  of  the  setiology  of  typhoid  fever  must  be  directed  to  ascer- 
taining in  what  manner  and  through  what  channels  the  specific  typhoid  bacilli 
penetrate  into  the  human  body,  and  what  circumstances  are  then  essential  to 
their  further  development  and  to  the  display  of  their  pathogenic  properties. 
It  is  almost  universally  believed  that  typhoid  bacilli,  as  a  rule,  do  not  have 
any  permanent  existence  outside  the  human  body.  Sometimes,  under  favor- 
able conditions,  they  may  remain  alive  for  months  in  .a  dry  state  (as  in  linens 
or  clothes)  as  well  as  in  moist  earth,  stagnant  water,  etc.  Often  the  conditions 
essential  to  an  abundant  development  and  transmission  of  the  bacilli  arise  in 
certain  places,  and  thus  make  it  possible  for  a  greater  or  less  number  of  per- 
sons to  absorb  the  pathogenic  poison,  and,  as  a  result,  to  be  attacked  by  typhoid 
fever.  In  this  way  occur  the  numerous  greater  or  smaller  epidemics  of  typhoid 
fever  in  contrast  to  the  sporadic  cases,  which  are  likewise  possible,  and  are 
not  infrequent.  If  an  epidemic  of  typhoid  appears  in  a  place  till  then  entirely 
free  from  the  disease,  we  must  always  refer,  it  to  an  importation  of  the 
disease  germs,  and  seek  their  source  in  some  previous  case  of  typhoid.  In 
some  manner,  therefore,  the  typhoid  poison  must  come  from  patients  already 
infected  with  the  disease.    The  stools  of  the  typhoid  patients  are  undoubtedly 


TYPHOID   FEVER  3 

the  greatest  factor  in  this  connection,  but  the  urine  also  often  contains  a  greal 
number  of  virulenl  typhoid  bacilli.  Of  especial  importance  is  the  fact  that, 
in  a  typhoid  epidemic,  there  are  numerous  ambulanl  individuals  who  carry 
and  discharge  typhoid  hacilli — individuals  who  do  not  seem  to  be  seriously  ill 
and  complain  of  only  indefinite  symptoms,  or  are  apparently  entirely  well. 
It  is  obvious  that  such  "  bacillus  carriers  "  are  often  greater  factors  in  the 
spread  of  the  disease  than  the  really  sick  patients  who  an-  in  bed  and  isolated. 
It  is  also  of  epidemiological  significance  that  individuals  who  have  recovered 
from  typhoid  fever  may  for  months  [and  even  years]  discharge  virulent  ty- 
phoid bacilli  in  their  dejecta. 

As  to  the  exact  manner  of  transmission  of  the  disease  (i.  e.,  the  way  in 
which  the  typhoid  bacillus  enters  the  body  of  a  well  person  from  the  external 
world)  there  were,  till  recently,  widely  differing  views.  There  were  chiefly 
two  contrasting  theories,  called,  respectively,  the  "ground-soil"  and  the 
"  drinking-water"  x  theories.  According  to  the  former,  which  was  maintained 
principally  by  Pettenkofer  and  his  pupils,  the  ground  soil  was  regarded  as 
the  chief  place  of  development  for  the  schizomycetic  fungus  of  typhoid  fever. 
The  poison  in  the  stools  must  first  be  changed  by  the  soil  before  it  becomes 
infectious.  The  "  ground  air,"  which  is  continually  rising,  carries  the  poison. 
The  chief  support  of  the  ground-soil  theory,  beyond  the  results  of  comparing 
the  character  of  the  soil  with  the  extent  of  the  epidemics,  consisted  in  the 
proof  which  Buhl  and  Pettenkofer  have  given  (taking  Munich  as  an  example, 
and  later  Berlin  and  other  places)  that  a  relation  exists  between  the  varia- 
tions of  the  standing  water  in  the  soil  and  the  frequency  of  typhoid  cases. 
It  appears  that,  when  the  water  stands  high  (near  the  surface),  fewer  cases 
occur,  and  when  it  falls  below  the  mean  height  cases  are  more  numerous. 
Pettenkofer  explained  this  relation  by  the  fact  that  the  level  of  the  ground 
water  is  certainly  an  index  of  the  moisture  and  other  conditions  of  the  soil 
upon  which  the  development  of  the  typhoid  bacilli  depends. 

This  "  ground-soil "  theory  is  no  longer  tenable.  The  observations  of  Pet- 
tenkofer only  indicate  that  the  upper  strata  of  the  soil  are  but  partial  factors 
in  the  spread  of  the  typhoid  bacilli.  Above  all,  it  is  highly  improbable  that 
the  typhoid  poison  enters  the  organism  by  inhalation.  All  experiences  show 
that  the  typhoid  bacilli  commonly  gain  entrance  by  being  swallowed;  it  is 
unquestionable  that  the  most  common  source  of  infection  is  water  used  for 
drinking  and  domestic  purposes.  This  may  become  infected  with  typhoid 
bacilli  in  the  most  varied  ways.  In  numerous  typhoid  epidemics  of  recent 
years,  a  definite  relationship  between  the  spread  of  the  disease  and  the  source 
of  the  water  has  been  demonstrated.  In  addition,  the  typhoid  bacilli  have 
often  been  found  in  the  suspected  water.  The  infection  depends,  in  many 
cases,  on  well  water  that  becomes  tainted  from  near-by  privies  or  from  other 
sources.  It  may  also  come  from  running  water.  Thus,  for  example,  wTe  so 
strikingly  often  have  outbreaks  of  typhoidal  disease  among  the  employees  in 
the  Oder  Eiver  service  at  Breslau.  Of  especial  importance,  however,  are  those 
epidemics  of  typhoid  which  arise  from  infected  water  flowing  through  pipe- 
mains  into  towns — the  sources  of  the  water  having  been  polluted  and  the  filtra- 

1  Compare  with  what  follows  the  statements  concerning  the  aetiology  of  cholera,  in  which 
disease  the  same  disputed  points  were  in  the  past  considered. 

2 


4  ACUTE   GENERAL   INFECTIOUS   DISEASES 

tion  being  insufficient.  The  yearly  endemic  prevalence  of  typhoid  in  certain 
cities  (Hamburg,  Munich,  St.  Petersburg,  etc.)  is  explained  by  the  condition 
of  the  water  in  the  conduits ;  it  has  already  been  frequently  shown  that  typhoid- 
can  be  almost  completely  checked  by  improvement  in  that  direction.  Not 
infrequently  the  transmission  of  the  typhoid  bacilli  from  water  occurs  indi- 
rectly— as,  for  example,  by  means  of  ice,  artificial  mineral  waters,  washed 
vegetables  and  other  food  stuffs,  and,  above  all,  by  watered  milk,  which  is  an 
especially  good  culture  medium  for  typhoid  bacilli. 

Direct  contagion  of  typhoid  through  the  air  does  not  exist.  Although  its 
importance  is  not  to  be  overestimated,  there  is  a  certain  amount  of  danger 
of  transmission  of  the  disease  from  a  typhoid  patient  to  his  environment. 
Nurses,  physicians,  and,  in  hospitals,  other  patients  in  the  same  ward,  not 
infrequently  become  infected  by  soiling  of  the  hands  with  stools  or  urine,, 
kitchen  utensils,  linens,  etc.  The  more  unfavorable  the  surroundings  (over- 
crowded neighborhoods,  filth)  the  more  readily  can  such  types  of  contact- 
infection  occur.  The  isolation  of  the  typhoid  patient  is  therefore  desirable 
under  any  circumstances.  Physicians  may  also  become  infected  by  post-mor- 
tem examination  of  typhoid  cases. 

[It  is  not  probable  that  sewer  gas  in  itself  is  an  exciting  cause  of  typhoid 
fever.  Especially  in  large  cities  typhoid  dejections  are  constantly  finding  their 
way  into  the  sewers,  which  afford  all  the  conditions  favorable  to  the  further 
growth  and  development  of  the  poison.  If,  then,  the  drainage  of  any  house 
is  defective,  the  seeds  of  the  disease  can  readily  gain  access  to  the  interior 
of  the  house  and  infect  susceptible  individuals. 

One  of  the  most  instructive  epidemics  on  record  is  that  in  Plymouth, 
Pa.,  a  town  of  eight  thousand  inhabitants.  In  the  spring  of  1885  a  dis- 
ease, at  first  supposed  to  be  of  a  strange  character,  broke  out  in  the  place,  and, 
before  it  ceased,  affected  twelve  hundred  persons,  causing  one  hundred  and 
thirty  deaths.  It  was  soon  found  that  the  malady  was  typhoid  fever,  which 
arose  from  one  case,  briefly  in  this  wise:  In  January,  February,  and  March 
there  was  a  case  of  typhoid  in  a  house  .on  a  hill  sloping  toward  a  water  supply 
of  the  town.  The  dejections  were  thrown  out  on  the  snow,  under  which  the 
ground  was  deeply  frozen.  On  March  25th  a  sudden  and  great  thaw  occurred,, 
the  water  did  not  sink  into  the  ground,  but  ran  immediately  into  the  natural 
surface  channels,  and  on  April  10th  the  epidemic  began.  There  were  reasons,, 
which  it  is  not  necessary  here  to  detail,  why  the  above  source  of  water  supply 
was  drawn  upon  to  an  unusual  degree  just  at  that  time,  but  it  has  been  shown 
that  those  who  derived  their  water  from  other  sources  were  spared  by  the 
disease.     The  original  case  came  from  Philadelphia.] 

In  almost  all  cases  the  intestine  seems  to  be  the  actual  point  of  entrance 
for  the  typhoid  poison  into  the  human  system.  This  is  shown  by  the  fact 
that  in  all  cases  which  come  to  autopsy  in  early  stages  of  the  disease,  the 
typhoid  bacilli  are  mainly  confined  to  the  lymphatic  tissues  of  the  intestine. 
The  typhoid  poison  is  swallowed,  either  directly  with  water  or  polluted  food,. 
or  after  being  in  some  other  way  introduced  into  the  mouth.  [Eaw  oysters 
grown  in  impure  waters  may  convey  the  infection. — V.]  If  not  destroyed 
in  the  stomach,  it  passes  on  in  a  viable  state  into  the  alkaline  contents  of  the 
intestine,  and  here  finds  the  conditions  essential  to  its  further  development. 
It  penetrates  at  first  into  the  lymphatic  follicles  and  Peyer's  patches,  and 


TYPHOID    HA'KR  7, 

thence  goes  on  into  the  mesenteric  glands,  the  blood  current,  the  spleen,  and 
other  organs. 

As  in  the  case  of  most  other  infectious  diseases,  the  occurrence  of  infection 
in  typhoid  is  dependent  not  only  on  outward  conditions,  but  also  on  an  indi- 
vidual predisposition,  namely,  a  varying  individual  power  of  destroying  the 
poison  that  has  entered  the  organism  before  any  harmful  effects  of  the  poison 
have  resulted.  Even  in  the  worst  typhoid  centers,  where  the  possibility  of 
infection  must  be  universal,  many  escape  the  disease. 

Age  has  an  indubitable  influence  upon  the  liability  to  the  disease.  Typhoid 
is  especially  a  disease  of  youthful,  vigorous  individuals,  of  fifteen  to  thirty 
years.  Above  that  age  it  is  much  less  frequent,  although  cases  do  occur  at 
sixty  and  even  seventy  years.  Formerly  it  was  often  said  that  young  children 
were  never  attacked;  but  this  was  because  the  disease  was  not  recognized,  for 
in  reality  it  is  only  children  under  one  year  old  who  seem  to  be  seldom  infected. 
At  a  later  age,  cases  aTe  by  no  means  rare. 

Sex  cannot  be  shown  with  certainty  to  have  an  especial  predisposing  influ- 
ence upon  the  frequency  of  typhoid  fever. 

Mental  excitement  and  gross  errors  in  diet  seem  to  predispose  to  the  disease. 
On  the  other  hand,  a  certain  immunity  has  been  alleged  to  be  given  by  many 
circumstances,  especially  pregnancy,  the  puerperal  state,  and  other  diseases 
already  existing  (tuberculosis,  heart  disease).  Most  of  these  statements  are 
shown,  however,  by  more  extended  experience,  to  be  very  doubtful.  It  is  cer- 
tain, however,  that  the  occurrence  of  typhoid  fever  gives  very  probable  though 
not  absolute  immunity  against  any  later  new  attack.  This  established  fact  of 
immunity,  not  only  for  typhoid  fever  but  also  for  several  other  infectious  dis- 
eases, has  till  recently  been  empirical.  At  the  present  time  Buchner,  Behring, 
Ehrlich,  Pfeiffer,  and  numerous  others  have  thrown  considerable  light  on  the 
problems  of  natural  and  artificial  immunity,  and  on  the  presence  of  specific  an- 
tibodies in  blood  serum  and  tissues  (antitoxins,  bacteriolysins,  agglutinins,  etc.). 

Finally,  it  must  be  mentioned  that  the  necessary  conditions  for  an  abun- 
dant development  and  conveyance  of  the  typhoid  germs  are  beyond  doubt 
dependent  on  the  season.  According  to  statistics,  most  of  the  typhoid  epi- 
demics come  in  the  months  from  August  to  November,  while  generally  the 
number  of  cases  greatly  diminishes  from  December  to  spring. 

General  Course  of  the  Disease.— Extended  experience  shows  that,  after 
infection  with  the  typhoid  poison  has  taken  place,  a  certain  time  must  elapse 
before  the  symptoms  of  the  disease  appear.  The  length  of  this  time,  the 
"  stage  of  incubation,"  is,  unlike  that  of  many  other  infectious  diseases,  not 
perfectly  definite.  On  the  average,  it  lasts  two  to  three  weeks,  sometimes  less 
time,  sometimes  longer.  During  this  period  the  patient  either  feels  perfectly 
well,  or  has  certain  slight  symptoms,  to  which  he  pays  more  or  less  attention, 
according  to  his  individual  susceptibility.  These  prodromata  consist  of  lan- 
guor, disinclination  to  exertion,  anorexia,  slight  headache,  pain  in  the  limbs, 
etc.  Often  they  last  only  a  few  clays.  Not  infrequently  the  patients  state 
afterwards  that  they  had  felt  the  disease  coming  on  for  weeks. 

The  transition  of  the  prodromata  into  the  regular  disease  takes  place 
sometimes  so  gradually  that  it  is  utterly  impossible  to  take  any  one  day  as 
the  first  of  the  illness,  in  order  to  reckon  from  it  its  duration.  It  is  usually, 
however,  the  first  symptoms  of  a  high  temperature,  chilliness,  feverishness, 


6  ACUTE   GENERAL   INFECTIOUS   DISEASES 

and  the  accompanying  increase  in  general  discomfort,  which  allow  one  to  fix, 
with  at  least  some  accuracy,  the  beginning  of  the  disease.  A  decided  initial 
rigor  is  exceptional.  After  the  fever  begins,  most  patients  soon  take  to  their 
beds,  although  it  happens  often  enough  that  the  sick  feel  either  unable  or 
unwilling  to  give  up,  and  keep  on  at  work  for  days ! 

There  have  been  manifold  attempts  to  divide  the  whole  course  of  the 
disease  into  separate  periods.  The  most  natural  division  seems  to  be  into 
the  three  stages  of  development,  height  or  fastigium,  and  decline  (stadium 
incrementi,  s.  acmes,  s.  decrementi).  Usually,  however,  physicians  reckon 
according  to  the  week  of  the  disease.  The  first  week  corresponds  to  the 
developmental  stage,  the  second,  and  in  all  severer  cases  the  third  as  well,  to 
the  fastigium,  the  fourth  (in  light  cases  the  third)  to  the  decline.  The  fol- 
lowing brief  survey  of  the  course  of  the  disease  holds  only  for  the  fully  devel- 
oped cases.  It  is  to  be  noted  that  in  individual  epidemics  there  may  be 
peculiarities  in  connection  with  the  severity  of  the  course  of  the  disease,  the 
development  of  certain  complications,  relapses,  etc. 

In  the  first  week,  the  initial  period,  the  general  symptoms  augment  rap- 
idly. The  patients  become,  in  severe  cases,  very  languid  and  feeble,  have 
generally  an  intense  frontal  headache,  and  complete  anorexia,  with  great 
thirst.  The  fever,  which  is  all  the  time  gradualty  rising,  is  recognizable  sub- 
jectively by  alternating  sensations  of  heat  and  cold,  and  objectively  by  the 
hot,  dry  skin,  the  parched  lips,  and  the  dry  and  coated  tongue.  The  sleep 
is  disturbed.  Tor  the  most  part  there  are  no  prominent  thoracic  symptoms, 
except  that  at  times  there  is  a  sense  of  oppression  in  the  chest,  or  some 
cough.  The  pulse  is  decidedly,  but  generally  not  greatly,  accelerated,  some- 
times even  now  dicrotic.  There  is  often  a  temporary  epistaxis.  The  belly 
is  not  much  swollen,  as  a  rule,  and  but  little  if  at  all  tender.  However,  the 
patients  sometimes  complain  of  abdominal  pain  as  well  as  of  backache.  There 
is  generally  constipation.  Usually  the  spleen,  even  at  this  time,  exhibits  a 
swelling  that  can  be  easily  demonstrated. 

Generally  the  fastigium  has  begun  before  the  end  of  the  first  week.  The 
severe  general  symptoms  persist  or  even  increase.  The  fever  maintains  con- 
stantly a  considerable  elevation.  The  patients  become  more  stupid.  Often 
delirium  appears,  especially  at  night.  In  the  lungs  there  is  developed  a  more 
or  less  intense  and  extensive  bronchitis.  The  abdomen  becomes  more  swollen. 
On  the  skin  of  the  trunk  appear,  generally  at  the  beginning  of  the  second 
week,  a  number  of  small,  pale-red  spots,  roseolas.  Instead  of  constipation, 
there  is  a  moderate  diarrhea.  There  are  daily  about  two  to  four  soft,  thin, 
bright-yellow  dejections. 

The  third  week,  during  which  in  the  severe  cases  the  symptoms  already 
mentioned  persist,  is  the  chief  time  of  the  numerous  complications  and  of 
especial  clinical  events,  about  which  we  shall  speak  below  at  length.  If  the 
disease  takes  a  favorable  course,  there  comes  at  the  end  of  the  third  week  a 
decline  of  the  fever;  and  then  the  general  symptoms  also  improve,  as  a  rule. 
The  mind  becomes  clearer,  the  patient  sleeps  better,  and  gains  some  appetite. 
The  pulmonary  and  digestive  symptoms  abate ;  convalescence  gradually  begins. 

We  will  begin  the  presentation  of  the  chief  peculiarities  by  speaking  of 
the  course  of  the  fever. 


TYPHOID   FEVER 


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Course  of  the  Fever. — Observation  of  the  temperature   in   typhoid   i-   so 

absolutely  essential  for  the  estimation  of  each  individual  case  that  no  scien- 
tific physician  ought  to  treat  a  case 

without  regular  measurement  of  the 
temperature.  The  measurements 
should  be  taken,  if  possible,  in  the 
rectum.  Their  frequency  must,  of 
course,  be  modified  by  circum- 
stances, but  it  will  probably  be  pos- 
sible to  have  three  or  four  measure- 
ments daily.  At  night,  especially  if 
the  patients  are  asleep,  it  is  gen- 
erally not  requisite  to  take  the 
temperature.  A  general  idea  of 
the  course  of  the  fever  can  be 
gained  only  by  representing  the 
separate  measurements  graphically 
in  a  continuous  "temperature 
curve." 

The  typical  curve  of  typhoid 
fever  (see  Fig.  3)  falls  naturally 
into  three  or  four  divisions.  The 
first  division  is  the  initial  period, 
or  the  pyrogenetic  stage,  and  is  sel- 
dom observed,  since  at  this  time  the 
patients  are  generally  not  yet  under 
the  doctor's  care.  The  initial  pe- 
riod of  the  fever  lasts,  as  a  rule, 
some  three  or  four  days,  seldom 
longer;  and  during  this  time  the 
temperature  rises,  generally  by 
gradual  steps,  so  that  the  morning 
as  well  as  the  evening  temperature 
is  each  clay  about  2°  or  3°  F.  (1°  to 
1.5°  C.)  higher  than  on  the  day 
before.  A  sudden  and  considerable 
rise  of  temperature,  such  as  occurs 
in  many  other  diseases,  is  very 
rarely  seen  in  the  beginning  of  ty- 
phoid fever. 

The  second  division  of  the  curve 
represents  the  so-called  fastigium, 
and  corresponds  to  the  height  of 
the  disease.  During  this  time  the 
fever  presents,  in  most  of  the  se- 
verer   cases,    the    general    character  3  g  §§  £  M  fa 

of  " febris  continua" — i.e.,  the 

spontaneous   remissions   of  the   fever   seldom   exceed   2°    F.    (1°    C).      Al- 
most always  the  lower  temperatures   come   in  the  morning  hours,   and  the 


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8  ACUTE   GENERAL   INFECTIOUS   DISEASES 

higher  in  the  evening.  In  cases  of  average  severity  the  morning  remissions 
touch  102°  to  103°  F.  (39°  to  39.5°  C),  and  the  evening  exacerbations  104° 
to  105°  F.  (40°  to  40.5°  C).  Temperatures  which  reach  or  exceed  106°  F. 
(41°  C.)  are  seen  only  in  very  severe  cases.  Considerable  morning  remissions 
are  always  a  favorable  symptom,  while  morning  temperatures  of  104°  F. 
(40°  C.)  or  higher  generally  show  the  case  to  be  severe.  The  duration  of  the 
fastigium  varies  with  the  severity  and  obstinacy  of  the  case.  It  may  last  only 
a  few  days  or  one  and  a  half  to  two  weeks;  in  violent  cases  still  longer. 

In  many  cases  of  slight  or  average  severity  the  period  of  decline  follows 
directly  on  the  fastigium;  but  in  severe  cases  there  frequentty  intervenes 
another  stage,  which  Wunderlich  has  graphically  named  the  "  ambiguous " 
period.  The  temperature  curve  becomes  irregular  and  more  variable.  The 
morning  remissions  may  be  great,  even  reaching  the  normal,  while  the  even- 
ing temperatures  are  often  still  very  high.  This  stage  has  accordingly  been 
termed  the  "  period  of  the  steep  curves."  It  may  be  said  that  in  general  the 
longer  a  case  of  typhoid  lasts  the  more  irregular  will  be  the  course  of  the  fever. 

The  last  stage — i.e.,  in  cases  of  slight  or  average  severity  the  third  stage, 
and  in  severe  cases  commonly  the  fourth — is  the  period  of  defervescence  or 
recover}''.  The  peculiarit}^  of  this  period  in  typhoid  fever  is  that  the  fall  of 
the  fever  is  never  by  crisis,  but  always  gradually,  by  lysis.  Commonly  the 
temperature  descends  by  degrees,  so  that  on  each  new  day  the  morning  remis- 
sions as  well  as  the  evening  exacerbations  are  1°  to  2°  F.  (0.5°  to  1°  C.)  lower. 
The  zigzag  form  of  curve,  in  which  there  are,  of  course,  very  frequently 
slight  irregularities,  must  be  taken  as  the  rule.  The  duration  of  the  defer- 
vescence generally  exceeds  that  of  the  initial  period.  It  lasts  five  to  eight 
days,  often  longer.  It  is  not  very  seldom  that  in  defervescence  the  morning 
remissions  become  from  the  first  very  marked,  even  reaching  the  normal  tem- 
perature, while  the  evening  exacerbations  become  daily  less  and  less,  until 
they,  too,  are  not  above  the  normal.  A  third  form  of  decline  is  much  less 
frequent,  in  which  the  morning  remissions  become  every  day  greater,  while 
the  evening  temperature  persists  for  some  clays  at  about  the  same  height. 
Several  times  we  have  seen  the  fever  take  on  a  tertian  type  during  recovery. 

To  this  outline  must  be  added  a  number  of  observations  of  jDractical 
importance. 

The  initial  period  does  not  exhibit  especial  variations  from  the  course 
we  have  stated.  Its  entire  duration  is  bounded  by  certain  relatively  narrow 
limits. 

The  fastigium  presents,  as  already  mentioned,  the  greatest  varieties  in  its 
duration.  In  light  cases  it  is  wholly  wanting,  so  that  these  consist  only  of  a 
period  of  gradually  rising  fever,  and  of  a  gradual  defervescence  almost  imme- 
diately consecutive  to  the  rise.  The  entire  duration  of  such  light  cases  is 
only  one  and  a  half  to  two  weeks.  In  other  and  tolerably  frequent  cases, 
which  are  often  tedious,  but  still  for  the  most  part  are  light,  the  fever  is  not 
continuous,  but  remittent.  The  difference  between  the  morning  and  evening 
temperatures  amounts  to  3°  or  4°  F.  (1.5°  to  2°  C),  but  the  absolute  height  of 
the  temperature  is  often  not  very  considerable,  so  that  the  temperature  curve 
at  first  leads  to  error  and  excites  suspicion,  for  example,  of  tuberculosis.  We 
have  seen  in  Leipsic  a  number  of  cases  in  which  the  fever  was  perfectly  inter- 
mittent during  almost  the  entire  illness,  and  for  two  to  three  weeks  after- 


TYPHOID   FEVER  9 

noon  elevations  reaching  lor  F:  (40°  C.)  or  more  daily  succeeded  normal 
morning  temperatures.     These  cases  had  the  general  course  of  lighl  attacks. 

Various  influences,  not  to  speak  of  therapeutic  interference,  may  produce 
a  considerable  temporary  remission  of  temperature  in  the  course  of  the  fas- 

tigium.  Such  a  remission  sometimes  occurs  spontaneously  from  the  seventh 
to  the  tenth  clay  of  the  disease.  If  a  marked  intestinal  hemorrhage  happene 
(vide  infra),  the  temperature  generally  falls  several  degrees  centigrade,  and 
the  less  frequent  instances  of  severe  epistaxis  have  the  same  o  fleet.  If,  in  female 
patients,  abortion  or  premature  delivery  occurs,  we  often  observe  a  similar 
considerable  fall  of  temperature,  even  without  severe  attendant  hemorrhage. 
Perforation  of  the  intestine  often  causes  the  temperature  to  fall  rapidly.  At 
times  the  occurrence  of  mental  disturbances  effects  a  moderate  though  notice- 
able lowering  of  temperature.  Those  great  and  sudden  depressions  of  tem- 
perature remain  to  be  mentioned  which  are  accompanied  by  a  very  small  but 
exceedingly  rapid  pulse  and  general  prostration.  Every  such  collapse,  if 
severe,  is  a  most  dangerous  event,  and  demands  prompt  and  energetic  medical 
treatment   (vide  infra). 

The  development  of  local  complications,  such  as  pneumonia,  inflamma- 
tion of  the  parotid  gland  or  of  the  middle  ear,  etc.,  is  generalby  accompanied 
by  a  considerable  rise  of  temperature.  The  fever  in  such  cases  often  becomes 
more  irregular.  This  indicates  the  great  practical  value  of  thermometry. 
Almost  every  new  rise  of  temperature  or  any  considerable  change  in  the  ordi- 
nary course  of  the  temperature  has  its  special  cause,  and  is,  therefore,  a  warn- 
ing to  the  attending  physician  to  be  vigilant.  The  cause  of  the  change  in 
the  temperature  is  often  not  apparent  until  two  or  three  days  later. 

The  period  of  defervescence  departs  most  frequently  from  its  typical 
behavior  by  being  lengthened  out  into  a  "  stage  of  retardation."  The  morn- 
ing temperature  is  then  generally  normal,  while  in  the  evening  slight  or 
moderate  elevations  continue.  The  reason  for  this  long  continuance  of  the 
fever  may  frequently  be  found  in  some  not  yet  completely  healed  local  com- 
plication, but  often  no  such  lesion  can  be  demonstrated.  Then  we  are  com- 
monly inclined  to  surmise  sluggish  intestinal  ulcers  which  will  not  heal,  or 
trouble  in  the  mesenteric  glands,  etc.  This  slow  fever  may  continue  for 
weeks.  It  is  prone  to  follow  severe  cases,  but  lighter  attacks,  especially  in 
elderly  or  feeble  patients,  may  also  take  on  this  sluggish  character  at  a  rela- 
tively early  period.  To  these  last-mentioned  cases  must  finally  be  added  a 
few  others  in  which,  during  the  whole  course  of  typhoid  fever,  no  febrile  tem- 
perature at  all,  or  only  a  very  slight  rise,  can  be  detected. 

Entrance  into  complete  convalescence  is  shown  with  far  greater  certainty 
by  the  absence  of  elevations  of  temperature  than  by  any  other  single  symp- 
tom. There  sometimes  come,  however,  temporary  elevations  of  temperature 
•during  convalescence,  following  some  error  in  diet,  long-continued  constipa- 
tion, or  mental  excitement.  In  other  cases  the  new  fever  depends  on  some 
local  sequela?,  e.g.,  a  boil  or  a  glandular  abscess.  Often,  however,  the  most 
accurate  investigation  fails  to  demonstrate  a  cause.  Especially  in  the  begin- 
ning of  convalescence  there  sometimes  comes  a  high  fever,  or  even  a  rigor, 
which  may  recur  several  times,  but  which  soon  gives  place  to  a  normal  tem- 
perature. Generally  no  definite  cause  for  these  brief  but  decided  elevations 
of  temperature  can  be  pointed  out.     Perhaps  we  might  consider  the  possi- 


10  ACUTE   GENERAL  INFECTIOUS   DISEASES 

bility  of  some  affection  of  the  mesenteric  lymph-glands.  These  sudden  and 
great  elevations  have  seldom  any  grave  significance. 

This  new  fever  which  we  have  just  described  is  best  termed  febrile  recru- 
descence, or  febrile  sequela,  in  contrast  with  the  proper  typhoid  relapse. 
That  is,  after  typhoid  fever  has  ended,  the  whole  process  may  be  repeated; 
and  this  occurrence  is  called  a  relapse.  Particulars  as  to  the  behavior  of  the 
fever  in  such  cases  will  be  considered  below,  in  connection  with  all  the  other 
peculiarities  of  typhoid  relapses. 

Phenomena  and  Complications  Relating  to  the  Separate  Organs.1 — Before 
we  undertake  a  detailed  discussion  of  the  individual  symptoms  of  typhoid 
fever,  we  must  first  make  a  brief  general  statement  which  is  of  very  great 
significance  for -the  correct  understanding  of  almost  every  infectious  disease. 
We  include  among  the  direct  typhoidal  symptoms  all  those  morbid  phenomena 
which  are  produced  immediately  by  the  typhoid  bacillus  itself  or  by  its  toxic 
chemical  action;  but,  on  the  other  hand,  every  patient  sick  with  typhoid 
fever  is  exposed  to  many  secondary  infections  (so-called  mixed  infections) 
from  the  intestinal  ulcers,  from  the  mouth,  in  the  lungs,  etc.,  whose  invasion 
is  rendered  possible,  or  at  least  rendered  easier,  by  the  preexisting  typhoid 
infection.  All  the  morbid  symptoms  arising  in  this  way,  which  unite  with 
the  pure  typhoidal  symptoms  in  making  up  the  whole  picture  of  the  disease, 
must,  strictly  speaking,  be  termed  complications  of  typhoid.  In  the  indi- 
vidual case  it  is  often  hard  to  decide  whether  a  particular  symptom  is  of  a 
typhoidal  nature  or  a  complication.  We  must,  however,  hold  fast  to  the 
essential  difference  between  these  two  kinds  of  morbid  phenomena,  if  we 
would  obtain  a  deep  insight  into  the  nature  and  origin  of  the  whole  course 
of  the  disease. 

1.  Digestive  Organs,  Mouth,  Ears,  Parotid. — We  think  it  best  to  begin 
our  consideration  of  the  more  special  symptoms  with  the  phenomena  refer- 
able to  the  intestinal  canal,  for  the  reason  that  the  anatomical  changes  in 
the  intestine  are  pathognomonic.  Indeed,  these  alterations  may  sometimes 
become  of  surpassing  import  in  a  clinical  point  of  view,  although  in  the 
majority  of  cases  the  intestinal  symptoms  are  clinically  not  nearly  so  promi- 
nent as  the  general  symptoms  that  result  from  the  infection  of  the  system 
as  a  whole. 

The  characteristic  typhoid  lesion  of  the  intestine  consists  of  an  affection 
of  Peyer's  patches,  most  marked  in  the  lower  part  of  the  ileum.  In  the  first 
week  the  patches  swell  gradually  (stage  of  medullary  infiltration).  The  rest 
of  the  mucous  membrane  exhibits  at  the  same  time  more  or  less  marked 
symptoms  of  simple  catarrhal  inflammation.  In  the  second  week,  necrotic 
crusts  form  on  the  surface  of  the  patches,  which  are  cast  off  in  the  third 
week,  leaving  behind  the  typhoid  ulcers.  Toward  the  end  of  the  third  week 
the  ulcers  clean  up,  and  then  in  the  fourth  week,  if  the  case  takes  a  favor- 
able course,  the  ulcers  heal.  Smooth  scars  are  formed,  often  diffusely  pig- 
mented. Experience  shows  that  these  scarcely  ever  lead  to  stricture  of  the 
intestine.  The  same  process  also  goes  on  in  a  greater  or  less  number  of  the 
solitary  follicles  as  well  as  in  the  Peyer's  patches  themselves.     We  may  add 

1  To  avoid  repetition,  we  have  in  what  follows  united  a  description  of  the  anatomical  changes- 
with  the  presentation  of  the  clinical  symptoms. 


TYPHOID   FEVER  ]  1 

that  probably  in  lighter  cases  oiTtyphoid  (vide  infra)  there  is  often  qo  actual 
ulceration.  The  swelling  of  the  lymphatic  tissue  subsides  in  tin-  case  before 
sloughing  occni's.  We  have  already  mentioned  the  occurrence  of  typhoid 
bacilli  in  Peyer's  patches  and  the  intestinal  follicles. 

The  number  and  size  of  the  ulcers  formed  have  no  direct  relation  what- 
ever to  the  severity  of  the  case.  Although  very  extensive  lesions  in  the  intes- 
tine are  often  found  in  cases  that  end  fatally,  yet,  on  the  other  hand,  we 
observe  fatal  cases  in  which  only  a  few  ulcers  are  found  in  the  intestine.  In 
cases  with  extensive  intestinal  lesions  we  often  see  follicular  ulcer-  in  the 
colon  as  well  as  in  the  small  intestine   (colo-typhoid) . 

The  clinical  symptoms  referable  to  the  intestinal  canal  are,  as  we  have 
said,  prominent  only  in  exceptional  cases.  In  the  beginning  of  typhoid  Ei 
there  is  usually  constipation.  This  may  last  throughout  the  illness,  so  thai 
the  patients  have  but  one  dejection  in  every  two  or  three  days,  or  often  none 
at  all  unless  an  enema  be  given.  As  a  rule,  a  moderate  diarrhea  begins 
during  the  second  week.  There  are  two  to  four  stools,  or  sometimes  more, 
each  day.  These  usually  have  a  characteristic  bright-yellow  color.  On  stand- 
ing, they  divide  into  an  upper,  cloudy,  and  quite  liquid  layer,  and  a  lower 
layer  composed  of  yellow,  crumbly  masses.  They  have  generally  an  alkaline 
reaction,  and  upon  microscopic  examination  they  are  found  to  contain,  besides 
remnants  of  the  ingesta  and  granular  detritus,  a  few  epithelial  cells,  round 
cells,  many  crystals  of  triple  phosphate,  and  numberless  bacteria.  Pfeiffer 
and  other  investigators  have  been  able  frequently,  although  not  invariably, 
to  demonstrate  the  true  typhoid  bacilli  in  the  dejecta  by  means  of  special 
methods  of  cultivation. 

Severe  diarrhea  (ten  or  more  stools  daily)  is  relatively  infrequent.  In 
some  bad  cases  we  have  seen  the  stools  take  on  a  dysenteric  character.  The 
autopsy  showed  in  these  cases  unusually  severe  lesions  of  the  colon  and  a 
diphtheritic  inflammation  of  its  mucous  membrane.  They  were  probably  sec- 
ondary complications. 

Gaseous  distention  affecting  the  intestine,  and  especially  the  colon,  is  very 
frequent ;  a  slight  but  evident  gaseous  distention,  with  a  fluctuating,  "  air- 
cushion  "  feeling,  is  a  very  valuable  symptom  in  the  diagnosis  of  typhoid 
fever,  but,  as  a  rule,  the  meteorism  is  moderate.  Indeed,  severe  cases  of 
typhoid  are  observed  in  which  the  abdomen  always  remains  concave.  Marked 
tympanites  is  always  an  unpleasant  complication.  We  saw  one  case,  which 
ended  fatally,  with  very  great  tympanites,  in  which  the  lesions  were  almost 
exclusively  in  the  colon,  and  it  was  the  enormous  distention  of  its  entire 
length  which  had  so  swollen  the  abdomen.  The  gurgling  noise  that  can  often 
be  produced  by  pressure  in  the  ileocecal  region,  even  at  the  beginning 
of  the  disease,  depends  on  the  localized  distention  of  the  bowel  in  that  region. 
It  is  to  a  certain  degree  characteristic,  although,  of  course,  of  no  great  diag- 
nostic importance.  Abdominal  pain  is  often  entirely  absent.  Some  patients, 
however,  complain  of  abdominal  pain  during  almost  the  entire  illness.  On 
pressure,  the  belly  is  generally  somewhat  sensitive,  but  the  tenderness  is 
seldom  extreme.  It  is  more  apt  to  be  marked  when  there  is  constipation. 
Often  such  tenderness  is  due  to  a  participation  of  the  peritoneum  in  the  dis- 
ease, even  when  there  is  no  perforation  (vide  infra). 

There   still   remain  two  symptoms  of  the  greatest  practical  importance, 


12  ACUTE   GENERAL   INFECTIOUS   DISEASES 

both  of  which  have  a  direct  connection  with  the  intestinal  lesions :  they  are 
intestinal  hemorrhage  and  perforation. 

Intestinal  hemorrhages  in  the  course  of  typhoid  are  almost  always  due  to 
the  erosion  of  the  walls  of  blood  vessels  in  connection  with  the  formation 
and  throwing  off  of  the  crusts  of  the  ulcers.  The  hemorrhages  occur,  there- 
fore, most  frequently  toward  the  end  of  the  second  and  during  the  third  week. 
The  blood  pours  out  into  the  intestine,  and  is  passed  with  the  stools.  Its 
amount  may  be  small,  or  it  may  reach  to  one  or  two  pints,  or  even  more. 
Its  color  is  generally  rather  dark.  The  later  discharges  are  generally  tarry. 
Liebermeister  states  that  he  has  observed  intestinal  hemorrhages  in  7.3  per 
cent  of  typhoid  patients,  and  Griesinger  in  5.3  per  cent.  We  have  ourselves 
found,  in  earlier  statistics  from  the  medical  wards  in  Leipsic,  45  intestinal 
hemorrhages  in  472  cases,  i.  e.,  in  9.5  per  cent.  In  individual  epidemics  the 
frequency  varies  greatly.    It  rose  in  one  year,  for  example,  to  eighteen  per  cent. 

Intestinal  hemorrhage  is  always  a  grave  symptom.  Even  slight  hemor- 
rhages deserve  consideration,  for  they  may  be  the  precursors  of  severer  ones. 
Yet  intestinal  hemorrhage,  even  if  profuse,  is  not  necessarily  fatal.  Of  the 
above  forty-five  eases  of  typhoid  with  hemorrhage,  twenty-six  ended  in  com- 
plete recovery.  In  eight  cases,  death  occurred  as  the  immediate  result  of 
the  loss  of  blood.     Eleven  ended  fatally  after  a  time. 

After  every  considerable  intestinal  hemorrhage,  the  symptoms  of  general 
ana?mia,  often  even  of  collapse,  appear.  The  fall  of  the  bodily  temperature 
has  been  already  mentioned.  The  hemorrhage  has  sometimes  a  favorable  influ- 
ence on  severe  cerebral  symptoms,  for  consciousness  succeeds  to  the  previous 
stupor  or  delirium.  Often  the  hemorrhage  is  directly  followed  by  recovery 
from  the  disease. 

Much  more  ominous  than  the  intestinal  hemorrhage  is  the  occurrence  of 
perforation,  as  a  result  of  the  breaking  through  of  a  typhoid  ulcer  into  the 
abdominal  cavity,  because,  almost  without  exception,  this  is  followed  by  a 
purulent  or  even  ichorous  peritonitis.  Peritonitis  is  never  caused  by  the 
typhoid  bacillus  itself,  but  by  pyogenic  organisms  (cocci,  perhaps  bacterium 
coli?)  which  enter  the  abdominal  cavity  with  the  contents  of  the  intestine. 
Tbe  amount  of  fluid  peritonitic  exudation  is,  as  a  rule,  not  very  great.  The 
serous  membrane  is  often  found  covered  merely  with  a  fibrino-purulent  or 
purulent-hemorrhagic  deposit.  The  occurrence  of  perforation  is  sometimes 
marked  by  a  violent  pain  suddenly  felt  by  the  patient;  but  it  may  also,  in 
severe  cases  associated  with  profound  prostration,  take  place  insidiousty.  The 
abdomen  is  generally  (not  always)  greatly  distended  and  very  tender  on 
pressure,  so  that,  even  in  stupor,  patients  groan  while  being  examined.  If  gas 
has  entered  through  the  opening  into  the  peritoneal  cavity,  we  often  observe 
absence  of  the  ordinary  dullness  over  the  liver;  but  this  symptom  is  to  be 
employed  cautiously  as  a  factor  in  diagnosis,  for  absence  of  hepatic  dullness 
may  also  result  from  distended  intestines  lying  in  front  of  the  liver.  When 
perforation  has  occurred,  the  patient  soon  looks  collapsed,  with  cheeks  fallen 
in  and  sharp,  cool  nose.  Frequent  eructations  and  vomiting  often  follow. 
The  pulse  becomes  small  and  very  frequent.  The  temperature  generally  falls 
as  the  peritonitis  begins,  and  later  it  usually  undergoes  great  variations. 

Perforation  of  the  intestine  occurs  most  frequently  in  the  third  or  fourth 
week  of  the  disease,  and  much  oftener  in  men  than  in  women.     In  sluggish 


TYPHOID    FEVER  13 

cases,  however,  we  cannot  be  without  apprehensions  of  it  till  a  late  period. 
The  perforation  generally  takes  place  in  a  coil  of  the  lower  pari  of  the  small 
intestine,  in  the  right  side  of  the  pelvis,  seldom  in  the  vermiform  appendix 
or  in  the  colon.  With  few  exceptions,  death  conies  quickly,  after  a  \'<-w  daye 
at  latest.  Only  when  the  perforation  is  small  and  the  Intestines  have  become 
agglutinated  at  the  onset  is  the  course  of  the  peritonitis  slower,  bo  that  the 
symptoms  are  less  violent  and  cause  death  in  a  week  or  ten  days.  Oiii  of 
fifty-six  fatal  typhoid  cases  in  the  Leipsic  medical  clinic  we  lost  five,  or  nine 
per  cent,  from  peritonitis  following  perforation.  Here  and  there  a  case  of 
recovery  has  been  reported,  probably  resulting  from  a  limitation  of  the  peri- 
tonitis through  speedy  adhesion  of  the  intestines.  Regarding  the  possibility 
of  operative  cure,  vide  infra. 

It  should  be  mentioned  here  that  sometimes  in  typhoid  fever  a  local  or 
general  peritonitis  may  occur  through  direct  extension  of  the  process  to  the 
serous  membrane  without  actual  perforation.  We  have  seen  in  one  case,  as 
the  result  of  the  peritonitic  bands  and  false  membranes,  complete  occlusion 
of  the  intestine   (ileus),  and  death. 

Swelling  of  the  mesenteric  lymph-glands  (less  often  of  the  retro-perito- 
neal glands  as  well)  is  found  in  typhoid  almost  as  constantly  as  the  anatom- 
ical changes  in  the  intestine.  Sometimes  they  break  down,  i.  e.,  suppurate. 
In  cases  that  have  passed  through  the  disease  we  often  find  considerable 
deposits  of  lime  in  the  glands.  These  changes  have  a  certain  clinical  impor- 
tance; for,  as  already  mentioned,  we  may  often  venture  to  refer  a  more  or 
less  tedious  recurrent  febrile  state  which  has  no  other  demonstrable  cause  to 
this  lesion  of  the  mesenteric  glands.  In  some  rare  cases  a  general  peritonitis 
has  been  observed  as  a  result  of  the  bursting  of  a  suppurating  gland. 

The  swelling  of  the  spleen  (acute  splenic  tumor)  is,  in  typhoid  fever  as 
well  as  in  many  other  acute  infectious  diseases,  one  of  the  most  constant 
symptoms.  The  enlargement  of  the  spleen  can  often  be  demonstrated  as  early 
as  the  end  of  the  first  week,  and  is,  therefore,  of  considerable  diagnostic  im- 
portance; but  percussion  of  the  spleen  is  sometimes  decidedly  difficult  and 
deceptive  in  this  disease  because  of  the  existence  of  tympanites.  The  surest 
demonstration  of  splenic  enlargement  is,  therefore,  always  by  means  of  palpa- 
tion, which,  after  a  little  practice,  gives  a  positive  result  in  the  majority  of 
cases.  Absence  of  splenic  tumor  in  typhoid  is  most  frequently  observed  in 
elderly  patients.  The  spleen  may  diminish  considerably  in  size  after  severe 
intestinal  hemorrhage.  Pain  in  the  splenic  region,  resulting  from  tearing  of 
the  distended  capsule,  is  comparatively  rare.  The' splenic  infarctions  which 
sometimes  occur  may,  in  exceptional  cases,  jjrove  the  starting  point  of  a 
peritonitis. 

Hepatic  symptoms  are  seldom  seen  in  typhoid  fever,  except  that  there  may 
be  a  moderate  swelling  of  the  liver.  The  anatomical  changes  of  "  parenchym- 
atous degeneration,"  and  the  frequent  formation  in  the  liver  of  the  small 
lymphomata  which  Wagner  discovered,  have  no  clinical  significance.  The 
bile  secreted  is  generally  pale  and  scanty.  This  is  a  partial  explanation  of 
the  light  color  of  the  stools.  The  frequent  presence  of  typhoid  bacilli  in  the 
bile  has  been  noted  above.  A  very  rare  complication,  which  we  ourselves 
observed  in  one  case,  is  acute  yellow  atrophy  of  the  liver. 

The  stomach  presents  no  especial  anatomical  changes  in  typhoid.     Ano- 


14  ACUTE   GENERAL  INFECTIOUS   DISEASES 

rexia  is  an  almost  invariable  symptom  in  the  beginning  and  during  the  course 
of  all  severer  cases.  There  is  seldom  any  desire  for  food  till  recovery  begins; 
but  then,  if  convalescence  is  undisturbed,  the  appetite  soon  attains  an  enviable 
keenness.  Vomiting  in  the  beginning  or  course  of  the  disease  is  an  excep- 
tion, unless  after  some  error  in  diet.  We  have  already  mentioned  it  as  a 
symptom  of  peritonitis.  Persistent  singultus  is  a  truly  tormenting  symptom 
that  has  been  repeatedly  observed  by  us. 

The  changes  in  the  mouth  and  throat  of  typhoid  patients  deserve  the  careful 
attention  of  the  physician.  The  lips  and  tongue  are  in  severe  cases  dry  and  fis- 
sured. The  lips  are  often  covered  with  dry,  black  crusts,  sometimes  described 
as  a  "  fuliginous  coating."  The  tongue  is  apt  to  be  thickly  coated  at  first,  but 
later  cleans  off  from  the  edges  and  tip.  In  severe  cases,  especially  if  the  mouth 
is  not  properly  cleansed,  a  rather  severe  stomatitis  may  occur  and  produce 
superficial  ulceration  of  the  buccal  mucous  membrane  and  of  the  edges  of  the 
tongue.  The  gums  sometimes  become  spong}^  and  are  apt  to  bleed,  as  if 
scorbutic. 

Actual  sore  throat  is  in  general  rare.  The  difficulty  in  swallowing,  often 
complained  of  by  patients,  is  generally  due  to  dryness  of  the  pharynx.  In 
certain  epidemics,  however,  the  occurrence  of  sore  throat  at  the  beginning  of 
the  illness  has  been  frequently  observed.  It  may  even  happen  that  this  early 
sore  throat  is  accompanied  by  an  erythema  diffused  over  the  body,  so  that  at 
first  susjjicions  of  scarlet  fever  arise.  The  cases  are  very  interesting  and  quite 
rare  (although  we  have  repeatedly  seen  them)  in  which  disturbances  of  swal- 
lowing exist  with  the  general  typhoid  symptoms  from  the  beginning.  On  ex- 
amining the  fauces  we  see  on  the  tonsils  peculiar  white,  slightly  elevated  spots, 
which  later  form  superficial  ulcers.  After  a  time  these  places  heal,  and  in 
other  respects  the  disease  pursues  a  normal  course.  The  suspicion  is  justified 
that  in  these  cases  there  is  a  specific  typhoidal  disease  of  the  tonsils  (due 
to  the  typhoid  bacillus  itself),  and  such  cases  are  called  tonsillar  or  pharyn- 
geal typhoid  (analogous  to  the  laryngeal  typhoid,  pneumo-typhoid,  and  nephro- 
typhoid,  to  be  mentioned  later).  In  such  cases  the  typhoid  bacilli  have  prob- 
ably attacked  the  tonsils  at  their  first  invasion.  It  should  also  be  mentioned 
that  in  severe  cases  there  is  often  an  extensive  growth  of  thrush  in  the  mouth 
and  throat,  and  this  may  spread  quite  a  distance  clown  the  oesophagus. 

The  changes  in  the  mouth  and  throat  are  of  especial  interest,  for  the  reason 
that  they  may  be  directly  propagated  to  important  neighboring  organs.  Start- 
ing from  the  pharyngeal  cavity,  the  pathogenic  agent,  probably  in  most  cases 
the  staphylococcus,  may  penetrate  through  the  Eustachian  tube  into  the  middle 
ear.  Thus  arise  those  inflammations  of  the  middle  ear  which  are  not  very  rare 
in  severe  cases  of  typhoid,  and  which  lead  to  perforation  of  the  membrana 
tympani  and  to  purulent  discharges  from  the  ear.  The  not  infrequent  inflam- 
mation of  the  parotid  gland  is  also,  as  we  believe,  occasioned  in  a  similar  way, 
the  inflammatory  agent  (sometimes  the  typhoid  bacilli  themselves)  reaching 
the  parotid  gland  from  the  mouth  by  way  of  Steno^s  duct.  We  do  not  regard 
the  otitis  and  parotitis  as  especial  localizations  of  the  typhoid  poison,  but 
as  secondary  diseases  for  the  occurrence  of  which  typhoid  fever  merely  fur- 
nishes the  occasion,  as  when  the  mouth  is  imperfectly  cleansed. 

Purulent  otitis  in  typhoid  fever  can  easily  be  overlooked  at  first,  since 
stuporous  patients  only  rarely  complain  of  pain  in  the  ear  or  of  deafness. 


TYPHOID   FEVER  15 

In  addition,  it  is  to  be  here  observed  thai  the  difficulty  in  hearing  does  not 
always  depend  on  middle-ear  disease.  We  have  seen  several  cases  of  almosi 
complete  (transient)  deafness,  combined  with  marked  tinnitus,  for  which 
absolutely  no  cause  could  be  found  on  examination  with  an  ear  speculum; 
in  all  probability  there  was  some  disease  of  the  inner  ear  or  of  the  audi! 
nerve.  The  parotitis  appears  most  frequently  in  the  third  week,  and  generally 
on  one  side,  though  sometimes  on  both.  It  almost  always  becomes  purulent, 
and  discharges  either  externally  or  into  the  external  auditory  meatus,  unless 
there  is  a  timely  incision. 

2.  Organs  of  Respiration. — Affections  of  the  lungs  are  among  the  most 
frequent  and  important  complications  of  typhoid  fever,  hut  are  for  the  mosl 
part  not  a  direct  result  of  the  typhoid  infection,  but  pure  complications.  The 
bronchitis  very  often  found  in  severe  cases,  and  especially  in  patients  who  do 
not  come  till  late  under  proper  care,  certainly  is  dependent  on  the  imperfect 
expectoration  of  the  bronchial  secretions  and  on  the  inhalation  of  inflamma- 
tory agents  coming  from  the  mouth  and  throat. 

Numerous  cases  of  typhoid  of  slight  or  average  severity,  under  proper 
care,  rim  their  course  without  any  considerable  bronchitis.  In  many  other 
eases,  and  even  severe  ones,  the  bronchitis  remains  within  moderate  bounds, 
especially  if  the  patient  is  brought  promptly  under  proper  care  and  treatment ; 
but  in  severe  cases,  when  marked  disturbances  of  the  nervous  system  arise, 
and  the  patient  in  his  stupor  expectorates  little,  swallows  things  the  wrong 
way,  and  lies  all  the  time  on  his  back,  passive  and  collapsed,  the  occurrence 
of  a  severe,  diffuse  bronchitis,  especially  in  the  lower  lobes  of  the  lungs,  can 
hardly  be  avoided.  Nor  in  such  cases  is  there  generally  a  mere  bronchitis,  but 
a  more  or  less  extensive  catarrhal,  lobular  pneumonia,  to  be  classed  therefore 
under  the  so-called  inhalation  pneumonias  (cf.  chapter  on  lobular  pneumonia). 
What  was  formerly  termed  "  hypostatic  pneumonia  "  is  also  almost  invariably 
to  be  put  in  this  group. 

From  the  way  in  which  these  pulmonary  disorders  arise,  we  can  understand 
why  the  bronchitis  sometimes  takes  on  a  putrid  character,  and  why  the  lobular 
infiltrations  are,  in  severe  cases,  transformed  into  genuine  gangrene.  If  such 
spots  touch  the  pleura,  they  occasion  the  development  of  a  pleurisy  which  is 
almost  always  purulent.  In  rare  cases,  pneumothorax  may  arise  as  a  sequel  to 
the  perforation  of  a  gangrenous  infiltration  into  the  pleural  cavity.  Various 
circumstances  promote  the  occurrence  of  pulmonary  symptoms.  Thus  we  find 
it  especially  easy  for  a  severe  bronchitis  and  its  sequela?  to  be  developed,  in  the 
case  of  elderly  persons,  or  the  kyphoskoliotic,  or  the  corpulent,  or  patients  who 
have  previously  suffered  from  emphysema  or  cardiac  disease. 

The  subjective  thoracic  symptoms,  in  typhoid  patients  who  have  pulmonary 
complications,  are  generally  not  very  prominent.  It  is  only  occasionally  that 
patients  complain  in  the  early  stages  of  typhoid  fever  of  pain,  and  of  a  sense  of 
oppression  in  the  chest,  or  of  cough,  or.  of  a  stitch  in  the  side ;  and  even  when 
such  symptoms  exist,  the  physical  examination  may  give  comparatively  insig- 
nificant results.  The  severer  pulmonary  complications  are  seen  mainly  in 
those  whose  intelligence  is  more  or  less  blunted,  and  who,  therefore,  make  little 
complaint,  are  not  much  disturbed  by  the  dyspnoea,  and  cough  and  expectorate 
little.  A  careful  physical  examination  alone  can  enlighten  us  as  to  their  con- 
dition.    On  auscultation,  sibilant  rhonchi  are  the  chief  signs  observed  in  the 


16  ACUTE   GENERAL   INFECTIOUS   DISEASES 

milder  cases..  In  the  severer  ones  there  are  moist,  fine,  and  coarse  rales, 
especially  numerous  toward  the  base  of  the  chest.  If  there  are  abun- 
dant moist  rales,  we  may  infer  that  there  is  a  lobular  pneumonia,  although 
this  cannot  be  demonstrated  with  certainty  till  the  separate  islets  of  in- 
filtration unite  into  a  more  extensive  solidification,  so  as  to  afford  dullness  on 
percussion. 

Kontgen-ray  examination  affords  valuable  information  as  to  the  condi- 
tion of  the  lungs;  for  evident  reasons,  however,  such  an  examination  can  only 
rarely  and  with  difficulty  be  made. 

In  addition  to  the  pulmonary  lesions  already  mentioned,  genuine  croupous 
or  lobular  pneumonia  does  occur  in  typhoid  fever.  This  is  often  an  actual  com- 
plication, dependent  upon  a  secondary  infection  with  the  genuine  pneumonia 
diplococcus.  Such  a  pneumonia  may  come  on  early  or  sometimes  during  con- 
valescence, and  affect  both  the  upper  and  lower  lobes.  There  is  probably  also 
a  true  typhoid  pneumonia  caused  by  the  entrance  of  typhoid  bacilli  into  the 
lungs.  Such  a  pneumonia  cannot  at  present  be  recognized  anatomically,  but 
only  by  bacteriological  investigation.  Especial  interest  attaches  to  those  cases 
of  typhoid  fever  which  begin  with  a  lobar  pneumonia.  Often  there  is  at  first 
not  the  slightest  suspicion  of  a  typhoid  fever,  for  the  disease  is  regarded 
as  an  ordinary  croupous  pneumonia ;  but  it  is  usually  to  be  noticed  that  the 
illness  does  not  begin  suddenly  with  a  rigor,  but  more  gradually,  and  that 
from  its  incipiency  the  constitutional  symptoms,  the  headache  and  splenic 
tumor,  are  more  prominent  than  is  usually  the  case  in  pneumonia.  At  the  end 
of  the  first  week's  illness  there  is  no  crisis,  but  persistent  fever.  Now  the  pul- 
monary symptoms  often  retreat  more  and  more  to  the  background,  while,  on 
the  contrary,  diarrhea  and  rose-spots  appear.  The  spleen  is  enlarged.  In 
short,  the  clinical  picture  of  typhoid  is  developed.  It  is  not  unnatural  to  sup- 
pose, although  there  is  yet  no  absolute  proof  of  the  fact,  that  in  these  cases, 
which  are  fittingly  termed  "  pneumo-typhoid,"  the  infection  with  the  typhoid 
bacilli  has  taken  place  exceptionally  in  the  pulmonary  tissue,  and  that,  there- 
fore, the  first  pathological  changes  are  developed  in  the  lungs. 

Laryngeal  Lesions. — The  same  causes  which  produce  the  bronchitis  result 
also  in  a  simple  catarrhal  laryngitis,  with  hoarseness.  This  is  in  severe  cases 
accompanied  by  superficial  ulcers  on  the  vocal  cords  or  the  posterior  wall  of  the 
larynx.  Sometimes,  again,  the  lesion  is  due  to  mechanical  causes,  constituting 
the  so-called  "  decubitus  laryngis."  The  disorders  which  attack  the  less  super- 
ficial structures  of  the  larynx  are  fortunately  rare.  Chief  among  them  is  a 
laryngeal  perichondritis  affecting  the  arytenoid  cartilages.  This  complica- 
tion is  justly  regarded  as  of  bad  omen,  and  may  lead  to  the  rapid  develop- 
ment of  oedema  of  the  glottis,  with  great  laryngeal  obstruction  and  threat- 
ening suffocation.  These  severe  laryngeal  affections  in  typhoid  are  regarded 
by  some  authorities,  especially  by  Klebs,  as  always  the  direct  effect  of  the 
infecting  poison;  but  in  most  cases  they  are  probably  due  to  an  invasion 
of  staphylococci  or  some  similar  microbes.  We  have  several  times  seen  croup 
in  typhoid  fever,  and  it  is  a  very  dangerous  symptom.  In  regard  to  their 
origin  most  of  these  mild  and  severe  laryngeal  affections  in  the  course  of 
typhoid  fever  are  to  be  regarded  as  secondary  inflammations;  but  specific 
typhoid  disease  of  the  larynx  also  seems  to  exist.  The  cases  are  of  interest 
where  the  whole  morbid  process  begins  with  a  severe  laryngitis   ("  laryngeal 


TYPHOID    FEVER  17 

typhoid")  and  is  followed  later  by  the  ordinary  symptoms  of  typhoid  (vide 
supra,  pharyngeal  typhoid). 

Among  symptoms  referable  to  the  mucous  membrane  of  the  nose,  epis- 
taxis  is  important.  It  occurs  in  the  beginning  of  typhoid  with  tolerable  fre- 
quency, and  is  in  one  way  not  unfavorable,  for  ii  often  mitigates  the  patient's 
headache.  At  a  later  period  nosebleed  may  become  a  most  unpleasant  com- 
plication, as  it  is  sometimes  very  difficult  to  check.  We  have  even  seen  one 
fatal  case  due  to  persistent  nosebleed.  Other  nasal  symptoms  are  exceptional. 
There  is  an  old  saying  that  typhoid  never  begins  with  a  coryza. 

3.  Nervous  System. — The  old  term  "nervous  fever/'  which  is  still  used 
by  the  laity,  shows  how  frequent  and  severe  are  the  nervous  derangements 
which  occur  in  typhoid.  In  cases  of  any  severity  there  is  almost  always  a  cer- 
tain dullness  of  intellect,  often  amounting  to  apathy  and  somnolence.  The 
patients  give  monosyllabic  and  incomplete  answers  to  all  questions,  and  their 
statements  about  their  previous  history  are  often  disordered,  and  contradic- 
tory. There  may  even  be  sopor  or  a  deep  coma  in  the  worst  cases.  All  cases 
of  this  sort  in  which  there  was  a  condition  of  intellectual  enfeeblement  were 
termed  by  the  old  physicians  "  febris  nervosa  stupida"  ■  in  contrast  to  the 
"  febris  nervosa  versatilis,"  that  form  in  which  abnormal  mental  activity  or 
delirium  predominates.  In  severe  cases  delirium  is  very  frequent.  It  is  gen- 
erally worse  at  night,  and  at  times  when  the  patient  happens  to  be  left  alone. 
Very  often  he  tries  to  leave  his  bed,  because  of  his  delusions,  and  talks  of  per- 
sons and  things  with  which  he  was  formerly  familiar;  or  he  is  very  noisy  and 
restless,  sometimes  shrieking  from  groundless  fears.  We  may  add  that  these 
diverse  nervous  symptoms  frequently  succeed  one  another,  or  appear  in  com- 
bination. Sometimes  a  soporose  patient  may  be  heard  softly  whispering  to 
himself  in  "  muttering  delirium." 

Certain  motor  disturbances  are  often  combined  with  considerable  impair- 
ment of  consciousness.  There  is  a  slight  twitching  of  the  muscles  of  the  face 
and  extremities.  The  old  authorities  gave  the  name  subsultus  tendinum  to  the 
sudden  leaping  into  prominence  of  the  sinews  thus  caused.  It  is  best  seen  on 
the  back  of  the  hands.  In  severe  cases  the  patient  is  sometimes  observed  to 
grind  the  teeth  together;  this  is  due  to  a  cramplike  condition  of  the  muscles 
of  mastication,  and  is  justly  regarded  as  ominous.  We  often  see  persistent 
tremor  of  the  extremities  and  lower  jaw;  and  it  is  especially  in  these  cases, 
as  we  have  demonstrated  upon  numerous  patients,  that  the  tendon  reflexes 
and  the  mechanical  excitability  of  the  muscles  are  much  increased.  If  deep 
coma  comes  on,  the  muscles  become  lax,  the  motions  of  the  eye  are  not  co- 
ordinated, and  reflex  excitability  diminishes,  or  is  wholly  extinguished. 

Headache  is  one  of  the  most  constant  symptoms  in  the  beginning  of  the 
disease.  It  is  usually  referred  to  the  forehead  or  temples.  The  pain  may  be 
very  violent,  and  sometimes  takes  on  almost  a  neuralgic  character.  It  almost 
always  subsides  in  the  second  week. 

If  we  seek  the  cause  of  these  nervous  symptoms,  which  are  often  so  severe, 
we  find  that  the  anatomical  changes  in  the  nervous  system,  including  the  brain, 
bear  no  relation  whatever  to  the  severity  of  the  symptoms  observed  during 
life.  We  sometimes  meet  with  minute  hemorrhages  in  the  cerebral  meninges, 
or  meningeal  opacity  or  edema,  or  a  moist  condition  of  the  cerebral  paren- 
chyma; but  the  connection  of  these  and  similar  changes  with  the  symptoms 


18  ACUTE   GENERAL   INFECTIOUS   DISEASES 

of  the  disease  is  often  more  than  doubtful.  Nor  can  the  microscopic  alterations 
in  the  brain,  which  have  been  reported,  be  regarded  as  important  and  authori- 
tative. It  is  only  in  very  rare  cases  that  large  cerebral  hemorrhages  or  puru- 
lent meningitis  have  been  found.  As  to  this  last,  we  should  always  be  very 
cautious  in  making  a  diagnosis,  as  symptoms  which  would  seem  to  be  most 
conclusively  meningeal — such  as  stiffness  of  the  neck,  rigidity  of  the  whole 
spinal  column,  and  occipital  headache — may  appear  in  typhoid  patients,  and 
yet  the  autopsy  may  show  no  trace  of  meningitis. 

For  a  long  time  it  was  thought  that  the  nervous  symptoms  were  mainly  a 
result  of  the  fever ;  i.  e.,  the  effect  of  the  overheated  blood  on  the  nervous 
system  (Liebermeister  and  others).  But  this  belief  is  not  supported  by  un- 
biased clinical  observation. 

Although  it  is  undeniable  that  elevated  temperature  has  a  harmful  influ- 
ence on  the  nervous  system,  yet  in  numerous  cases  there  is  no  relation  between 
the  height  of  the  fever  and  the  severity  of  the  nervous  derangements.  There 
are  cases  in  which  the  fever  remains  continuously  high  for  days,  while  the 
patient  feels  perfectly  comfortable  and  presents  no  symptoms  of  any  impor- 
tant cerebral  disturbance.  The  opposite  class  of  cases  is  still  more  numerous, 
in  which  from  the  very  start  there  is  always  a  low  temperature,  and,  not- 
withstanding, the  most  severe  nervous  symptoms  •  arise.  Friintzel  and  others 
have  published  very  striking  cases  of  this  sort.  Hence  we  must  seek  for 
some  other  special  cause  of  the  nervous  symptoms,  and  according  to  our  pres- 
ent views  this  cause  should  be  sought  in  the  intoxication  from  the  toxins  result- 
ing from  the  infection.  That  the  appearance  of  the  nervous  symptoms  is 
dependent,  not  only  on  the  material  causes,  but  also  on  the  susceptibility  of 
the  individual,  is  shown  by  the  fact  that  certain  patients  are  especially  prone 
to  exhibit  marked  nervous  phenomena ;  for  example,  hard  drinkers,  "  nervous  " 
individuals,  those  who  have  suffered  violent  emotional  disturbances  shortly 
before  the  onset  of  the  disease,  etc. 

The  true  psychoses  most  often  take  the  form  of  mental  confusion.  The 
patients  lose  their  orientation  of  time  and  of  place  as  well  as  of  persons  and 
of  the  nature  of  their  environment.  By  careful  examination,  disturbances 
of  memory  in  reference  to  recent  events  and  illusions  of  memory  can  readily 
be  demonstrated.  Occasional^,  after  delusions  of  a  terrifying  nature,  states 
of  violent  excitement  may  ensue.  In  other  cases  the  mental  state  takes  on 
more  of  a  depressive  character. 

We  have  repeatedly  seen  patients  in  such  a  state  that  they  would  lie  almost 
motionless  in  bed,  with  eyes  open,  and  perhaps  assert  that  they  were  dead !  In 
other  cases  there  is  mental  excitement,  sometimes  combined  with  hallucinations, 
or  there  is  confusion  of  ideas.  In  one  case,  in  a  girl  who  was  evidently  pre- 
disposed to  nervous  disorders,  we  saw  typical  hysterical  insanity  break  out 
during  the  fever.  Sometimes  the  mental  excitement  at  the  beginning  of  a 
relapse  terminates  in  actual  insanity.  All  these  typhoid  psychoses  have,  in 
general,  a  favorable  prognosis.  They  end  in  complete  cure  after  a  number 
of  weeks  or  at  most  after  several  months. 

We  have  still  to  mention  a  number  of  nervous  diseases  that  develop  in  the 
course  of  typhoid  or  after  its  decline.  Neuralgia  is  sometimes  seen,  as  well  at 
the  beginning  as  at  the  end  of  the  disease.  It  is  most  frequent  in  the  regions 
supplied  by  the  trigeminus  and  the  occipital  nerves.     Great  hyperesthesia  of 


TYPHOID   FEVER  19 

the  skin  and  muscles  is  not  rare  during  convalescence.     It  attacks  the  lower 
•extremities  by  preference.     Paralysis  of  single  muscles  (e.g.,  of  the  sern 
magnus),  or  paralysis  of  a  single  extremity,  has  been  repeatedly  observed  ae  a 
sequela.    The  paralysis  is  generally  of  the  atrophic  variety,  and   ie  probably, 

as  a  rule,  due  to  neuritis.     Ataxia  and   spastic  paralysis  of  the  lower  ex- 
tremities  are   rare   sequelae.      They    probably   depend   on   secondary    myelitic 

disease. 

Finally,  there  are  sometimes  developed,  either  in  the  course  or  a1  the 
conclusion  of  typhoid  fever,  the  symptoms  of  a  localized  cerebral  disorder 
(e.  g.,  hemiplegia,  aphasia,  etc.),  the  anatomical  cause  of  which  varies.  There 
may  he  a  hemorrhage  or  an  embolism,  and  probably  in  still  other  eases  a  local- 
ized encephalitis.  Other  nervous  diseases  (multiple  sclerosis,  for  example) 
rarely  follow  typhoid. 

4.  Circulatory  System. — Disturbances  of  the  heart  such  as  to  produce 
striking  anatomical  changes  are  rare.  The  pericardium  macroscopic-ally  almost 
always  appears  normal ;  the  slight  mitral  or  aortic  endocarditis  sometimes 
found  has  no  clinical  significance.  The  disturbances  in  the  cardiac  muscle 
seem  more  important.  It  is  often  more  flabby  than  normal.  The  cavities, 
especially  on  the  right  side,  are  often  dilated.  With  the  naked  eye  we  fre- 
quently see  in  the  muscle  itself  cloudiness  or  fatty  changes.  Microscopic 
lesions  are  usually  present  and  are  much  more  pronounced.  They  consist 
ordinarily  of  a  granular  ("albuminoid")  or  more  rarely  of  a  fatty  or  hyaline 
degeneration  of  the  fibers,  and  of  genuine  inflammatory  foci  of  interstitial 
myocarditis  (Hayem,  Komherg).  ISTo  marked  disease  of  the  cardiac  ganglia 
has  as  yet  been  found. 

The  clinical  significance  of  these  changes  should  not,  we  believe,  be  over- 
estimated. In  all  probability  they  are  often  without  serious  consequences  and 
disappear  completely  with  recovery  from  the  disease.  Sudden  death  (heart- 
failure?)  occurs  in  typhoid,  but  it  is  very  rare  (see  the  chapter  on  diphtheria). 
Permanent  disturbances  of  the  heart  after  typhoid  are  also  rare.  When  they 
occur  they  are  perhaps  due  to  the  passage  from  an  acute  myocarditis  to  a 
chronic  interstitial  degeneration. 

The  pulse  in  typhoid  is  almost  always  accelerated,  but  in  general  it  is  true 
that  in  this  particular  disease  the  frequency  of  the  pulse  is  not  increased  in 
proportion  to  the  height  of  the  temperature.  On  the  average,  the  heart  beats 
90  to  100  times  a  minute.  This  comparatively  low  pulse  rate  occurs  so  often 
that  it  has  some  diagnostic  value.  When  it  remains  at  140  or  higher,  in  adults, 
it  is  always  an  unfavorable  symptom.  The  more  accelerated  pulse  rates  gen- 
erally occur  with  the  onset  of  some  complication.  Temporary  accelerations 
are  easily  produced  by  mental  excitement  or  bodily  exertion,  as  by  sitting 
up  in  bed.    In  convalescence  the  rate  is  not  infrequently  subnormal. 

Slight  irregularities  of  the  pulse  are  not  rare,  either  in  the  acme  or  the 
decline  of  typhoid.  Marked  irregularity  is  always  a  grave  symptom,  although 
in  many  cases  it  passes  off  and  the  patient  recovers. 

Dicrotism,  due  to  loss  of  tension  in  the  wall  of  the  artery,  is  so  common 
that  it  is  still  regarded  by  elderly  physicians  as  characteristic  of  typhoid, 
although  it  often  occurs  in  the  same  way  in  other  acute  diseases.  In  many 
severe  cases  the  height  and  strength  and  fullness  of  the  pulse  may  cause  no 
alarm,  but  often  the  pulse  is  notably  weak  and  small.  This  is  due  not  only 
3 


20  ACUTE   GENERAL   INFECTIOUS   DISEASES 

to  the  influence  of  the  disease,  but  also  to  the  previous  condition  of  the  indi- 
vidual (vide  infra). 

The  diminished  cardiac  activity  may  result  in  venous  thrombosis,  espe- 
cially in  the  lower  extremities  and  in  a  crural  vein.  This  sometimes  causes 
swelling  of  one  of  the  lower  extremities  during  the  later  stages  or  convales- 
cence. The  swollen  member  generally  regains  its  normal  size  after  some  weeks. 
In  other  cases  the  thrombosis  occurs  earlier,  and  in  patients  who  are  still  too 
vigorous  to  suffer  from  cardiac  weakness,  so  that  we  are  forced  to  the  conclu- 
sion that  there  is  some  local  specific  cause,  a  local  thrombo-phlebitis  due 
either  to  the  typhoid  bacillus  itself,  or,  more  probably,  to  the  invasion  of 
the  walls  of  the  vein  by  some  secondary  infection.  A  possible,  but  fortunately 
infrequent,  result  of  these  thrombi  in  the  lower  limbs  is  pulmonary  embolism 
and  sudden  death. 

In  severe  cases,  which  end  in  death,  cardiac  thrombi  are  sometimes  found, 
with  emboli  in  the  lungs,  spleen,  kidneys,  or  other  organs. 

(Edema  of  the  ankles  and  legs  is  very  often  seen  in  convalescents,  especially 
when  they  first  get  out  of  bed.  It  is  due  to  the  weakness  of  the  heart  and 
changes  in  the  vesicular  walls.  Once  we  saw  a  general  dropsy  develop  at 
the  end  of  a  severe  attack  in  a  girl  of  fourteen.  The  autopsy  disclosed 
no  other  possible  cause  for  it  than  the  extreme  atrophy  and  flabbiness  of  the 
heart. 

5.  The  Blood. — As  in  most  febrile  diseases  associated  with  great  emacia- 
tion, so  in  typhoid  in  severe  cases  the  number  of  red  blood  corpuscles  (and  cor- 
respondingly the  amount  of  hemoglobin  in  the  blood)  is  much  diminished. 
We  found,  for  example,  2,800,000  to  3,200,000  in  a  cubic  millimeter.  In 
milder  cases  the  figures  do  not  differ  materially  from  normal.  It  is  a  fact  of 
greater  interest  and  also  of  distinct  diagnostic  importance  that  it  has  been 
found  (first  by  Halla,  later  confirmed  by  all  subsequent  observations)  that  in 
typhoid,  in  contrast  with  numerous  other  acute  febrile  diseases— pneumonia, 
erysipelas,  sepsis,  etc. — there  is  no  persistent  leucocytosis.  On  the  other  hand, 
following  the  transient  leucocytosis  of  the  first  week,  there  is  a  pronounced 
leucopenia — i.  e.,  a  diminution  in  the  number  of  leucocytes  in  the  blood. 
The  white  blood  cells  drop  to  5,000  to  3,000  per  cubic  millimeter,  and  in  severe 
cases  even  lower.  The  decrease  chiefly  affects  the  neutrophile  cells;  however,, 
the  eosinophiles  also  almost  entirely  disappear.  At  the  onset  of  the  disease 
there  is  a  marked  diminution  in  the  number  of  lymphocytes;  they  are  greatly 
increased  in  the  later  stages.  After  the  fever  disappears,  the  leucocytic  count 
rises  rapidly,  and  now  there  is  not  infrequently  observed  a  distinct  lympho- 
cytosis and  an  eosinophilia.  In  the  presence  of  inflammatory  complications 
the  blood  picture  often  changes — great  increase  in  the  neutrophiles.  Concern- 
ing the  presence  of  typhoid  bacilli  in  the  blood,  see  below. 

6.  The  Skix. — The  eruption  seen  in  typhoid  fever  is  characteristic  and  ex- 
tremely important  in  diagnosis.  The  roseolas  or  rose  spots  (light  red,  slightly 
elevated  spots)  appear  at  the  beginning  of  the  second  week,  usually  on  the 
trunk,  and  chiefly  on  the  abdomen  and  back.  The  number  varies  greatly. 
Barely  they  are  entirely  absent,  most  often  in  elderly  persons.  Sometimes  they 
are  very  abundant,  and  extend  to  the  thighs,  the  arms,  and  even  to  the  neck 
and  face.  Often  they  vanish  after  a  few  days,  but  they  may  persist  much 
longer.     In  the  latter  case  they  may  become  to  a  very  slight  degree  petechial,. 


TYPHOID   FEVER  21 

so  that  they  will  not  entirely  disappear  on  pressure.  They  often  occur  in  suc- 
cessive crops.  We  have  even  seen  several  cases  where  new  rose  spots  kept  com- 
ing for  some  days  after  the  fever  had  disappeared. 

As  to  other  cutaneous  eruptions,  we  may  mention  first  of  all  that  herpes 
lahialis  is  so  rare  in  typhoid  that  in  cases  of  doubtful  diagnosis  it  is  a  factor  in 
excluding  that  disease.  Miliaria,  urticaria,  and  superficial  pustules  are  some- 
times observed.  Occasionally  little  bluish  spots  appear,  especially  on  the  trunk. 
These  used  to  be  called  "  taches  bleuatres"  (pelioma  typhosum)  :  but  later 
observations  show  that  they  are  not  connected  with  typhoid  fever.  They 
are  due  to  pediculi.  We  might  use  the  term  pelioma  typhosum  to  designate  the 
kind  of  vesicles  which  we  have  repeatedly  seen  on  the  abdomen  in  severe  cases. 
They  are  about  the  size  of  peas,  and  have  sero-hemorrhagic  contenl  -.  Moils  and 
superficial  abscesses  are  frequent,  especially  as  disagreeable  sequela?  in  convales- 
cence from  severe  attacks.  There  are  often  abscesses  of  the  sweat  glands  in  the 
skin  of  the  axilla  during  convalescence.  All  these  and  similar  cases  of  suppura- 
tion in  typhoid  fever  do  not  depend,  as  a  rule,  upon  the  original  cause  of  the 
disease,  but  upon  secondary  pathogenic  germs,  especially  the  staphylococcus, 
for  whose  entrance  the  typhoid  process  has  merely  prepared  the  way.  Exten- 
sive ecchymoses  are  very  rare,  and  are  symptomatic  of  a  general  hemorrhagic 
diathesis.  Petechia?  are  frequent  during  recovery.  They  are  generally  seen 
in  the  follicles  of  the  skin  below  the  knee.  There  have  been  a  few  cases  of  gan- 
grene in  the  lower  extremities,  especially  in  the  toes.  We  saw  in  one  patient 
an  extensive  gangrene  of  the  skin  of  the  abdomen,  probably  due  to  the  ice  hag 
employed. 

Finally,  we  must  mention  that  bedsores  are  prone  to  develop  in  severe  or 
neglected  cases.  The  localities  most  often  attacked  are  the  nates,  the  furrow 
between  them,  and  the  heels.  A  bedsore  may  be  so  extensive,  and  accompanied 
by  such  undermining  of  the  skin,  as  to  be  a  dangerous  or  even  fatal  com- 
plication. 

The  epidermis  often  scales  off  to  a  considerable  extent  during  convalescence 
after  a  severe  attack  of  typhoid.  Everybody  knows  how  the  hair  falls  out  after 
the  fever,  but  it  is  sure  to  grow  again.  The  nails  also  are  not  infrequently 
affected,  becoming  rough  and  brittle,  or  even  falling  off. 

7.  Muscles,  Bones,  Joints. — Zenker  has  discovered  a  degeneration  of  the 
voluntary  muscles  which  occurs  in  typhoid  as  well  as  in  other  severe  diseases. 
It  is  called  the  "  granular  "  or  "  waxy  "  degeneration.  Whether  it  has  clinical 
symptoms  cannot  be  determined.  Perhaps  it  may  explain  the  great  muscular 
hyperesthesia  which  is  often  observed,  and  the  muscular  pains,  which  may  be 
very  trying.  Severe  cases  sometimes  have  hemorrhages  into  the  muscles,  par- 
ticularly the  rectus  abdominis. 

Lesions  of  the  bones  and  joints  occur  but  seldom,  although  other  observers 
and  we  ourselves  have  repeatedly  seen  periostitis  and  osteomyelitis  in  the  ribs, 
tibia,  etc.,  following  typhoid. 

Quincke  first  described  a  typhoid  spondylitis  with  secondary  symptoms  due 
to  pressure  on  the  nerve  roots.  Its  causation  was  demonstrated  by  E.  Erankel, 
who  found  numerous  small  foci  of  typhoid  bacilli  surrounded  by  localized 
areas  of  necrosis  in  bone  marrow,  especially  in  that  of  the  vertebral  column. 
Perhaps  the  frequent  bone  pains  of  typhoid  patients  may  be  due  to  such  foci. 
The  occurrence  of  leucopenia  in  typhoid  (vide  supra)  may  also  be  due  to  these 


22  ACUTE   GENERAL  INFECTIOUS   DISEASES 

changes  in  the  bone  marrow.  The  typhoid  bacilli  are  almost  always  to  be 
found  in  the  larger,  purulent,  periostitic,  or  osteitic  areas. 

8.  Gentto-urinary  Apparatus. — Genuine,  acute,  hemorrhagic  nephritis  is 
a  very  rare  complication.  It  does  occur,  however,  and  has  even  given  rise  to 
the  establishment  of  a  special  "  renal  form  of  typhoid  fever "  (nephro- 
typhoid).  This  name  applies  especially  to  those  cases  in  which  a  severe  acute 
nephritis  is  the  predominant  symptom  at  the  start,  while  at  a  later  period 
the  course  of  the  fever,  the  intestinal  symptoms,  the  rose  spots,  etc.,  show  the 
disease  to  be  typhoid  fever.  Nephro-typhoid  is  analogous  to  pneumo-typhoid 
and  tonsillo-typhoid.  A  simple  so-called  febrile  albuminuria  occurs  very  fre- 
quently at  the  acme  of  typhoid,  and  is  not  to  be  interpreted  unfavorably.  It  is 
probably  the  result  of  that  slight  parenchymatous  degeneration  of  the  kidneys 
which  occurs  in  typhoid  with  the  same  frequency  as  in  most  of  the  other  severe 
infectious  diseases.  In  the  albuminous  urine  of  typhoid  patients  the  bacilli  are 
almost  invariably  present.  In  other  respects  the  urine  in  typhoid  presents 
the  same  peculiarities  as  in  most  other  severe  febrile  diseases :  its  amount 
is  diminished;  its  color  dark;  its  specific  gravity  increased.  The  rare  pres- 
ence of  urates  in  the  sediment  is  worthy  of  note;  this  may  bear  some  relation 
to  the  leucopenia  of  typhoid  (vide  supra).  After  cessation  of  the  fever  there 
is  often  a  marked  polyuria  (3  to  5  liters  daily  of  a  urine  of  a  low  specific 
gravity)  that  may  last  for  weeks.  It  should  be  added  that  the  urine  often 
contains  indican  and  at  the  height  of  the  disease  almost  always  gives  Ehr- 
lich's  "  diazo-reaction."  The  disappearance  of  the  latter  reaction  indicates  a 
favorable  prognosis.  If  the  reaction  persists  after  the  fever  has  disappeared, 
one  may  be  prepared  for  a  relapse.  Cystitis  occurs  not  infrequently  toward 
the  end  of  the  illness;  it  is  often  a  secondary  complication  (a  catheter  infec- 
tion, for  example),  but  may  be  a  specific  typhoid  infection. 

In  men,  orchitis  is  sometimes  observed.  Women  often  have  their  catamenia 
at  the  beginning  of  typhoid.  Later  in  the  course  of  the  disease,  and  in  con- 
valescence from  severe  attacks,  the  menses  are  often  absent  for  several  periods. 
In  pregnant  women  there  is  considerable  danger  of  abortion  or  miscarriage. 

Peculiarities  in  the  Course  of  the  Disease. — The  above  statements  show  an 
almost  inexhaustible  variet}'  in  the  possible  symptoms  and  complications  of 
typhoid.  The  course  of  the  disease  as  a  whole  may  likewise  present  many 
diverse  forms  and  peculiarities.  We  shall  attempt  merely  to  cite  the  most 
essential. 

The  numerous  light  and  rudimentary  attacks  (typhus  levissimus)  are  first 
to  be  mentioned.  It  was  not  recognized  till  lately  that  they  belonged  to 
typhoid  fever  at  all  (Griesinger).  They  used  to  have  all  sorts  of  names 
applied  to  them,  the  favorite  term  being  "  gastric  fever."  This  light  form 
lasts  from  eight  to  fourteen  days.  The  fever  is  moderate  and  often  decidedly 
remittent.  There  is  almost  no  proper  fastigium.  The  typhoid  symptoms 
are  but  slightly  developed.  There  is  no  severe  pulmonary  or  cerebral  dis- 
turbance. There  is  generally  a  moderate  diarrhea,  the  spleen  is  plainly 
enlarged,  and  often  rose  spots  can  be  found.  The  diagnosis  of  these  cases  is, 
of  course,  difficult  in  proportion  to  the  scanty  development  of  typhoid  symp- 
toms. It  is  best  established  by  demonstrating  an  etiological  relation  between 
these  cases  and  others  which  are  plainly  typhoid  fever.  A  positive  diagnosis 
can  only  be  made  by  bacteriological  methods   (vide  infra). 


TYPHOID  FEVER  23 

Abortive  typhoid  is  justly  distinguished  by  Liebermeister  from  typhus 
levis.  The  name  belongs  to  cases  which  begin  with  severe  symptoms  and 
high  fever,  as  if  they  were  going  to  be  grave,  but  in  which  these  violent 
symptoms  disappear  after  a  few  days  and  give  place  to  a  rapid  convalescence. 

On  the  other  hand,  there  are  eases  which  for  a  long  time  cause  so  little 
subjective  discomfort  that  the  patient  does  not  even  go  to  bed  (walking 
typhoid).  It  is  not  till  quite  late  that  there  occurs  a  sudden  change  \'<>\'  the 
worse,  or  some  severe  complication.  Thus  it  has  happened  that  persons  who 
were  apparently  healthy  have  suddenly  had  all  the  symptoms  of  a  Bevere 
peritonitis  due  to  perforation  and  have  died,  the  autopsy  disclosing  the  lesions 
of  the  third  week  of  typhoid  fever;  or  a  mild  typhoid  assumes  the  walking 
type  and  is  not  detected,  but  later  a  severe  or  dangerous  relapse  may  occur. 

The  individual  circumstances  are  very  important  in  weighing  each  case, 
for  they  may  modify  the  disease  in  many  ways. 

In  children  it  is  a  remarkable  fact  that  typhoid  ulcers  are  much  less  fre- 
quent than  in  adults.  This  explains  why  intestinal  hemorrhages  and  peri- 
tonitis are  much  rarer  in  children.  Marked  cerebral  symptoms  are,  on  the 
other  hand,  very  frequent.  In  severe  cases  children  sometimes  exhibit  the 
peculiar  symptom  of  a  continuous  penetrating  screaming.  In  other,  mild, 
cases  the  children  are  soporose. 

In  the  aged  the  diagnosis  of  typhoid  is  often  very  difficult,  since  the 
course  of  the  disease  is  frequently  irregular.  Generally  the  fever  is  not  very 
high,  and  it  very  seldom  exhibits  distinctly  the  type  described  above.  The 
pulmonary  or  cerebral  symptoms  predominate  as  a  rule. 

In  the  corpulent,  typhoid  fever  is  often  very  severe,  so  that  our  prognosis 
must  always  be  rather  grave,  especially  if  pulmonary  symptoms  arise. 

Hard  drinkers  are  also  in  especial  peril  in  this  as  in  all  other  acute  dis- 
eases. Dangerous  cardiac  weakness  is  prone  to  appear.  Severe  cerebral  symp- 
toms are  frequent.  It  is,  however,  surprising  that  true  delirium  tremens  is 
relatively  infrequent,  although  so  common  in  pneumonia. 

The  influence  of  previous  strong  mental  excitement  and  of  certain  already 
existing  diseases  (cardiac  disease,  emphysema,  kyphoskoliosis,  etc.)  has  been 
already  mentioned.  Finally,  we  repeat  that  often  the  different  epidemics 
present  certain  peculiarities.  For  instance,  in  one  the  type  of  the  disease 
will  be  severe,  in  another  mild.  In  one  epidemic  relapses  are  comparatively 
frequent,  in  another  exceptional.  The  same  is  true  with  regard  to  the  fre- 
quency of  the  appearance  of  certain  symptoms,  such  as  intestinal  hemorrhage, 
perforation,  pneumonia,  or  nephritis.  Indeed,  it  has  even  been  observed  that 
those  cases  which  occur  during  a  given  epidemic  in  the  same  family  or  house 
or  block  sometimes  present  striking  resemblances  to  one  another  ("group 
typhoid  "  of  E.  Wagner  and  others) . 

Eelapses  of  Typhoid  Fever. — Typhoid  fever  exhibits  in  many  cases  the 
peculiarity  of  repeating  itself  completely  after  having  run  its  entire  course 
and  disappeared.  This  process  is  called  a  relapse.  It  is  in  all  probability 
the  result,  not  of  a  fresh  infection  of  the  system  from  without,  but  of  a 
renewed  development  (a  new  generation)  of  the  germs  already  present.  One 
must  think,  however,  of  the  possibility  of  a  fresh  autoinfection.  Errors  in 
diet,  psychical  disturbances,  etc.,  sometimes  appear  to  cause  the  relapse;  usu- 
ally, however,  the  exciting  cause  cannot  be  discovered. 


24  ACUTE   GENERAL   INFECTIOUS   DISEASES 

A  typical  relapse  is  like  a  first  attack  in  all  clinical  and  anatomical  par- 
ticulars, with  this  difference,  that  everything  is  more  condensed,  and  lasts  a 
shorter  time  than  in  the  first  attack.  The  interval  between  the  two,  during 
which  there  is  no  fever,  lasts  seven  to  ten  daj^s.  It  may  be  longer,  and  is 
often  shorter.  Sometimes  the  relapse  follows  immediately  upon  recovery. 
Indeed,  it  may  even  happen  that,  before  the  patient  has  completely  recovered, 
his  temperature  begins  to  rise  again  in  the  characteristic  steplike  way.  To 
such  cases  as  this  last  the  term  recrudescence  is  applied.  Except  in  the  time 
of  its  beginning,  it  maj  be  just  the  same  as  a  genuine  relajjse.  In  the  inter- 
val between  the  two  attacks  many  persons  are  perfectly  comfortable,  and 
appear  to  be  fully  convalescent.  There  is  often,  however,  a  slight  evening 
rise  of  temperature.  It  is  noticeable  that  the  splenic  tumor  does  not  com- 
pletely disappear  after  the  first  attack  in  many  cases  which  are  followed  by  a 
relapse.    The  persistence  of  the  "  diazo-reaction  "  has  already  been  referred  to. 

The  relapse  is  generally  briefer,  as  we  have  said,  than  the  first  attack, 
seldom  lasting  more  than  fifteen  to  eighteen  days.  The  temperature  rises 
more  rapidly,  perhaps  in  two  or  three  clays.  The  fastigium  is  shorter,  the 
decline  more  abrupt.  The  absolute  height  of  the  temperature  may  be  very 
considerable,  even  exceeding  that  in  the  first  attack.  Rose  spots  appear  as 
soon  as  the  third  or  fourth  day.  The  stools  become  liquid,  the  spleen  enlarges 
again,  and  all  sorts  of  complications  may  arise.  The  danger  occasioned  by 
a  relapse  ma}^,  however,  be  overestimated.  On  the  whole,  a  relapse  is  not  so 
very  dangerous,  and  it  is  especially  noticeable  that  the  subjective  symptoms, 
such  as  headache,  are  often  slight.  A  severe  relapse  may,  however,  follow 
both  mild  and  severe  attacks.  In  other  instances  the  relapse  may  prove 
merely  rudimentary. 

The  frequency  of  relapses  varies  considerably  in  different  epidemics.  In 
Leipsic  we  had  relapses  in  about  nine  per  cent  of  all  cases,  but  in  separate 
years  the  percentage  varied  between  four  and  sixteen.  Out  of  about  five 
hundred  cases  we  have  seen  three  in  which  there  were  two  successive  and 
typical  relapses. 

Diagnosis. — The  diagnosis  of  typhoid  fever  may  be  perfectly  easy,  but,  if 
the  case  be  anomalous,  or  come  under  observation  at  a  late  period,  it  may 
be  extremely  obscure.  It  depends,  above  all,  on  the  purely  clinical  manifes- 
tations of  the  disease.  Important  factors  are  the  gradual  onset,  then  the 
height  and  course  of  the  fever,  with  no  demonstrable  localized  disease  to 
account  for  the  fever,  and  the  rose  spots.  Less  characteristic,  but  still  of 
value,  are  the  stools,  the  tympanites,  and  the  swelling  of  the  spleen.  In 
doubtful  cases,  the  persistent  slow  pulse,  the  absence  of  leucocytosis,  and  the 
"  diazo-reaction  "  ma}^  aid  in  the  diagnosis.  ^Etiological  factors,  such  as  the 
occurrence  of  undoubted  cases  of  typhoid  in  the  neighborhood,  are  of  great 
diagnostic  value  in  obscure  cases.  Sometimes  the  diagnosis  cannot  be  estab- 
lished till  the  appearance  of  certain  symptoms,  like  intestinal  hemorrhage,  a 
characteristic  mode  of  convalescence — viz.,  by  lysis — or  a  relapse.  It  is  an 
important  rule  not  to  make  a  diagnosis  of  typhoid  after  a  single  examination. 
It  is  generally  necessary  to  observe  the  case  accurately  for  several  days  before 
the  diagnosis  can  be  established.  The  differential  diagnosis  from  other  acute 
diseases,  such  as  miliary  tuberculosis,  acute  endocarditis,  meningitis,  etc.,  will 
be  considered  in  discussing  these  diseases. 


TYPHOID   FEVER  25 

The  diagnosis  is  usually  most  difficult  in  the  cases  with  au  imperfect 
history  which  are  first  seen  in  a  severe  "  typhoidal  '"  state,  will)  high  l'< 
disturbances  of  consciousness,  etc.  These  are  the  cases  in  which  we  must  also 
•consider,  beside  typhoid  fever,  miliary  tuberculosis,  acute  septic  or  pyaemic 
infection  (including  acute  malignant  endocarditis),  meningitis,  severe  " 
phoid  pneumonia,"  etc.  The  clinical  differential  diagnosis  between  typhoid 
and  these  conditions  will  be  spoken  of  Later. 

It  is  just  in  these  doubtful  cases  that  the  newer  methods  of  bacteriological 
diagnosis  render  incalculable  aid. 

The  bacteriological  diagnosis  of  typhoid  fever  is  arrived  at  by  two  means 
— first,  the  examination  of  the  blood  for  specific  properties;  secondly,  the 
direct  examination  of  the  blood  for  typhoid  bacilli.  The  first  method  (serum 
diagnosis,  Gruber-Widal  reaction)  is  based  on  the  principle  that  the  typhoid 
infection  (like  many  other  infections)  stimulates  the  development  of  specific 
""antibodies"  in  the  blood  serum  of  the  infected  patient.  Pfeiffer  was  the 
first  to  discover  that  typhoid  bacilli,  injected  in  lethal  amount  into  a  rabbit's 
abdomen,  become  disintegrated  when  a  small  quantity  of  serum  from  an 
immunized  animal  is  simultaneously  added  ("bacteriolysis").  Gruber  found 
that  the  blood  serum  from  patients  recently  recovered  from  typhoid  had  a 
peculiar  grouping,  "  agglutinating  "  effect  on  living  typhoid  bacilli,  and  Widal 
was  the  first  to  show  that  this  "  agglutination  "  could  frequently  be  observed 
during  the  course  of  the  disease. 

When  the  necessary  precautions  are  taken,  the  Gruber-Widal  reaction  is 
of  great  practical  importance.  Although  not  absolutely  diagnostic,  it  is  of 
great  weight  both  when  present  and  when  absent.  The  macroscopic  and  the 
microscopic  reactions  are  to  be  differentiated.  The  former  is  carried  out  by 
adding  one  or  more  drops  of  the  blood  serum  of  the  patient  to  a  uniformly 
cloudy  suspension  of  living  typhoid  bacilli  in  5  c.c.  of  bouillon.  The  test 
tube  is  allowed  to  stand  for  a  few  hours  (best  in  a  thermostat  at  37°  C). 
If  the  reaction  is  positive,  the  bacilli  are  agglutinated  in  a  concentration  of 
l-to-100,  or  at  least  of  l-to-50.  They  become  clumped,  sink  to  the  bottom,  the 
bouillon  becomes  perfectly  clear.  Even  mere 
characteristic  is  the  microscopical  serum  di- 
agnosis. To  one  drop  of  a  fresh  bouillon 
culture  of  typhoid  bacilli  the  serum  of  the 
typhoid  suspect  is  added  in  varying  propor- 
tions. A  drop  of  the  mixture  is  examined 
under  the  microscope.  If  the  reaction  is 
present,  the  evenly  distributed  motile  rods 
become  clumped  and  immotile  in  a  few  min- 
utes or,  at  most,  in  half  an  hour  (see  Fig.  4). 
The  blood  serum  of  typhoid  patients  shows 
this  peculiarity  to  so  great  a  degree  that  one 
drop  is  sufficient  to  give  the  reaction  with  the 
typhoid  bacilli  in  suspension  in  twenty,  thir-    FlG-  4-~^!idf  t?™aT  ^gl£ina' 

/  L  ,  1  .         ,       ,      i  „         tion  of  the  typhoid  bacilli.     (Com- 

ty,   and   even  up   to   one   hundred    drops    of       pare  wjth  pig.  2.) 

bouillon.     On  the  other  hand,  the  serum  of 

healthy  individuals,  or  of  those  suffering  from  other  diseases  than  typhoid, 

does  not  possess  this  agglutinating  power  at  all,  or  only  to  a  very  much 


26  ACUTE   GENERAL   INFECTIOUS   DISEASES 

slighter  degree.  Typhoid  is  thus  almost  invariably  present  if  agglutination 
occurs  with  a  l-to-50  to  a  l-to-100  dilution.  The  reaction  is  sometimes 
present  on  the  third  or  fourth  day  of  the  disease,  but,  as  a  rule,  not  till  the 
beginning  of  the  second  week.  Very  rarely,  it  takes  place  only  at  a  later 
period.  If  there  is  no  sign  of  agglutination  in  a  case  of  fever  of  two  weeks' 
duration,  one  may  almost  absolutely  exclude  typhoid  fever.  The  reaction 
persists  for  a  considerable  time  (months  and  even  years)  after  the  attack  of 
the  disease.  The  Gruber-Widal  reaction  can  be  obtained  with  the  serum 
from  vesicles  or  with  serous  inflammatory  exudates  of  typhoid  patients. 

The  significance  of  the  Widal  reaction  is  somewhat  limited  (E.  Stern) T 
because,  on  the  one  hand,  it  is  not  present  in  some  cases  of  typhoid  fever, 
and,  on  the  other,  the  serum  in  other  diseases  (infections  with  colon  bacilli, 
with  B.  proteus  and  icterus)  may  agglutinate  the  typhoid  bacilli.  Despite 
this,  the  Widal  reaction,  in  combination  with  the  clinical  symptoms,  remains 
of  the  utmost  value  in  the  diagnosis.  Ficker's  observation,  that  a  suspen- 
sion of  killed  and  ground-up  typhoid  bacilli  is  agglutinated  by  typhoid  serum,, 
is  of  value  in  general  practice.  Ficker's  "  typhoid  diagnosticator "  (to  be 
obtained  from  E.  Merck,  of  Darmstadt)  is  based  upon  this  possibility  of  a 
macroscopic  examination  without  the  use  of  any  bacteriological  apparatus. 

The  ultimate  achievement  of  the  bacteriological  diagnosis  of  typhoid  must, 
however,  be  the  demonstration  of  the  bacilli  in  the  body  of  the  patient.  This 
can  only  be  clone,  to  be  sure,  in  a  bacteriological  laboratory,  and  is  therefore 
not  available  in  general  practice.  But  when  it  can  possibly  be  performed, 
the  direct  proof  of  the  presence  of  typhoid  bacilli  permits  a  certainty  of 
diagnosis  that  is  not  possible  by  any  other  means.  The  search  for  the  bacilli 
in  the  urine  is,  as  yet,  of  the  least  diagnostic  value.  Of  more  importance  is 
their  demonstration  in  the  feces.  Since  the  introduction  of  the  Drigalski- 
Conradi  culture  medium  the  differentiation  between  the  typhoid  and  the 
colon  bacilli  has  become  a  much  simpler  matter.  The  medium  is  an  agar 
plate  containing  milk  sugar,  sodium  carbonate,  nutrose,  and  litmus.  Most 
of  the  other  varieties  of  bacteria  are  excluded  by  the  addition  of  "  crystal 
violet"  to  the  medium,  thus  leaving  behind  the  colon  and  typhoid  colonies. 
The  colon  bacilli  generate  lactic  acid,  and  therefore  the  colonies  are  red;  the 
typhoid  bacilli  grow  in  blue  colonies.  The  nature  of  the  latter  is  established 
by  further  examination  (agglutination,  etc.).  The  bacteriological  examina- 
tion of  the  blood  has,  however,  gained  the  greatest  significance  (Schott- 
muller).  About  20  c.c.  of  blood  are  removed  from  one  of  the  veins  of  the 
arm  by  means  of  a  Luer  syringe,  and  is  at  once  mixed  in  several  tubes  with 
liquefied  agar  at  a  temperature  of  45°  C.  (113°  F.)  and  poured  into  Petri 
dishes,  which  are  placed  in  the  incubator  at  37°  C.  (98.6°  F.).  In  positive 
cases  small  gray  colonies  appear  in  the  blood  agar  in  twenty-four  to  forty- 
eight  hours.  The  deeper  colonies  look  black,  owing  to  the  formation  of  sul- 
phid  of  iron.  The  deeper  colonies  are  typhoidal  and  must  be  subjected  to 
further  microscopical  examination.  With  careful  technic  the  method  gives 
excellent  results.  It  is  employed  in  all  typhoid  and  typhoid-suspect  cases 
in  the  Breslau  clinic.  The  positive  finding  of  typhoid  bacilli  in  the  blood 
occurs  in  at  least  ninety  per  cent  of  all  cases  of  typhoid,  and  has  made  the 
positive  diagnosis  for  us  in  many  cases  in  which  the  diagnosis  was  otherwise 
uncertain  or  even  impossible.     Even  in  the  first  days  of  the  fever  the  bacilli 


TYPHOID   FEVEB  27 

can  often  be  demonstrated  in  the  blood.  In  fatal  cases  the  bacilli  in  the 
blood  increase  greatly  in  number  shortly  before  death.  The  attempts  rec< 
made  to  grow  the  bacilli  from  smaller  quantities  of  Mood  (l-to-2  c.c.)  are  of 
great  practical  importance.  For  this  purpose  there  must  firsl  be  a  prelim- 
inary "enrichment"  of  the  bacilli.  This  is  accomplished  through  the  addi- 
tion of  sterile  bile  or  pepton  solution  to  the  blood,  and  then  placing  the 
mixture  for  twenty-four  hours  in  the  incubator. 

Prognosis. — A  perfectly  favorable  prognosis  should  never  be  made.  I 
which  seem  the  mildest  may  become  dangerous  (from  intestinal  perforation, 
etc.).  Yet,  if  there  are  good  nursing  and  good  treatment,  typhoid  fever  is 
not  a  particularly  dangerous  disease,  and  we  may  hope  for  recovery  even  in 
very  severe  attacks.  The  danger  lies,  first,  in  the  severity  of  the  infection, 
as  shown  .chiefly  (though  not  wholly)  by  the  height  of  the  fever  and  the 
intensity  of  the  general  symptoms.  A  further  danger  is  the  appearance  of 
the  complications  already  enumerated  and  discussed.  Thirdly,  the  constitu- 
tion and  condition  of  the  individual  are  important.  The  circumstances  com- 
ing under  this  head  have  likewise  been  repeatedly  mentioned  above.  All 
these  factors  must  be  carefully  estimated  before  we  decide  as  to  the  danger 
in  each  case  and  make  our  prognosis. 

The  mortality  in  typhoid  varies  greatly  in  the  separate  epidemics.  The 
severe  cases  are  undoubtedly  more  frequent  at  some  times  than  at  others. 
This  renders  it  difficult  to  give  statistics  which  are  universally  applicable. 
"We  may  in  general  reckon  on  an  average  mortality  of  about  ten  per  cent, 
and  measure  the  severity  of  separate  epidemics  by  this  standard.  Numerous 
observers  agree  that  the  treatment  now  in  vogue  has  decidedly  diminished 
the  mortality.  It  was  formerly  not  rare  for  it  to  reach  twenty  or  twenty- 
five  per  cent. 

Treatment. — A  specific  cure  for  typhoid — i.  e.,  some  remedy  to  destroy 
the  specific  cause  of  the  disease  within  the  system,  or  to  render  it  harmless — 
is  as  yet  unknown.  Bacteriologists  are  now  attempting  to  discover  a  specific 
remedy,  in  the  same  way  that  they  are  attempting  it  in  all  of  the  other  seri- 
ous infectious  diseases.  An  effort  has  been  made  to  stimulate  the  formation 
of  immune  bodies  by  the  injection  of  small  quantities  of  killed  typhoid  bacilli 
into  the  typhoid  patient.  The  injection  of  other  kinds  of  bacteria  (especially 
the  Bacillus  pyocyaneus)  has  also  been  tried.  Becent  investigations  have  dealt 
with  a  serum  therapy,  the  immune  sera  being  obtained  from  animals.  All 
these  studies  are  of  great  scientific  interest,  but  their  practical  results  are  still 
very  doubtful. 

Under  these  circumstances  the  treatment  of  typhoid  must  still  be  chiefly 
dietetic  and  symptomatic,  and  in  one  sense  prophylactic.  We  must  fight  the 
symptoms  already  present,  and  further  seek,  as  far  as  possible,  to  defend  the 
patient  from  the  attack  of  certain  dangerous  secondary  disorders.  Starting 
out  with  this  view,  the  proper  treatment  of  typhoid  fever  is  a  task  of  the 
highest  importance,  and  by  no  means  a  thankless  one. 

We  will  begin  by  considering  the  general  treatment.  The  sick-room  must 
not  be  too  warm,  and  must  be  frequently  and  thoroughly  aired.  The  sick- 
bed must  be  well  cared  for.  If  effort  be  made  to  prevent  bedsores,  we  shall 
obviate  one  source  of  pain  and  danger  (vide  supra),  and  save  ourselves  and 
the  nurse  much  trouble.     Those  who  are  very  ill  should  therefore  be  laid  on 


28  ACUTE   GENERAL   INFECTIOUS   DISEASES 

an  air  cushion  or,  if  possible,  a  water  bed.  The  patient  should  be  told  not 
to  lie  always  upon  his  back,  but  to  change  now  and  then  upon  his  side.  The 
back,  the  region  of  the  sacrum,  and  the  heels  are  to  be  often  bathed  with 
French  brandy,  etc.,  and  anointed.  The  minutest  bedsore  is  to  be  treated 
carefully.  It  should  be  cleansed  twice  a  day  and  dressed  with  a  mercurial 
ointment  or  one  containing  Peruvian  balsam  (l-to-30),1  etc.  If  the  bedsore  be 
extensive,  careful  dusting  with  powdered  dermatol,  or  a  similarly  acting  dust- 
ing powder,  is  very  efficient  treatment.  We  should  be  particularly  careful 
not  to  let  the  skin  be  undermined.  If  this  has  already  occurred,  we  must  be 
prompt  in  the  use  of  the  knife. 

We  cannot  too  strongly  recommend  that  the  mouth  should  be  kept  clean. 
In  a  light  case  the  patient  can  see  to  this  himself,  but  otherwise  the  mouth 
and  tongue  must  be  frequently  cleansed  with  a  linen  cloth  wet  in  cold  water 
or  a  solution  of  borax  (l-to-30).  Perhaps  we  need  hardly  repeat  the  reason 
for  this  excessive  cleanliness.  It  lies  in  the  causative  relation  between  stoma- 
titis and  inflammation  of  the  parotid  gland,  and  of  the  middle  ear.  If  the 
tongue  and  lips  be  dry,  they  may  be  touched  with  glycerin. 

The  diet  must  be  at  once  liquid  and  nourishing.  Milk  is  excellent,  and  it 
should  always  be  ordered,  but  it  can,  unfortunately,  be  taken  by  very  few 
patients  continuously.  It  is  often  better  borne  if  coffee,  tea,  or  a  little  brandy 
be  added  to  it.  Cocoa  made  with  milk  may  also  be  given  for  a  change.  In 
severe  cases  we  have  frequently  employed  the  various  baby  foods,  such  as 
h'ygiama,  with  benefit.  Besides  milk,  the  thick  soups,  gruels  (oatmeal),  soups 
containing  sago,  rice,  farina,  and  the  like,  are  to  be  ordered.  Meat  broths  are 
also  allowable,  and  may  be  made  more  nutritious  by  various  additions  (meat 
juice,  sanatogen,  nutfose,  perhaps  an  egg).  Sometimes  calf's-foot  jelly  is  of 
value.  The  demands  that  patients  often  make  for  more  solid  nourishment 
may  be  acceded  to  without  risk  by  feeding  them  on  rolls  or  zwieback  that 
have  been  soaked.  Cakes,  sweet  crackers,  biscuits,  and  the  like  are  also  useful. 
When  the  strength  of  the  patient  Is  dangerously  reduced,  beef  tea  or  expressed 
meat  juice  should  be  ordered.  The  newer  artificially  prepared  meat  juices  and 
albuminous  preparations  may  also  be  employed  with  benefit. 

When  the  fever  takes  a  sluggish  course,  we  must  often  begin  to  give 
stronger  nourishment  before  the  fever  has  ended.  The  best  drink  is  cold 
water,  which  must  be  offered  to  the  patient  even  when  he  does  not  ask  for  it. 
Lemonade  and  similar  preparations  generally  become  distasteful  in  time. 
Drinks  containing  carbon  dioxid  are  to  be  avoided,  because  they  increase 
the  meteorism.  Cold  tea  with  milk  as  well  as  with  the  fruit  juices  (especially 
the  cranberry)  is  good.  In  severer  cases  we  should  give  some  good  strong 
wine,  such  as  port,  Malaga,  or  Hungarian  wine,  but  it  is  not  necessary  to  force 
the  patient  to  take  wine  if  he  does  not  care  for  it.  If  the  patient  desires  beer, 
we  need  not  hesitate  to  give  it  in  moderate  amount.  During  convalescence 
we  should  be  very  careful  about  diet,  since  errors  often  have  disagreeable  con- 
sequences. We  must  wait  till  there  has  been  no  fever  at  all  for  one  to  two 
weeks  before  we  allow  a  solid,  animal  diet,  and  return  by  degrees  to  common 
sorts  of  food. 

1  The  unguentum  balsami  peruviani  is  made  by  mixing  one  part  of  balsam  very  thoroughly 
with  thirty  parts  of  the  glycerite  of  starch  (B.  P.).     It  is  not  officinal  in  Germany. — Trans. 


TYPHOID  FEYER  29 

The  general  and  dietetic  treatment  which  we  have  thus  far  discussed  is  very 
important.  Outside  of  this,  it  is  our  opinion  thai  there  is  only  one  method  of 
treatment  to  be  chiefly  considered — at  least  under  the  present  limitations  of  our 
therapeutic  ability.  This  method  consists  in  the  persistent  use  of  cool  baths, 
first  practiced  by  Brand  in  Stettin.  Although  the  indications  £or  this  method 
■of  treatment  are  no  longer  exactly  what  its  original  promoter  held  them  to  be, 
and  although,  therefore,  some  of  the  minutiae  of  the  treatment  must  be  changed, 
there  is  at  present  no  other  single  method  of  treating  typhoid  fever  which  has 
so  numerous  and  evident  advantages  for  the  patient  when  properly  and  moder- 
ately used.  To  carry  it  out  in  private  practice  may  often  be  more  difficult  than 
in  a  well-appointed  hospital.  However,  even  in  private  houses  it  will  generally 
he  possible  to  manage  it,  and  we  regard  it  as  the  duty  of  every  physician  who 
undertakes  to  treat  a  severe  case  of  typhoid  to  try  his  best  to  have  the  baths 
employed. 

The  great  advantages  of  the  treatment  by  baths  are:  1.  The  haths  diminish 
the  fever,  if  their  temperature  be  only  sufficiently  low,  by  direct  absorption  of 
heat.  The  baths  thus  obviate,  as  far  as  possible,  all  the  bad  effects  which  might 
result  from  a  rise  of  temperature.  2.  The  direct  influence  of  the  baths  upon 
the  nervous  system  is  still  more  important.  The  intellect  becomes  clearer,  the 
apathy  and  dullness  diminish.  In  fact,  if  baths  be  used,  we  do  not  see  nearly 
so  often  as  formerly  the  grave  "  typhoid  condition."  It  is  thus  evident  that 
bathing  not  only  causes  an  improvement  in  the  subjective  sensations  of  the 
patient,  hut  brings  in  its  train  many  other  beneficial  effects.  The  patient 
takes  his  nourishment  better,  does  not  so  often  swallow  the  wrong  way,  coughs 
more  effectively,  is  easier  to  move,  and  his  body  and  his  mouth  can  be  better 
cleansed.  3.  The  influence  of  the  baths  upon  the  respiratory  organs  is  of  the 
greatest  importance.  We  refer  especially  to  the  stimulation  to  deeper  inspira- 
tion, and  the  promotion  of  expectoration.  The  best  proof  of  the  benefit  of  this 
influence  is  the  circumstance  that  if  patients  are  subjected  to  baths  from  the 
start,  it  is  comparatively  a  rare  thing  for  severe  bronchitis,  atelectasis,  and 
catarrhal  pneumonia  to  develop.  4.  The  good  care  of  the  skin,  which  the 
bathing  makes  possible,  is  not  to  he  despised.  Since  this  treatment  has  been 
introduced,  bedsores  are  much  rarer  in  typhoid  than  before.  5.  Lastly,  the 
baths  are  sometimes  observed  to  have  a  diuretic  effect. 

What  has  been  said  shows  that  the  height  of  the  fever  is  by  no  means  the 
sole  indication  for  the  employment  of  baths,  at  least  in  our  opinion.  The 
condition  of  the  nervous  system  and  of  the  respiratory  organs  is  also  to  be  con- 
sidered. It  is  true  that  numerous  mild  cases  run  a  favorable  course  without 
a  single  hath;  but  we  should  always  remember  that  this  treatment  is  not  only 
directed  against  the  symptoms  already  existing,  but  has  also  a  prophylactic 
importance,  since  it  tends  to  prevent  any  severe  cerebral  or  pulmonary  mani- 
festations. 

We  will  pass  on  to  the  special  method  of  carrying  out  balneo-therapeutics 
in  typhoid.  Full  baths  are  generally  employed,  immersing  the  patient  to  his 
neck.  The  tub  must  stand,  if  possible,  by  the  bedside.  In  hospitals,  where 
there  are  beds  on  rollers,  it  is  a  better  way  to  wheel  the  patients  into  the  bath- 
room. All  who  are  severely  ill  should  be  lifted  into  the  bath  and  there  held 
and  supported,  to  avoid  any  bodily  fatigue.  During  the  bath  the  skin  should 
be  gently  rubbed.     This  averts  unpleasant  sensations  of  chilliness.     The  tern- 


30  ACUTE   GENERAL   INFECTIOUS   DISEASES 

perature  of  the  water  should  not  be  set  too  low,  especially  for  the  first  baths. 
We  begin  at  85°  to  90°  F.  (30°  to  32°  C),  or,  if  the  individual  be  elderly  or 
sensitive  and  timid,  at  even  warmer  temperatures.  When  the  patient  has  be- 
come accustomed  to  the  temperature  of  the  water,  we  can  cool  off  the  bath 
still  further.  Baths  below  73°  F.  (22°  C.)  have  scarcely  ever  been  used  by 
us,  and  we  believe  that  they  are  seldom  needed.  A  very  satisfactory  average 
temperature  is  80°  to  85°  F.  (25°  to  30°  C).  A  bath  lasts,  on  the  average, 
ten  minutes.  If  the  patient  feels  very  cold  or  very  uneasy  in  the  bath,  it  must 
be  cut  short.  After  the  bath  the  patient  is  at  once  lifted  into  bed,  wrapped 
up  in  a  sheet  previously  made  ready,  and  wiped  dry,  with  rather  vigorous 
rubbing  of  the  extremities  and  back.  The  moist  sheet  is  then  removed.  The 
patient  is  covered  up  rather  warmly,  and  is  given  some  hot  broth  or  a  sip  of 
good  strong  wine.  The  effect  of  the  bath  upon  the  temperature  is  measured 
about  half  an  hour  later  by  the  rectum.  If  the  temperature  be  2°  to  3°  F. 
(1°  to  2°  C.)  lower  than  before,  the  result  is  deemed  satisfactory.  Often  the 
difference  is  greater,  but  in  severe  cases  the  fever  may  be  so  obstinate  that  the 
temperature  remits  only  a  small  fraction  of  a  degree.  In  such  cases  it  is  some- 
times permissible  to  lower  the  temperature  of  the  bath  still  more,  or  continue 
it  a  little  longer.  If  cool  baths  are  ill  borne,  protracted  baths  of  lukewarm 
water  are  sometimes  very  efficient  (Eiess,  and  others). 

In  so  far  as  the  height  of  the  fever  furnishes  an  indication  for  baths,  we 
may  accept  103.6°  F.  (39.8°  C.)  in  the  rectum,  as  the  temperature  calling  for  a 
bath,  but  spontaneous  variations  of  the  temperature  of  the  body  are  always  to 
be  regarded.  In  cases  which  show  a  low  morning  temperature  without  special 
interference,  the  height  of  the  evening  temperature  is  seldom  an  indication 
for  a  cold  bath.  We  regard  it  as  very  important  that  the  baths  be  not  given 
too  frequently,  since  their  advantages  may  thus  be  overbalanced  by  their  incon- 
testable evil  consequences.  At  present  we  rarely  prescribe  more  than  two  to 
four  baths  a  day.  At  night  we  have  given  baths  only  very  seldom,  when  forced 
to  by  extremely  high  temperatures  or  other  bad  symptoms.  It  must  be  a  mis- 
take to  wake  a  patient  who  is  quietly  sleeping,  and  put  him  into  cold  water, 
even  if  his  temperature  is  above  104°  F.  (40°  C).  On  the  other  hand,  even  if 
the  temperature  be  not  excessive,  or  even  if  it  be  normal,  there  is,  as  we  have 
said,  no  better  remedy  than  the  baths  for  severe  pulmonary  or  cerebral  symp- 
toms. In  such  cases  we  often  raise  the  temperature  of  the  baths  a  little,  and 
during  them  we  have  colder  water  poured  upon  the  head  and  back.  If  we  do 
this,  the  ears  must  be  stopped  with  cotton  wool,  lest  the  cold  water  find  its 
way  into  them. 

Advantageous  as  the  bath  treatment  of  typhoid  generally  is,  it  must,  how- 
ever, like  every  other  therapeutic  method,  be  used  with  wise  moderation  and 
with  constant  regard  to  individual  conditions.  If  the  patients  are  very  weak, 
show  a  strong  aversion  to  the  baths,  or  feel  dull  and  exhausted  instead  of 
refreshed  after  them,  it  is  well  to  consider  whether  we  really  do  good  by  con- 
tinuing their  employment.  In  such  cases  we  have  often  advised  cold  wet  packs 
of  the  whole  body  in  bed,  instead  of  the  baths,  and  we  consider  such  a  use  of 
cold  as'  very  advisable  in  these  cases.  The  antithermic  action  of  the  pack  is,  of 
course,  much  less  than  that  of  the  bath,  but  it  can  easily  be  aided  by  the  exhibi- 
tion of  antipyretics  internally.  The  respiration  and  the  nervous  system,  how- 
ever, are  almost  always  most  favorably  affected.    Most  patients  readily  consent 


TYPHOID   FEVEB  31 

to  tlie  packs  and  lie  < j n i < * t  for  an  hour  or  two  in  the  wet  envelope.  We  would 
urgently  recommend  the  more  Hrequenl  use  of  packs,  especially  in  private 
practice,  where  the  hath  treatment  often  meets  with  greater  difficulties  than  in 
hospitals.  We  should  here  always  begin  with  higher  temperatures,  and  only 
gradually  go  on  to  cold  packs. 

There  are  a  number  of  contraindications  to  the  use  of  baths  which  cannol 
be  disregarded.  First,  the  occurrence  of  intestinal  hemorrhage,  however  slight, 
and  likewise  the  suspicion  that  peritonitis  is  developing,  prohibit  bathing. 
In  these  cases  quiet  is  the  very  first  requirement  of  the  patient,  and  the  baths 
must  be  at  once  discontinued.  The  onset  of  otitis,  severe  laryngeal  affections, 
and  acute  nephritis  are  also  complications  in  which  we  should  properly  omit  the 
baths  entirely  or  employ  them  very  cautiously,  giving  them  warmer  and  less 
frequently.  Sometimes  rheumatic  pains  in  the  limbs  or  an  attack  of  boils 
render  the  continued  use  of  baths  difficult.  In  short,  we  see  that  nothing 
could  be  more  foolish  than  to  try  to  establish  a  general  rule  for  the  bath  treat- 
ment of  typhoid. 

In  many  cases  of  typhoid  fever  any  medication,  in  addition  to  dietary  and 
hydrotherapeutic  measures,  is  quite  unnecessary.  Under  some  circumstances 
certain  drugs,  however,  can  aid  the  treatment.  I  refer  especially  to  the  use 
of  calomel  at  the  beginning  of  the  disease.  Wunderlich  thought  he  noticed 
that  the  administration  of  two  to  three  calomel  powders  of  5  gr.  (gm.  0.3) 
each  in  the  first  week  of  the  disease  had  an  ameliorating  effect  on  its  course, 
and  sometimes  even  shortened  it.  This,  of  course,  can  scarcely  be  proved. 
However,  I  consider  the  exhibition  of  calomel  useful,  especially  in  those 
rather  frequent  instances  in  which  there  is  constipation  at  the  beginning  of 
the  disease.  I  do  not  employ  the  drug  in  the  later  stages,  but  when  there  are 
no  other  special  indications,  I  prescribe  onl}r  a  simple  muriatic-acid  mixture. 
The  question  has  been  widely  discussed  as  to  the  advisability  of  combating  the 
fever  through  the  administration  of  antipyretics. 

The  one-sided  point  of  view  which  considered  that  the  chief  task  of  the 
physician  in  the  treatment  of  acute  febrile  disease  was  to  low-er  the  temperature 
has  been  gradually  abandoned.  In  describing  the  bath  treatment  of  typhoid 
we  have  emphasized  the  fact  that  the  action  of  the  bath  in  reducing  the  tem- 
perature was  only  one  factor,  and  perhaps  neither  the  most  efficient  nor  the 
most  important  factor,  in  the  curative  action  aimed  at.  In  giving  antipyretics 
internally  their  antifebrile  action  is  of  chief  importance,  but  some  of  them 
also  have  a  certain  sedative  action  on  the  nervous  system.  The  important 
influence  of  the  bath  on  the  respiration  and  skin  they  do  not  possess.  If 
we  had  to  decide  whether  to  treat  typhoid  exclusively  by  baths  or  exclusively 
by  antipyrin  and  similar  drugs,  we  should  decidedly  prefer  the  former.  "We 
would  not  wholly  exclude  the  use  of  antipyretics  internally  in  the  treatment 
of  typhoid,  but  we  would  limit  their  use  more  than  is  often  the  case.  In  our 
opinion  they  are  indicated  only  when  with  existing  high  fever  baths  are  for 
any  reason  impossible  or  contraindicated  (vide  supra),  or  when,  in  spite  of  the 
baths,  the  fever  remains  constantly  high.  In  such  cases  the  baths  can  often 
be  judiciously  combined  with  the  use  of  antipyretics  internally  if  the  patient 
bears  the  drug  well  and  feels  better  subjectively  after  the  reduction  of  tem- 
perature than  before.  We  often  treat  typhoid  patients  by  baths  in  the  day, 
and,  if  the  fever  be  high,  by  a  dose  of  antipyrin  (15  to  30  grains,  gm.  1  to  2) 


32  ACUTE   GENERAL   INFECTIOUS   DISEASES 

at  night.  With  severe  headache,  nervous  restlessness,  etc.,  this  remedy  is 
especially  indicated;  but  we  regard  it  as  at  least  useless  and  often  improper 
to  give  a  patient  with  moderate  fever  large  doses  of  an  antipyretic  without  any 
sufficient  reason,  as  unfortunately  is  often  the  case  in  practice ;  the  only  perma- 
nent result  is  to  make  the  patient  feel  worse  and  upset  his  stomach.  [In 
America,  the  use  of  antipyretics  in  typhoid  and  other  acute  infectious  fevers  is 
exceptional.  They  may  occasion  collapse,  particularly  if  given  just  as  a  lysis 
or  crisis  is  about  to  begin.] 

In  regard  to  the  different  antipyretics  so  frequently  brought  forward  and 
recommended  of  late,  we  are  of  the  opinion  that  antipyrin  is  most  to  be  rec- 
ommended. It  was  introduced  by  L.  Knorr  and  first  recommended  by  Filelme. 
In  doses  of  15  to  30  gr.  (gm.  1  to  2),  best  given  in  wafers,  it  usually  reduces 
the  temperature  considerably,  although  we  may  find  that  the  height  and  the 
obstinacy  of  the  fever  are  not  identical  terms.  We  do  not  often  see  unpleas- 
ant effects  from  antipyrin  (such  as  vomiting,  profuse  sweating  with  deferves- 
cence, a  chill  when  the  temperature  rises  again,  and  sometimes  a  measles- 
like eruption).  The  patient  often  feels  better  than  before  while  under  the 
influence  of  antipyrin,  since  the  drug,  as  we  have  said,  also  acts  favorably 
on  the  nervous  symptoms  (headache,  restlessness).  The  dose  of  15  to  30  gr. 
(gm.  1  to  2)  can  in  severe  cases  be  repeated  several  times  a  day,  but,  as  a  rule, 
we  should  not  exceed  80  or  90  gr.  (gm.  5  to  6)  in  the  twenty-four  hours. 
One  or  two  doses  a  day  are  usually  all-sufficient.  Lactophenin  is  also  much 
recommended  and  even  held  as  a  specific  in  typhoid.  In  doses  of  7  to  15  gr. 
(gm.  0.5  to  1)  it  reduces  the  temperature  considerably  and  usually  causes  a 
marked  improvement  in  the  general  condition.  A  total  of  80  or  90  gr. 
(gm.  5  to  6)  can  be  used  in  a  day.  Of  the  many  other  antipyretics  which,  of 
course,  have  often  been  tried  in  typhoid,  we  may  first  mention  antifebrin 
(acetanilid),  which  in  doses  of  -1  to  7  gr.  (gm.  0.25  to  0.5)  has  a  similar 
action  to  antipyrin  (Cahn  and  Hepp),  and  it  should  be  used  in  practice 
among  the  poor  because  it  is  much  cheaper.  If  we  avoid  too  large  doses  we 
seldom  see  unpleasant  results.  The  appearance  of  a  pale  cyanotic  hue  of  the 
skin  is  the  only  disturbing  feature;  this,  as  in  anilin  poisoning,  is  probably 
due  to  a  change  in  the  coloring  matter  of  the  blood,  -and  therefore  warns  us 
to  be  cautious.  Other  new  antipyretics  are  phenacetin  (15  gr.,  gm.  1,  at  a 
dose),  pyramidon  (1  to  7.5  gr.,  gm.  0.25  to  0.5),  salipyrin,  etc.,  which  have, 
however,  no  special  advantages.  Of  the  older  antipyretics,  quinin  (in  doses 
of  15  to  22.5  gr.,  gm.  1.0  to  1.5)  is  to  be  specially  mentioned;  indeed,  it  has 
recently  been  claimed  that  quinin  has  a  favorable  effect  on  the  course  of  the 
disease. 

Another  important  symptom  which  needs  special  treatment  is  intestinal 
hemorrhage.  It  has  been  already  mentioned  that  if  this  occurs  the  baths 
should  cease  at  once.  Further  than  this,  the  chief  remedies  are  ice  and  opium. 
Flat  ice  bags,  cold-water  coils,  are  laid  upon  the  abdomen.  The  ice  bags  should 
not  be  too  heavy,  and  should,  if  possible,  be  suspended  from  a  hoop.  Inter- 
nally, the  patient  is  given  every  two  hours  15  or  20  drops  of  laudanum  or  a 
powder  of  0.5  gr.  or  1  gr.  (gm.  0.03  to  0.05)  of  opium,  either  pure  or  combined 
with  acetate  of  lead  (opii,  gr.  ss.,  gm.  0.03;  plumbi  acetatis,  gr.  j,  gm.  0.05; 
sacchari  albi,  gr.  j,  gm.  0.05).  The  object  of  the  opium  is  to  check  peristalsis, 
and  thus  promote  the  formation  of  a  clot  in  the  bleeding  vessel.      [Morphin 


TYPHOID   FEVER  33 

subcutaneously  (gr.  £  to  \)  accomplishes  the  same  purpose  and  more  promptly. 
Jt  should  be  repeated  every  half  hour  till  beginning  narcotism,  [f  neither  food 
nor  drugs  be  given  by  the  mouth  for  souk.'  hours,  there  will  be  more  chance 
for  the  intestinal  coils  to  keep  quiet.]  In  severe  cases  we  may  try  injections 
of  ergotin,  or  fluid  extract  of  hydrastis,  20  drops  three  or  \'<>\w  times,  or  a 
subcutaneous  infusion  of  about  7  ounces  (200  c.c.)  of  a  one-  to  two-per-eenl 
sterilized  solution  of  gelatin  in  seven-per-cent  salt  solution.  For  the  threat- 
ening anaemia  following  severe  hemorrhages,  subcutaneous  infusions  of  nor- 
mal salt  solution  are  to  be  employed.  The  baths  cannot  be  resumed  till 
there  lias  been  no  bleeding  for  at  least  four  or  five  'lavs — and  then  only 
cautiously. 

If  peritonitis  occurs,  the  treatment  is  much  the  same.  Above  all,  opium 
must  be  used  in  still  larger  doses,  but,  unfortunately,  as  a  rule,  in  vain.  The 
surgical  treatment  of  peritonitis  has  rather  more  of  a  future  and  more  success, 
but  experience  of  this  is  still  scanty. 

If  there  is  considerable  diarrhea,  we  can  give  mistura  gummosa  [P.  G.,  gum 
arabic  and  sugar,  each  15  parts;  water,  170  parts]  or  small  doses  of  opium,  the 
latter  sometimes  combined  with  tannin,  tannigen,  etc.  In  general  it  is  cer- 
tainly proper  not  to  check  the  ordinary  moderate  diarrhea  of  typhoid.  Per- 
sistent constipation  is  always  to  be  avoided.  Constipation  at  the  beginning  of 
the  disease  is  overcome  by  calomel  (vide  supra).  In  later  stages  we  always 
try  enemata  first,  to  produce  an  operation.  If  this  does  not  succeed,  then  we 
must  employ  rhubarb  or  castor  oil.  Great  tympanites  may  be  diminished  by 
laying  cold  wet  cloths  or  ice  hags  upon  the  belly.  Considerable  amounts  of 
gas  may  often  be  removed  by  introducing  a  long  rectal  tube.  As  to  punctur- 
ing the  greatly  inflated  intestines,  a  method  practiced  by  some  physicians,  we 
have  no  personal  experience. 

If  there  are  severe  pulmonary  symptoms,  baths  or  wet  packs  are,  as  we 
have  said,  the  best  remedies.  Internally  we  may  try  liquor  ammonii  anisatus 
[P.  G.,  olei  anisi,  1  part;  aqua?  destillata?,  24  parts;  aquas  ammonia?,  5  parts] 
and,  especially  with  weak  heart,  benzoic  acid  (gr.  ij  to  iij,  gm.  0.1  to  0.2, 
in  powder)  and  gr.  iij,  gm.  0.2  of  camphor.  If  the  pulse  be  very  rapid,  we 
may  try  an  ice  bag  over  the  heart.  If  at  the  same  time  the  pulse  is  small 
and  weak,  we  give  stimulants  (camphor,  strophanthus,  caffein,  and  strong 
wine).  We  only  rarely  use  digitalis  in  typhoid.  If  symptoms  of  severe  cardiac 
weakness — so-called  collapse — suddenly  occur,  a  rapid  and  energetic  interfer- 
ence is  urgently  demanded.  Hypodermic  stimulation  should  be  employed 
and,  above  all  other  drugs,  camphor  in  oil.  Besides  camphor,  caffein  injec- 
tions (caffein  nitrobenz.,  2.0  in  10.0  =  gr.  xv  in  oijss.  aqua?  destillata?,  two  to 
three  syringefuls)  ma}^  be  employed,  and  wine,  strophanthus,  etc.,  internally. 
If  the  respiration  stops  it  can  sometimes  be  started  up  again  by  douches  of 
cold  water  on  the  back  of  the  neck.  -  We  may  sometimes  restore  it  by  artificial 
respiration. 

For  nervous  symptoms  the  baths  and  douching  are  the  most  effective  reme- 
dies. The  head  is  meanwhile  covered  by  an  ice  bag.  Antipyrin  sometimes 
acts  favorably.  If  there  be  great  excitement,  as  shown  by  excessive  restlessness 
or  delirium,  small  doses  of  morphin  internally,  or,  better,  subcutaneously,  are 
often  very  useful. 

For  insomnia,  veronal  in  doses  of  7.5  to  12  gr.  (gm.  0.5  to  0.75),  perhaps 


34  ACUTE  GENERAL  INFECTIOUS  DISEASES 

in  combination  with  15  gr.  (gm.  1)  of  sodium  bromid,  may  be  tried  without 
hesitation. 

The  numerous  other  complications  and  sequelas  which  may  occur,  but 
which  cannot  all  be  mentioned  here,  should  be  treated  on  general  principles. 

The  prophylactic  measures  to  avoid  the  spreading  of  the  disease  can  be  only 
briefly  referred  to.  The  most  careful  isolation  of  the  patient  is  naturally  of 
the  first  importance.  If  this  be  not  possible  in  his  home,  he  should  be  trans- 
ferred to  a  hospital.  Special  attention  should  be  paid  to  the  very  mild  cases 
("bacilli  carriers,"  vide  supra).  The  careful  disinfection  of  the  excreta 
(urine  and  feces)  is  of  great  importance.  The  best  disinfectant  is  "  Kresol- 
wasser,"  as  prescribed  by  the  Eoyal  Bureau  of  Health  (2  ounces  of  liq.  cresoli 
saponatus  in  a  liter  of  water),  which  is  added  in  equal  parts  to  the  feces,  urine, 
or  vomitus.  Milk  of  lime,  chlorid  of  lime,  a  two-per-cent  solution  of  corro- 
sive, sublimate,  lysol,  etc.,  may  also  be  employed. 

We  should  further  take  care  that  bedpans,  bedclothes,  linen,  the  rectal 
thermometer,  etc.,  should  be  handled  by  other  persons  as  little  as  possible, 
and  should  be  carefully  disinfected. 

The  extensive  investigations  into  the  question  of  vaccination  against 
typhoid  have  not  led  to  any  definite  results,  although  they  are  by  no  means 
hopeless.     [Late  reports  are  encouraging.] 


APPENDIX 
PARATYPHOID  FEVER 

Schottmuller  and  others  have  repeatedly  observed  a  typhoid-like  disease, 
usually  having  a  favorable  course,  in  which  the  bacilli  found  in  the  blood, 
stools,  and  roseolas  have  certain  differential  cultural  characteristics  which  dis- 
tinguish them  from  the  typhoid  bacilli.  Thus  far  two  types  (Types  A  and  B) 
have  been  identified.  The  blood  serum  of  paratyphoid  patients  does  not 
agglutinate  typhoid  bacilli,  but  does  agglutinate  the  paratyphoid  organisms. 
This  circumstance  is  especially  valuable  in  the  diagnosis.  The  paratyphoid 
bacilli  axe,  however,  usually  agglutinated  by  true  typhoid  serum.  Further 
observations  must  be  made  to  show  the  practical  significance  of  the  discovery 
of  paratyphoid.  It  is  worthy  of  mention  that  the  so-called  Bacillus  paratypho- 
sus  B  is  often  the  cause  of  cases  of  "  meat  poisoning." 


CHAPTER    II 

TYPHUS    FEVER 

(Spotted  Fever.     Petechial  Typhoid.     Febris  exanthematica.) 

Typhus  fever  is  an  acute  infectious  disease,  perfectly  distinct  from  typhoid 
fever,  but  formerly  often  confounded  with  it.  The  similarity  of  the  two  dis- 
eases, which  led  to  their  similar  names,  consists  only  in  the  grave  general  con- 


TYPHUS    FEVER  35 

dition  with  fever,  and  in  a  number  of  complications  which  may  appear  in  both. 
There  is,  however,  an  essential  difference  in  the  whole  course  of  the  two 
eases,  and  especially  in  the  circumstance  that  the  intestinal  lesion  which 
characteristic  of  typhoid  is  never  seen  in  typhus.  The  chief  distinction  be- 
tween the  two  affections,  which  must  undoubtedly  lie  in  the  difference  in  their 
causes,  cannot  yet  be  demonstrated.  We  do  not  yet  know  the  organized  patho- 
genic agents  of  typhus  fever,  although  it  must  be  presupposed  that  they 
exist. 

.ZEtiology. — As  to  the  way  in  which  infection  occurs,  we  have  much  less 
information  even  than  in  relation  to  typhoid.  We  know  nothing  as  yet  as  to 
the  specific  agents  which  produce  typhus,  although  microorganisms  have  been 
repeatedly  found  in  the  blood.  It  is  an  incontestable  fact  that  the  appear- 
ance of  typhus  in  a  place  previously  free  from  the  disease  is  always  to  be 
referred  to  an  importation  of  the  pathogenic  poison  from  without.  It  is  like- 
wise determined,  through  numerous  observations,  that  typhus  is  one  of  the  con- 
tagious diseases — that  is,  that  the  specific  poison  can  be  directly  transferred 
from  the  patients  to  others  around  him.  How  it  is  transferred  we  have  no  cer- 
tain knowledge.  Perhaps  the  poison  is  contained  in  the  expired  air;  or,  as  is 
still  more  probable,  in  the  scales  of  epidermis ;  or,  perhaps,  in  the  other  excre- 
tions and  secretions  of  the  patient.  We  are  equally  ignorant  through  what 
channel  the  infectious  agent  enters  the  system — whether  it  is  inspired  or  swal- 
lowed. It  is  certain  that  the  poison  may  be  transferred  in  the  clothes,  etc., 
of  the  patient  (fomites). 

Favorable  hygienic  surroundings  decidedly  diminish  the  contagiousness  of 
typhus  fever.  For  example,  in  the  well-ventilated  pavilions  of  the  Leipsic  hos- 
pital there  have  rarely  been  cases  of  transfer  of  the  disease  to  physicians,  nurses, 
or  other  patients.  On  the  other  hand,  if  the  hygienic  influences  be  unfavorable, 
typhus  fever  may  appear  in  very  widespread  epidemics.  Those  terrible  epi- 
demics which  have  been  described  under  the  names  of  "  famine  fever,"  "  camp 
fever"  (Hungertyphus,  Ivriegstyphus),  etc.,  were  for  the  most  part  typhus 
fever.  In  the  smaller  epidemics  it  is  often  possible  to  trace  the  disease  to 
some  wretched,  overfilled  tenement  house. 

At  present  typhus  fever  appears  constantly  in  Great  Britain.  Ireland  has 
been  notorious  for  many  years  as  a  breeding  place  of  the  disease.  It  is  also 
frequent  in  the  eastern  part  of  Germany  (Posen,  East  Prussia  and  West  Prus- 
sia, Silesia),  in  Poland,  Galicia,  Russia,  and  in  parts  of  southern  Europe.  The 
isolated  cases  which  occur  every  year  here  and  there  in  central  Germany, 
though  more  or  less  numerous,  are,  almost  without  exception,  to  be  referred  to 
an  importation  of  the  disease. 

Typhus  fever  attacks  by  preference  young  adults  of  twenty  to  forty  years ; 
but  it  occurs  in  children,  and  is  comparatively  frequent  in  elderly  persons. 
There  is  no  marked  dependence  of  the  epidemics  upon  any  particular  season 
of  the  year.  As  in  the  case  of  typhoid  fever,  a  person  who  has  once  had  the 
disease  seems  to  enjoy  immunity  from  any  fresh  attack. 

[The  practical  acquaintance  of  American  physicians  with  typhus  fever  is, 
fortunately,  limited.  Many  of  the  outbreaks  which  have  occurred  were  trace- 
able to  immigrants,  especially  from  Ireland. 

During  our  Civil  War  the  disease  broke  out  neither  among  the  armies  in 
the  field  nor  among  the  prisoners  of  war.    A  number  of  cases  were  reported  at 
4 


36  ACUTE   GENERAL   INFECTIOUS   DISEASES 

the  time,  but  great  doubt  has  since  been  thrown  upon  the  correctness  of  the 
diagnosis.] 

Course  and  Symptoms  of  the  Disease. — If  we  try  to  sketch  the  characteristic 
behavior  of  typhus  fever,  especially  as  contrasted  with  typhoid,  we  may  say 
that  the  disease  begins  much  more  abruptly  and  rapidly,  and  that  the  fever 
quickly  becomes  very  high  and  the  general  disturbance  very  severe,  but  the 
illness  lasts  a  shorter  time,  seldom  more  than  two  weeks,  and,  with  a  favorable 
course,  passes  by  crisis  into  recovery. 

The  duration  of  the  period  of  incubation  seems  to  vary.  It  is  usually  about 
twelve  days — never  less  than  four,  or  more  than  fourteen  days.  Sometimes, 
though  not  invariably,  slight  prodromata  precede  by  some  days  the  actual  out- 
break of  the  disease.  These  are  languor,  anorexia,  headache,  and  pain  in  the 
limbs.  Then  the  regular  illness  begins,  as  a  rule,  rather  suddenly,  and  often 
with  a  pronounced  rigor.  With  this  the  temperature  rises  quickly,  and  may  on 
the  very  first  evening  reach  104°  or  105°  F.  (40°  to  40.5°  C).  Vomiting  is  not 
rare,  and  may  be  repeated.  A  grave  general  condition,  with  fever,  is  developed 
in  a  few  days.  The  patient  feels  exhausted.  There  is  often  violent  pain  in 
the  loins  and  extremities.  Nervous  symptoms  soon  appear:  persistent  and 
intense  headache,  vertigo,  spots  before  the  eyes,  ringing  in  the  ears,  and  in 
many  cases  quickly  increasing  stupor  and  delirium.  In  severe  cases  the  fever 
often  reaches  106°  F.  (41°  C),  and  may  be  even  higher,  and  it  is  almost 
constant,  with  but  slight  morning  remissions.  The  skin  is  hot  and  dry,  the 
tongue  dry  and  thickly  coated,  the  respiration  moderate,  the  pulse  very  rapid. 
We  very  frequently  find  in  the  chest  the  signs  of  an  extensive  bronchitis. 
N/asal  catarrh  and  conjunctivitis  also  occur.  Serious  intestinal  symptoms  are 
generally  absent.  The  spleen  is  almost  always  greatly  enlarged.  The  urine  is 
concentrated  and  scanty,  and  sometimes  has  a  trace  of  albumen.  There  is 
usually  a  moderate  leucocytosis  (in  contrast  to  typhoid  fever). 

On  the  third  to  the  seventh  clay  of  the  disease  the  characteristic  eruption 
appears.  To  this  the  disease  owes  its  name  of  "  spotted  fever."  The  eruption 
consists  of  rose  spots,  generally  very  numerous  and  widespread,  upon  the 
trunk  and  extremities,  often  also  on  the  face.  Sometimes  the  spots  are  larger, 
and  may  then  bear  great  resemblance  to  a  fresh  eruption  of  measles.  The  skin 
between  the  separate  rose  spots  is  not  infrequently  diffusely  reddened.  After 
two  or  three  days  the  roseolas  become  hemorrhagic,  and  change  into  lighter 
or  darker  petechias.  It  is  commonly  only  in  the  lighter  cases  that  the  rose 
spots  facie  away  without  first  becoming  petechial.  In  rare  though  well-substan- 
tiated cases  the  eruption  has  been  scanty,  or  even  wholly  wanting.  Herpes 
does  occur,  but  only  seldom. 

The  fever  begins  to  abate  in  light  cases  as  early  as  the  second  week,  coin- 
cidently  with  an  improvement  in  the  general  symptoms.  Often  this  change  is 
indicated  about  the  seventh  day  by  a  considerable  remission  in  the  temperature. 
On  the  other  hand,  in  severe  cases,  all  the  symptoms  grow  worse.  The  weak- 
ness increases.  The  nervous  derangement  reaches  the  extreme  of  a  severe 
"  typhoidal  state,"  expressed  either  by  marked  stupor,  which  sometimes  passes 
into  complete  coma,  or  by  violent  delirium.  Lobular  pneumonia  attacks  the 
lungs,  and  the  fever  continues  with  unabated  violence.  These  symptoms  may 
end  with  death,  but  in  favorable  cases  they  decline  rapidly.  Sometimes  this 
decline  is  preceded  by  a  great  rise  in  temperature  (perturbatio  critica),  espe- 


TYPHUS   FEVER  37 

cially  about  the  seventeenth  day,  rarely  a  few  days  earlier  or  later.  In  such 
cases  the  temperature  is  apt  to  fall  by  crisis,  sinking  in  a  day  or  two,  with  but 
slight  interruption,  down  to  the  normal  level.  Even  in  those  cases  in  which 
the  descent  is  by  gradations  it  is  always  decidedly  more  abrupt  than  in  typhoid. 
The  eruption  quickly  fades,  the  patients  gradually  improve,  and,  as  a  rule, 
become  completely  and  permanently  convalescent.  Ii  is  true  thai  some  observ- 
ers have  seen  relapses,  but  they  are,  at  least  in  our  present  epidemics,  extremely 
rare. 

Complications  and  Varieties  in  the  Course  of  the  Disease. — From  what  we 
have  said  of  its  course,  it  is  evident  that  the  symptoms  are  essentially  those  of 
an  intense  general  infection  of  the  system.  The  sole  demonstrable  local  lesion 
which  is  almost  invariably  present  is  the  characteristic  eruption,  and  this  has 
evidently  no  causal  relation  to  the  severe  symptoms  of  the  disease.  It  is  like- 
wise extremely  probable  that  most  of  the  complications,  which  not  infrequently 
arise  in  severe  cases,  are  secondary,  and  occur  in  the  way  already  described 
with  considerable  detail  in  the  preceding  chapter.  They  are  just  such  com- 
plications as  are  possible  in  any  severe  constitutional  disease,  and  embrace 
otitis,  parotitis,  extensive  lobular  pneumonia,  more  rarely  gangrene  of  the 
lungs,  and  pleurisy;  also  furunculosis,  purulent  cellulitis,  bedsores,  dysentery, 
icterus,  etc.  Whether  some  of  the  local  lesions  which  are  observed  may  not  be 
direct  results  of  the  pathogenic  poison,  we  cannot  at  present  decide.  Among 
these  would  come,  first  of  all,  the  rare  cases  of  lobular  pneumonia  and  nephritis. 
Sequelae  are,  on  the  whole,  rare,  though  sometimes  there  is  a  tedious  anaemic 
condition,  or  neuralgia,  paralysis,  etc. 

The  separate  epidemics  of  typhus  present  considerable  variety,  not  only  as 
regards  the  occurrence  of  individual  complications,  but  more  especially  in  the 
general  course  and  character  of  the  cases.  For  instance,  some  epidemics 
are  distinguished  by  the  greater  frequency  of  light  attacks  (typhus  exanthemati- 
cus  levissimus).  Here  the  entire  attack  runs  its  course  in  five  to  eight  days. 
The  fever  is  generally  comparatively  moderate;  there  are  no  severe  general 
symptoms,  and  complications  are  exceptional. 

Diagnosis. — It  may  be  very  difficult  for  a  time  to  distinguish  typhus  from 
typhoid.  The  following  factors  are  of  chief  importance :  1.  The  onset  is  much 
more  abrupt  in  typhus  than  in  typhoid,  and  is  often  accompanied  by  a  pro- 
nounced rigor.  2.  In  typhus,  the  nervous  disturbances  usually  appear  earlier 
and  are  more  severe  than  in  typhoid.  3.  The  rash  is  seldom  so  extensive  in 
typhoid  as  in  typhus,  and  in  typhoid  it  hardly  ever  becomes  petechial.  4.  In 
typhus  the  pains  in  the  loins  and  limbs  are  generally  much  more  pronounced. 
5.  The  characteristic  intestinal  symptoms  in  typhoid.  6.  The  leucocytosis  in 
typhus.  7.  If  we  still  find  it  hard  to  decide,  the  manner  of  recovery  will 
almost  always  settle  the  question.  Eecovery  in  severe  cases  of  typhoid  is,  on 
the  average,  much  more  tardy  and  gradual,  by  lysis.  In  typhus  it  occurs  gen- 
erally by  the  seventeenth  day,  and  by  crisis.  Aside  from  these  clinical  differ- 
ences, the  surest  means  of  excluding  typhoid  are  the  Widal  reaction  and 
the  bacteriological  examination  of  the  blood  (vide  supra).  It  may,  at  the 
beginning,  be  difficult  to  distinguish  typhus  from  smallpox,  as  well  as 
from  measles.  The  differentiation,  however,  is  soon  made  by  the  general 
epidemiological  considerations,  and,  above  all,  by  the  further  course  of  the 
disease. 


38  ACUTE   GENERAL   INFECTIOUS   DISEASES 

Prognosis. — The  prognosis  is  chiefly  determined  by  the  severity  of  the  fever 
and  of  the  nervous  symptoms.  Extensive  lobular  pneumonia  is  the  most  fre- 
quent dangerous  complication.  The  mortality  varies  greatly  in  the  separate 
epidemics.  It  is  sometimes  only  six  or  seven  per  cent,  but  may  rise  to  twenty 
per  cent. 

Treatment. — Treatment  is  based  on  the  same  principles  as  in  typhoid  fever. 
'There  is  no  specific  remedy.  Besides  good  nursing,  a  judicious  employment 
of  baths  is  certainly  our  chief  reliance  for  lessening  the  severity  of  many  of  the 
symptoms,  such  as  febrile,  nervous,  and  pulmonary  disturbances,  as  well  as  for 
averting  many  dangerous  complications.  Potassium  bromid  (30  to  45  gr., 
gm.  2  to  3 )  is  said  to  have  a  favorable  effect  on  the  delirious  patients.  Because 
of  the  marked  contagiousness  of  the  disease,  typhus  eases  should,  as  soon  as 
possible,  be  most  carefully  isolated.  All  the  rules  for  disinfection  should,  of 
course,  be  carried  out  with  the  greatest  care. 


CHAPTER    III 

RELAPSING   FEVER 

(Relapsing  Typhus — Febris  recurrens) 

iEtiology. — This  disease  was  first  named  by  English  pathologists  relapsing 
fever,  and  by  Griesinger  febris  recurrens.  It  has  a  peculiar  course,  made  up 
of  separate  attacks,  and  is  further  of  great  interest  because  it  is  one  of  the  first 
infectious  diseases  in  which  the  specific  pathogenic  organisms  became  known, 
and,  being  easily  demonstrable  in  each  separate  case,  were  utilized  for  the 
speedy  and  certain  diagnosis  of  the  disease.  Obermeier  discovered  in  Berlin, 
in  the  year  1873,  that  in  relapsing  fever  the  blood,  at  certain  times,  invariably 
contains  peculiar  threadlike  microorganisms.  This  discovery  has  since  been 
universally  confirmed;  and  it  may  be  maintained  that  if  once  the  presence  of 
these  "  spirilli "  be  demonstrated  in  the  blood,  we  are  justified  in  making  an 
absolute  diagnosis  of  relapsing  fever. 

In  Germany  the  disease  did  not  become  epidemic  till  the  year  1868.  In 
1872  and  1873  there  were  considerable  epidemics  in  Breslau  and  Berlin.  Its 
last  extensive  appearance  was  in  1879  and  1880,  when  it  spread  over  most  of 
northern  and  central  Germany,  and  was  accurately  studied  by  numerous  ob- 
servers. People  of  the  poorer  classes  were  almost  exclusively  attacked,  and 
especially  the  "  tramps."  The  uncleanly  dens  where  these  people  lodge  were 
found  everywhere  to  be  the  chief  centers  of  infection. 

The  transmission  of  the  disease  probably  occurs  mainly  through  bedbugs; 
they  carry  the  spirilla-containing  blood  from  the  infected  to  healthy  indi- 
viduals. 

The  disease  cannot  be  very  contagious  if  the  hygienic  influences  be  good. 
At  least  the  results  of  our  late  epidemics  would  imply  this.  In  the  Leipsic 
hospital,  where  at  that  time  over  two  hundred  and  fifty  cases  were  treated,  and 
isolation  could  not  be  at  all  perfectly  carried  out,  not  one  case  of  infection 
occurred.     It  is  certain  that  the  disease  can  be  transmitted  by  direct  inocu- 


RELAPSING   FEVER  39 

lation  with  the  blood  of  patients.     This  has  been  established  by  a  Ku- 
physician,  by  the  experimental   inoculation  of  healthy  person-,     hoetors  I 
been  repeatedly  inoculated  at  the  autopsy  of  those  who  have  died  of  relapsing 
fever.     The  disease  may  likewise  be  transferred   by   inoculation  to  monkeys, 
while  other  mammals  seem  to  enjoy  an  immunity  from  it. 

[The  first  cases  of  relapsing  fever  observed  in  this  country  were  in  Irish 
immigrants  coming  over  in  the  same  vessel  in  the  year  181  1.  At  several  peri- 
ods since  then  more  or  less  limited  outbreaks  traceable  to  immigration  have 
occurred,  but  the  disease  has  never  acquired  any  foothold  with  us,  and  com- 
paratively few  physicians  have  ever  seen  it.  So  far  as  can  be  learned,  only 
one  case  has  ever  been  seen  in  Boston,  and  that  was  in  the  person  of  a  physi- 
cian from  another  city,  who  brought  the  disease  with  him  and  passed  through 
it  in  the  Massachusetts  General  Hospital.] 

Clinical  History. — The  stage  of  incubation  lasts  about  five  to  eight  days. 
It  is  only  exceptionally  that  some  slight  prodromal  symptoms  present  them- 
selves just  before  the  outbreak  of  the  disease  proper.  As  a  rule,  it  begins  sud- 
denly, with  a  more  or  less  pronounced  chill  and  intense  constitutional  symp- 
toms. There  are  violent  headache,  great  languor,  anorexia,  and  especially 
marked  pains  in  the  loins  and  extremities.  The  temperature  rises  rapidly, 
reaching  generally  106°  F.  (41°  C.)  or  higher  as  early  as  the  first  or  second 
day.  The  skin  is  hot  and  dry,  and  usually  quickly  assumes  a  very  characteristic 
dirty-yellowish  color.  In  Leipsic  we  often  saw  herpes  labialis,  which  seems, 
however,  to  have  been  rarer  in  epidemics  elsewhere.  The  tongue  becomes  dry 
and  thickly  coated.  Sometimes  there  is  vomiting.  The  bowels  are  consti- 
pated, or  there  is  a  slight  diarrhea.  The  spleen  becomes  rapidly  enlarged, 
being,  as  a  rule,  even  larger  than  in  typhoid  or  typhus.  The  liver  is  slightly 
enlarged.  The  chest  presents  the  signs  of  a  bronchitis,  generally  moderate, 
but  in  exceptional  instances  severe.  The  pulse  is  much  quickened.  It  is  sel- 
dom that  there  are  severe  cerebral  symptoms  beyond  a  certain  apathy  and 
stupor.  We  have  seen  delirium  tremens,  sometimes,  in  drunkards.  A  very 
characteristic  symptom,  already  mentioned,  is  the  marked  hyperesthesia  of 
the  muscles,  especially  in  the  calves. 

After  these  symptoms,  accompanied  by  persistent  and  generally  very  high 
fever,  have  lasted  five  days  to  a  week,  there  is  a  critical  decline  of  temperature, 
with  profuse  sweating.  The  patient  now  improves  so  rapidly  and  decidedly 
that  he  thinks  himself  completely  cured,  and  generally  gives  little  credence  to 
the  physician's  prophecy  of  a  relapse.  In  rare  but  well-attested  cases  there 
has  been  really  but  one  attack.  The  rule  is  that,  after  about  a  week,  a  second 
attack  occurs,  often  a  third  after  that,  and,  infrequently,  even  a  fourth  and 
fifth.  In  each  of  these,  the  above-mentioned  symptoms  are  repeated  more  or 
less  completely  and  violently.  As  the  only  certain  and  constant  sign  of  the 
recurring  attacks  (the  so-called  relapses)  is  a  fresh  rise  of  temperature,  it  will 
be  well  to  consider  their  peculiarities  at  the  same  time  that  we  describe  the 
course  of  the  fever.  During  the  intervals  of  normal  temperature  the  other 
objective  symptoms  of  disease  are  usually  absent,  except  an  evident  splenic 
tumor,  and,  not  infrequently,  the  peculiar  pale-yellow  hue. 

Course  of  the  Fever  (see  Fig.  5). — The  beginning  of  the  fever  in  the 
first  attack  is,  as  we  have  said,  almost  always  sudden,  so  that  it  may  even  in  a 
few  hours  reach  a  considerable  height.    The  fever  lasts,  as  a  rule,  five  to  seven 


40 


ACUTE   GENERAL  INFECTIOUS   DISEASES 


days,  but  not  infrequently  as  short  a  time  as  three  or  four  days,  or  as  long 
as  ten  or  twelve  days.  During  this  time  it  may  keep  a  tolerably  uniform 
height,  but  oftener  there  are  considerable  remissions,  which  may  even  come  to 
deserve  the  name  of  pseudo-crises.  In  such  cases  the  temperature  sinks  in  the 
morning  to  normal  or  even  lower,  so  that  we  might  believe  the  fever  ended; 


42.0° 
41.0° 
40.0° 
39.0° 
38.0° 
37.0° 
36.0° 
35.0° 


12   3  4  5 


7  8 


10  11  12  13  14  15  16  17  18  19  20  21  22  23  24 


S  ■■■■■■■■■■  liSliaMMIBBBEBMBB  MB  ■fflmaiBMBIl— BM 
*»»sbbssessssbbsbsbb5sbbsem^^ 

HiiiEjjHjnHy  ivbbhi  SSgSgaSSiu'iESSSEHSEEiiEMMBiaSaSS 


■■■■■iBBiHiiwiHHHiiBHHniunMniBiHimnHin 

■  SSSSS'SS5!  HHBBnHBDBBH9BK  IHVIIHiniBHHHflH 

BIHKBBJEBBinnHBiBIHXBIBiBIBinBiBIBBIBiEiBBBlfllBIBBSnilBIBIBIfllilBiBiBBIBi 


Fig.  5. — Example  of  the  temperature  curve  in  relapsing  fever. 

but  in  the  evening  the  temperature  rises  again  to  its  former  level.  These 
pseudo-crises  are  most  frequent  toward  the  end  of  the  attack,  but  do  occur 
sometimes  in  the  very  first  days.  The  absolute  height  of  the  fever  is,  as  a  rule, 
very  considerable.  Temperatures  between  105.5°  and  106.5°  F.  (11°  and 
41.5°  C.)  are  very  often  observed,  and  in  themselves  are  not  especially  ominous 
in  relapsing  fever.  The  highest  temperature  we  have  observed  was  107.9°  F. 
(42.2°  C).  Sometimes  the  temperature  is  more  moderate  (between  102°  and 
104°  F.,  39°  and  40°  C).  The  fever  almost  always  ends  at  the  close  of  the 
attack  by  crisis,  only  rarely  by  a  rapid,  gradual  decline.  The  crisis  is  often 
preceded  by  an  especially  great  rise  the  evening  before  (perturbatio  critica) ; 
so  that  the  subsequent  fall  of  temperature  is  very  considerable.  It  generally 
occurs  at  night,  and  is  accompanied  by  profuse  perspiration.  The  fall  may 
amount  to  9°  or  10°  F.  (5°  to  6°  C).  The  temperature  sinks  almost  always 
below  normal,  often  as  low  as  95°  F.  (35°  C.)  or  thereabouts.  Once  we  saw 
it  fall  to  92.1°  F.  (33.4°  C). 

To  the  first  attack  succeeds  an  interval  during  which  there  is  no  fever  (apy- 
rexia),  which  lasts  on  the  average  about  a  week,  sometimes  a  less  time,  and  often 
a  greater.  The  longest  interval  we  have  ever  observed  lasted  seventeen  days. 
During  this  interval  the  temperature,  which,  as  a  rule,  is  at  first  subnormal, 
rises  to  normal,  and  then  generally  remains  there.  Exceptionally  there  are 
slight  evening  exacerbations  to  above  100.5°  F.  (38°  C).  These  may  have  no 
demonstrable  cause,  or  may  result  from  some  complication,  such  as  otitis,  or  a 
furuncle.  Then  comes  another  change,  and  generally  a  sudden  one,  ushered 
in  with  a  chill,  and  a  new  rise  of  temperature,  the  beginning  of  the  second 
attack  or  first  relapse.  During  this  attack  the  fever  has  the  same  general 
peculiarities  as  in  the  first  attaek.  Generally  the  first  relapse  is  briefer  by  a 
day  or  two  than  the  first  attack,  but  the  reverse  is  sometimes  true.     We 


RELAPSING   FEVER 


41 


will  add  that  we  have  observed  not  infrequently  a  rather  high  evening  tem- 
perature (101.5°  F.,  38.5°  C.)  for  one  or  two  days  before  the  second  atl 

began,  as  also  before  the  third. 

Relapsing  fever  seems  in  many  epidemics  to  have  been  made  up  of  two 
attacks,  so  that  no  more  than  one  tenth  of  the  cases  had  a  third  attack.  On 
the  other  hand,  the  majority  of  the  cases  in  the  last  epidemic  had  two  relapses. 
In  these  cases  the  rule  was  for  the  interval  between  the  second  and  third 
attacks  to  be  one  or  two  days  longer  than  the  first  apyrexia ;  but  earlier  epi- 
demics seem  to  have  had  the  second  apyrexia,  if  there  was  one  at  all,  briefer 
than  the  first.  The  third  attack  is  set  down  in  all  reported  cases  as  decidedly 
shorter  than  either  of  its  predecessors.  It  lasts  generally  two  or  three  days. 
Exceptionally  we  have  seen  it  persist  for  four  or  even  six  days. 

A  fourth  and  even  a  fifth  attack  may  occur,  but  only  exceptionally.  If  they 
do  happen,  they  are  usually  imperfectly  developed,  and  often  are  limited  to  a 
fever  of  one  day's  duration.  The  more  accurately  and  persistently  we  take 
the  temperature  during  convalescence,  the  oftener  do  we  find  slight  rises  of 
temperature  occurring  at  intervals  late  in  the  history  of  the  case.  These  are 
probably  to  be  interpreted  as  final,  rudimentary  attacks. 

The  Spirilli. — The  number  of  cases  of  relapsing  fever  in  which  no  spirilli 
can  be  demonstrated  in  the  blood,  if  the  examination  be  accurate,  has  become 
so  small  that  it  can  be  disregarded, 
when  we  compare  it  with  the  much 
greater  number  of  cases  where  such 
demonstration  is  made  with  ease  and 
certainty.  The  best  way  is  to  get  a 
drop  of  blood  by  pricking  the  skin,  and 
examine  it  as  it  is,  without  mixing 
anything  with  it.  Staining  (with 
the  basic  anilin  colors)  is  easy  but  un- 
necessary. With  any  good  dry  lens  of 
400  to  500  diameters  the  spirilli  are 
seen  with  perfect  distinctness.  It  re- 
quires a  little  practice  to  make  them 
out,  but  this  is  easily  obtained.  Often 
the  attention  is  first  caught  by  little 
jogglings  and  motions  of  the  red  blood 
corpuscles,  and  then  we  see  the  deli- 
cate,   narrow    threads.      Their    length 

equals  about  three  to  six  times  the  diameter  of  the  red  globules  (Fig. 
6).  They  exhibit  an  active  and  almost  continuous  motion,  like  snakes. 
Often  the  whole  thread  bends  upon  itself  and  then  stretches  out  again. 
They  are  partly  separate  and  partly  tied  up  in  knots  composed  of  four 
to  twenty  individuals.  The  whole  number  visible  in  one  field  varies  greatly 
in  individual  cases,  and  has  no  direct  relation  to  the  severity  of  the  case. 
Often  it  requires  long  searching  to  find  a  few,  while  in  other  cases  there 
may  be  twenty  or  more  in  the  field  at  once.  A  very  interesting  fact  is 
that  their  appearance  in  the  blood  depends  upon  the  attacks  of  fever. 
On  the  first  day  of  the  attack  we  rarely  find  spirilli,  and  then  only 
one  or  two.     Upon  succeeding  days  their  number  increases.     Shortly  before 


Fig.  6. — Spirilli  of  relapsing  fever  in  the 
blood. 


42  ACUTE   GENERAL   INFECTIOUS   DISEASES 

the  end  of  the  attack — that  is,  before  the  crisis — they  generally  disappear 
entirely;  but  even  after  the  crisis  they  have  been  found,  exceptionally  and 
in  very  small  numbers.  They  have  very  often  been  found  by  the  author  as  well 
as  other  observers  during  the  pseudo-crisis  described  above,  so  that,  after  the 
temperature  has  become  normal,  the  presence  of  spirilli  makes  it  very  prob- 
able that  another  rise  of  temperature  is  impending.  The  spirilli  have  thus  far 
been  found  in  the  blood  only,  in  the  catamenia,  in  bloody  urine,  or  in  blood 
coughed  up  from  the  lungs,  and  never  in  the  organs  or  secretions  (urine,  milk, 
sweat,  contents  of  herpetic  vesicles).  There  can  hardly  be  any  doubt  that  the 
spirilli  which  appear  in  the  separate  attacks  are  to  be  regarded  as  separate 
generations.  As  to  their  manner  and  place  of  development  we  have  as  yet  no 
knowledge.  In  the  final,  rudimentary  attacks,  we  find  few  if  any.  If  the 
patient  dies  during  an  attack,  they  are  to  be  found  in  the  blood  after  death. 
Artificial  cultivations  have  not  been  very  successful ;  nor  have  pure  cultures  of 
them,  to  our  knowledge,  ever  succeeded.  Albrecht  states  that  they  will  sub- 
sequently develop  in  blood  taken  from  a  patient  during  the  interval  when  he 
has  no  fever. 

The  blood  is  otherwise  modified  during  relapsing  fever.  We  very  often 
find  a  slight  increase  in  the  white  corpuscles.  There  is  often  a  noticeable 
abundance  of  very  small  bodies,  so-called  granular  elements-  (Kornchenbildun- 
gen).  The  significance  of  these  (the  remains  of  white  corpuscles?)  is  still 
doubtful.  There  are,  finally,  peculiar  cells,  rather  large,  with  fat  granules. 
They  were  demonstrated  by  Ponfick  in  the  venous  blood,  and  are  said  to  come 
from  the  spleen.    We  also  find  fatty-degenerated  endothelium  in  the  blood. 

Complications. — Complications  are,  on  the  whole,  rare,  and  mostly  second- 
ary. Important  among  these  are  troublesome  ophthalmic  disturbances,  especially 
iritis  and  irido-choroiclitis.  Sometimes  j)arotitis,  laryngitis,  or  pneumonia 
occur.  Epistaxis  is  a  not  infrequent  complication.  It  is  usually  profuse  and 
persistent,  and  it  may  even  be  dangerous.  Sometimes  there  has  been  rather 
severe  dysenteric  trouble.  In  one  case,  which  ended  fatally,  we  observed  a 
very  peculiar  intestinal  lesion,  consisting  of  hemorrhagic-necrotic  foci  in  the 
colon  and  lower  ileum.  In  severe  cases  acute  hemorrhagic  nephritis  occurs 
with  comparative  frequency.  At  the  autopsy  an  important  and  character- 
istic phenomenon  are  the  wedge-shaped  white  spots  which  occur  in  the  spleen, 
like  infarctions.  They  have  a  clinical  interest,  as  they  may  become  the  starting 
point  of  pysemic  conditions  or  of  peritonitis.  Splenic  abscesses  have  been 
observed  in  a  few  cases. 

Variations. — Variations  in  the  course  of  the  disease  occur  in  this,  as  in  all 
other  acute  infectious  diseases.  First,  there  are  mild,  abortive  cases,  in  which 
the  attacks  are  few  and  brief.  Then  cases  have  been  described  resembling 
intermittent  fever.  Of  chief  importance  is  that  severe  variety  of  relapsing 
fever  first  observed  in  Egypt  by  Griesinger,  and  described  as  "  bilious  typhoid." 
"  Bilious  typhoid "  fever  occurs  in  successive  attacks,  exactly  like  those  of 
relapsing  fever.  The  type  is  much  more  severe.  As  a  rule,  there  appear 
marked  icterus,  grave  nervous  symptoms,  hemorrhages  into  the  skin  and 
mucous  membranes;  and  the  termination  is  frequently  fatal.  The  autopsy 
shows  a  greatly  enlarged  spleen,  often  containing  infarctions  and  abscesses, 
and  in  some  cases  hepatic  abscesses,  septic  nephritis,  and  similar  lesions. 

The  two  diseases  have  been  heretofore  considered  either  identical  or  closely 


SCARLET   FEVER 

related — the  association  being  based  upon  the  alleged  finding  of  thi 
spirilla  in  both  eases,  and  on  the  alleged  transmission  of  blood  from  a  patient 
with  "bilious  typhoid"  to  a  normal  individual,  with  a  resultanl  development 
in  the  latter  of  an  ordinary  recurrent  fever!  Recent  studies  cast  consider- 
able doubt  upon  these  observations,  so  that  the  nosological  situation  of  "  bilious 
typhoid  "  is  at  present  not  decided  upon. 

Prognosis. — The  prognosis  of  ordinary  relapsing  fever  is  or  the  whole  very 
favorable.  In  the  last  epidemics  the  usual  mortality  was  only  two  to  four 
per  cent.  The  fatal  cases  could  some  of  them  be  Laid  to  wretched  nursing.  In 
the  remaining  portion  death  resulted  from  complications,  such  as  pneumonia 
and  nephritis. 

Treatment. — The  treatment  must  as  yet  be  purely  symptomatic.  Anti- 
pyretic treatment  is  generally  needless,  since  the  fever  is  relatively  brief  and 
often  quite  intermittent.  Moreover,  most  patients  cannot  well  ejidure  cold 
baths,  because  the  muscles  are  so  painful.  As  a  rule,  good  nursing  and  proper 
food  amply  suffice.  If  the  muscular  pains  are  very  violent,  we  may  order 
chloroform  liniment  as  an  embrocation.  Complications  are  to  be  treated  on 
general  principles. 

We  are  not  acquainted  with  any  remedy  that  can  influence  the  disease 
itself  or  avert  the  relapses.  Large  doses  of  quinin,  salicylic  acid,  etc.,  have 
been  frequently  employed  for  this  purpose,  but  never  with  success.  Lately 
there  has  been  ascribed  to  calomel  a  favorable  influence  upon  the  general 
course  of  the  disease,  and  its  use  is  said  to  diminish  the  number  of  attacks. 
We  must  await  further  evidence  in  support  of  this  statement. 


CHAPTEE    IV 

SCARLET    FEVER 

(Scarlatina) 

We  now  begin  the  consideration  of  those  acute  infectious  diseases  which  are 
usually  embraced  under  the  name  of  the  "  acute  exanthemata."  In  this  group 
are  reckoned,  besides  scarlet  fever,  measles,  German  measles,  smallpox,  and 
varicella.  Typhus  may  also  be  included  in  this  group  with  a  certain  amount 
of  justice.  The  point  which  these  diseases  have  in  common  is  that  in  all  of 
them  is  developed  a  characteristic  eruption,  of  slight  clinical  significance  in 
itself,  in  most  cases,  but  of  thoroughly  characteristic  appearance  in  each  dis- 
ease, and  hence  of  essential  importance  in  diagnosis.  A  number  of  the  acute 
exanthemata  have  this  further  point  of  mutual  resemblance  that  they  appear 
chiefly  in  children.  These  diseases  are  scarlet  fever,  measles,  German  measles, 
and  varicella. 

etiology. — Infection  with  the  specific  scarlatinal  poison  occurs  almost  al- 
ways by  contagion,  which  takes  place  very  readily.  A  single  approach  to  a 
patient  ill  with  scarlet  fever  may  suffice  to  communicate  the  disease.  There  is 
no  doubt  that  the  disease  may  be  transferred  by  objects  which  the  patient 
has  touched,  such  as  linen,  clothing,  furniture,  or  toys.    Persons  who  have  been 


44  ACUTE   GENERAL   INFECTIOUS   DISEASES 

with  the  sick  may  be  the  means  of  transmitting  the  disease,  although  them- 
selves unaffected.  In  England  it  has  been  thought  that  the  contagium  may  be 
carried  by  milk.  [Similar  observations  have  been  made  in  America  (Kober, 
Taylor,  Bell).] 

Numerous  observations  show  that  the  scarlatinal  poison  is  with  great  diffi- 
culty destroyed,  and  that  it  may  keep  its  contagious  powers  for  months 
("  tenacity  ").  We  can  thus  see  how  difficult,  how  impossible,  it  may  be  in  an 
individual  case  to  point  out  the  source  of  contagion.  Scarlet-fever  patients 
can  communicate  the  disease  certainly  as  late  as  the  end  of  the  desquamative 
period,  or  perhaps  somewhat  longer. 

Details  as  to  the  manner  of  contagion,  or  as  to  the  specific  poison  itself,  are 
as  yet  unknown.  All  statements  made  in  regard  to  finding  alleged  specific 
microorganisms  of  scarlet  fever  are  extremely  doubtful.  The  exciting  agent 
of  scarlet  fever  must,  however,  be  contained  in  the  blood  and  in  the  contents 
of  the  miliary  vesicles  of  scarlet-fever  patients,  for  the  disease  has  repeatedly 
been  artificially  produced  in  healthy  persons  by  inoculation  with  these  fluids. 

Predisposition  to  scarlet  fever  is  far  less  universal  than  is  predisposition  to 
measles  or  smallpox.  In  families  with  several  children  often  only  one  or  two 
fall  sick,  while  the  rest  escape,  although  equally  exposed.  As  age  increases, 
liability  to  the  disease  greatly  diminishes,  although  there  are  cases  of  scarlet 
fever  among  adults.  The  majority  of  patients  are  between  two  and  ten  years 
of  age.  Scarlet  fever  is  rare  during  the  first  year  of  life.  It  is  an  interesting 
fact  that  children  with  fresh  wounds,  either  accidental  or  surgical,  are  espe- 
cially liable  to  scarlet  fever.  An  analogous  and  familiar  fact  is  that  women 
after  delivery  have  a  strong  tendency  to  the  disease.1  As  a  rule,  a  person  is 
attacked  but  once,  so  that,  after  the  disease  is  over,  an  immunity  from  con- 
tagion is  enjoyed;  but  there  are  exceptions  to  this  rule. 

Scarlet  fever  is  now  spread  over  the  entire  globe.  In  Germany  there  are 
almost  always  some  sporadic  cases  in  the  larger  towns,  while  from  time  to  time, 
especially  in  autumn,  there  are  more  or  less  extensive  epidemics  in  one  place  or 
another.  There  is  considerable  variation  in  the  different  epidemics  of  scarlet 
fever,  as  in  many  other  infectious  diseases,  in  the  general  character  of  the  dis- 
ease, and  above  all  in  the  prevailing  mildness  or  severity  of  the  cases  and  the 
frequency  of  certain  complications  (nephritis,  diphtheria),  etc. 

Clinical  History. — The  period  of  incubation  is  not  definitely  known.  Many 
observations  seem  certainly  to  indicate  a  short  period  of  two  to  four  days,  but 
the  incubation  stage  is  perhaps  often  somewhat  longer — four  to  seven  days, 
and  even  more.  There  are  hardly  ever  any  decided  prodromata.  The  disease 
begins  rather  suddenly,  with  fever,  often  introduced  Iry  chilliness,  and  some- 
times by  a  well-marked  rigor.  There  is  almost  invariably  a  painful,  scarlatinal 
sore  throat.  A  further  symptom,  in  all  cases  of  any  severity,  is  cerebral  dis- 
turbance, generally  rather  intense.  There  may  be  headache,  dullness,  uneasy 
sleep,  delirium,  and,  in  smaller  children,  sometimes  even  convulsions.  A  very 
frequent  and  characteristic  early  symptom  is  vomiting,  which  may  be  repeated. 

The  characteristic  rash  usually  appears  as  soon  as  the  close  of  the  first  day, 
or  on  the  second,  and  begins  on  the  neck  and  on  the  chest  and  face,  quickly 

1  In  puerperal  cases  genuine  scarlet  fever  and  septic  diseases  were  formerly  often  confounded. 
(See  Chapter  XIX.) 


SCARLET  FEVER 


45 


becoming  almost  universal.  The 'eruption  consists  at  firs!  of  numberless  small 
red  points,  crowded  thickly  together  and  soon  united  into  a  diffuse,  intense, 
scarlet-colored  erythema.  The  small  and  somewhal  elevated  points  almost 
always  correspond  to  the  swollen  hair  follicles.  The  diffuse  redness  is  the 
result  of  an  excessive  hyperemia  of  the  skin,  and  vanishes  completely  on  pres- 
sure. The  skin  as  a  whole  seems  slightly  swollen  and  thickened.  The  hack 
usually  presents  the  most  vivid  tint.  In  the  face  there  is  generally  pallor  of 
the  lips  and  chin,  presenting  a  very  striking  and  characteristic  contrast  to  the 
bright-red  cheeks.  If  some  object  like  the  end  of  a  penholder  be  drawn  over 
the  red  skin,  there  soon  arise  corresponding  while  lines,  due  to  contraction  of 
the  blood  vessels.  It  is  possible  thus  to  make  letters  or  pictures  upon  the  back 
of  the  patient.  We  should  add,  however,  that  this  is  not  a  peculiarity  of  the 
scarlatinal  eruption,  being  seen  in  other  erythematous  eruptions. 

The  rash  persists  for  some  three  or  four  days,  at  first  even  increasing  some- 
what in  vividness.  It  often  appears  more  intense  by  artificial  light  than  in  the 
•daytime.  Meanwhile  the  severe  general  symptoms  continue — the  fever,  the 
usually  excessively  rapid  pulse,  the  cerebral  symptoms,  and  the  throat  trouble. 
The  spleen  is  often  somewhat  swollen,  though  seldom  very  large.  Then  the 
eruption  begins  to  fade,  the  fever  gradually  ceases  by  lysis,  the  general  condi- 
tion and  the  difficulty  in  swallowing  improve.  With  the  end  of  the  first  week 
or  the  beginning  of  the  second,  the  cases  which  run  the  typical  course  become 
fully  convalescent.  When  the  rash  disappears,  the  epidermis  usually  begins 
to  peel  off,  in  a  very  characteristic  way,  in  pieces  of  considerable  size.  The 
exfoliation  upon  the  hands  and  feet  is  especially  pronounced,  and  the  little 
convalescents  often  amuse  themselves  by  peeling  off  the  epidermis  in  strips. 
Cases  which  are  apparently  the  mildest  and  most  benign  may  have  their 
convalescence  interrupted  by  the  oc- 
currence of  a  secondary  scarlatinal 
nephritis.  There  is  no  sure  proph- 
ylaxis against  this. 

We  will  now  pass  on  from  this 
general  summary  to  a  more  complete 
consideration  in  detail  of  general 
and  local  symptoms ;  and  we  shall 
see  how  manifold  are  the  clinical 
phenomena  presented  by  scarlet 
fever. 

1.  Fever  (see  Fig.  7). — Although 
in  a  few  undeveloped  cases  there  is 
no  fever,  or  scarcely  any,  almost  all 
cases  of  any  severity  have  high 
fever.  It  is  only  exceptionally  that 
severe   cases   are   observed   in   which 

the  bodily  temperature  is  little  if  at  all  elevated.  As  a  rule,  the  fever 
rises  rapidly  upon  the  very  first  day,  corresponding  to  the  sudden  on- 
set of  all  the  symptoms,  to  about  104°  to  105°  F.  (40°  to  40.5°  C).  The 
next  day  it  often  becomes  a  little  higher  still,  and  then  persists  with  but 
slight  variations,  as  a  rule,  so  long  as  the  eruption  it  at  its  height.  Dur- 
ing this   period  a   temperature   of   105°   F.   or   more    (40.5°   to   41°   C.)    is 


40.0° 


39.0° 


38.0° 


37.0° 


immm 
imvtm 

m*&m 

IIIHB 

mm 

III! 
II1BS 


mi 


im 


rami 


1MWa\ 


iies 

IB- 


1'W 


Fig.  7. 


Eruption. 

— Example  of  a  normal  scarlet-fever 
curve. 


46  ACUTE   GENERAL   INFECTIOUS   DISEASES 

not  infrequently  observed.  When  the  eruption  fades,  and  the  other  symp- 
toms dec-line,  defervescence  occurs.  This  happens  but  rarely  by  crisis, 
and  that  in  the  slight  attacks.  It  is  almost  always  by  prolonged  lysis,  as  in 
typhoid,  only  more  irregularly  and  more  rapidly.  If  the  fever  lasts  into  the 
second  week  of  the  disease,  it  is  almost  always  (though  not  without  excep- 
tions) caused  by  demonstrable  complications.  The  most  frequent  causes  are 
the  persistence  of  a  severe  sore  throat,  the  occurrence  of  inflammatory  changes 
in  the  cervical  glands,  or  a  purulent  otitis  media.  In  closing  what  we  have  to 
say  about  the  fever  in  this  disease,  we  would  emphasize  the  fact  that  the  pulse 
is  often  very  rapid  (140  to  160  a  minute),  even  in  comparison  with  the  height 
of  the  temperature. 

2.  The  Throat. — The  throat  presents  the  most  constant  local  lesion  of  scar- 
let fever.  Sore  throat  is  only  in  the  rarest  cases  wholly  absent ; x  but  its  form 
and  intensity  may  vary  extremely.  The  mildest  variety  is  a  simple,  erythema- 
tous catarrh,  without  much  swelling,  but  exhibiting  usually  a  vivid  and  often 
punctate  reddening  of  the  soft  palate  and  tonsils,  the  pharynx,  and  also  the 
mucous  membrane  of  the  hard  palate,  frequently  associated  with  enlargement 
of  the  little  mucous  follicles.  Sometimes  minute  hemorrhages  take  place  into 
the  mucous  membrane.  In  other  cases  the  scarlatinal  affection  of  the  throat 
is  from  the  start  associated  with  considerable  swelling  of  the  parts,  and  espe- 
cially of  the  tonsils,  justifying  the  term  "  parenchymatous  sore  throat."  Not 
infrequently  small  abscesses  form  in  the  lacunas  of  the  tonsils;  or  superficial 
spots  of  necrosis  develop  which  leave  behind  them  larger  or  smaller  ulcers,  and 
sometimes  occasion  considerable  hemorrhage.  There  may  even  be  a  circum- 
scribed gangrene  of  the  tonsils. 

The  most  important,  because  it  is  also  the  most  dangerous,  of  the  affections 
of  the  throat  resulting  from  scarlet  fever  is  the  so-called  scarlatinal  diphtheria 
— that  is,  a  "  diphtheritic,"  or  better,  a  necrotic  inflammation  of  the  tonsils 
and  soft  palate.  This  usually  develops  on  the  third,  fourth,  or  fifth  day  of  the 
disease,  replacing  a  simple  inflammatory  condition  of  the  parts.  Whitish, 
dirty-colored  spots  develop  on  the  tonsils,  the  arches  of  the  palate,  and  the 
uvula.  These  rapidly  increase  in  size,  and  cause  a  dry  necrosis  of  the  mucous 
membrane  and  subsequent  ulceration.  The  process  is  a  truly  "  diphtheritic  " 
one — that  is,  there  is  an  inflammation  combined  with  an  extension  into  the 
diseased  tissues  of  a  fibrinous  exudation. 

It  is  especially  characteristic  of  scarlatinal  diphtheria  that  there  is  almost 
invariably  a  considerable  swelling  of  the  cervical  lymph-glands,  except  in  those 
cases  which  die  very  quickly.  It  is  true  that  the  glands  are  usually  somewhat 
enlarged  in  the  milder  forms  of  pharyngitis  accompanying  scarlet  fever,  but 
they  seldom  attain  the  size  observed  in  the  true  diphtheritic  process.  In  this 
there  is  an  inflammatory  and  cedematous  infiltration  affecting  often  not  only 
the  glands  themselves,  but  also  the  surrounding  connective  tissue,  so  that  in 
severe  cases  the  whole  cervical  region  and  the  floor  of  the  buccal  cavity  present 
a  firm  and  usually  a  very  painful  enlargement.     It  should  be  added  that  the 

i  Absence  of  sore  throat  has  been  noted  by  others  and  by  myself,  especially  in  the  scarlet  fever 
of  women  in  childbed.  I  suspect  that  the  reason  for  this  is  that  the  infection  does  not  enter  in 
the  usual  way  through  the  mouth,  but  from  some  wound  due  to  parturition.  On  the  other  hand, 
it  is  to  be  noted  that  in  the  scarlet  fever  from  wounds,  when  the  infection  follows  an  injury  to  the 
finger,  etc.,  a  sore  throat  occurs. 


SCARLET    FEVER  47 

severity  of  the  throat  symptome  and  the  extent  of  the  glandular  swelling  are 
not  always  commensurate.  Almost  always  the  scarlatinal  diphtheria  is  asso- 
ciated with  a  marked  stomatitis,  ami  very  often  also  with  a  severe  purulent 
or  even  diphtheritic  rhinitis,  although  an  invasion  of  the  larynx  (vide  infra) 
is  only  exceptionally  seen.  At  the  alae  of  the  nose  and  the  corners  of  the  mouth 
there  are  often  superficial  ulcers  from  this  cause.  Otitis  is  also  a  frequent 
complication  of  scarlatina  (vide  infra). 

The  influence  of  the  scarlatinal  diphtheria  upon  the  general  condition  of 
the  patient  is  always  considerable.  Apart  from  the  marked  local  discomfort, 
there  is  often  a  severe  general  septic  condition.  Grave  signs  of  cardiac  weak- 
ness (a  very  rapid,  small  pulse)  are  very  apt  to  appear  early.  Moreover,  cases 
of  scarlet  fever  associated  with  pharyngeal  diphtheria  often  .-how  at  the  same 
time  other  severe  septic  complications  (inflammation  of  several  joints,  sim- 
ple or  purulent  inflammation  of  the  serous  membranes,  nephritis,  etc.).  Many 
cases  end  fatally  in  a  few  days,  while  others  pursue  a  more  tedious  course, 
lasting  perhaps  several  weeks  before  death  comes.  These  are  often  associated 
with  pyaemic  processes  in  other  parts  of  the  body. 

With  regard  to  the  pathogenesis  of  the  throat  troubles  seen  in  scarlet  fever, 
the  more  simple  forms  are  in  all  probability  directly  associated  with  the  scar- 
latinal process — that  is,  they  are  direct  sequences  of  the  affection.  In  regard, 
however,  to  the  severer  forms,  and  especially  to  the  diphtheritic  variety,  it  is 
almost  certain  that  these  are  not  a  direct  result  of  the  scarlatinal  poison,  but 
are  due  to  some  secondary  infection  which  occurs  on  the  soil  furnished  by  the 
primary  scarlatinal  angina.  The  severe  necrotic  disease  of  the  mucous  mem- 
branes and  the  secondary  changes  in  the  lymph-glands  and  other  septic  com- 
plications are  due  chiefly  to  streptococci  (Loftier).  Jochmann  could  also  find 
the  streptococci  in  the  blood  in  almost  all  the  severe  cases.  There  seems  to  be  a 
certain  intimate  relationship  between  the  scarlatinal  and  the  streptococcus  in- 
fection; otherwise,  it  is  very  difficult  to  explain  why  such  a  characteristic  sec- 
ondary condition,  the  "  scarlatinal  diphtheria,"  develops  only  in  scarlet  fever. 
The  latter  and  true  diphtheria  are,  however,  not  identical.  From  a  purely 
clinical  standpoint  they  present  several  important  points  of  difference.  In 
particular,  the  scarlatinal  diphtheria,  in  contrast  with  the  primary  form  of  the 
disease,  seldom  spreads  to  the  larynx.  The  severe  dyspnoea  which  sometimes 
develops  in  the  course  of  scarlet  fever  is  probably  caused  by  an  inflammatory 
oedema  of  the  glottis.  Paralysis  of  the  soft  palate,  the  ocular  muscles,  and 
other  parts,  is  scarcely  ever  a  sequel  of  scarlatinal  diphtheria.  Besides  the 
streptococcus  diphtheria,  true  diphtheria  with  all  its  sequelae  (laryngeal  croup, 
etc.),  sometimes  complicates  scarlet  fever.  It  is  identified  by  the  presence  of 
true  diphtheria  bacilli  in  the  cultures. 

3.  Parts  Adjacent  to  the  Throat. — We  proceed  by  a  natural  sequence  to 
the  consideration  of  the  affections  of  certain  parts  adjacent  to  the  throat, 
troubles  which  must  be  regarded  as  chiefly  the  result  of  direct  extension,  or  of 
a  conveyance  of  the  inflammatory  process  from  the  throat. 

The  stomatitis  we  have  already  mentioned,  as  well  as  the  disturbance  in  the 
neighboring  lymph-glands  and  the  surrounding  tissue.  Parotitis  is  not  rare  in 
severe  cases.  Of  special  importance  is  the  scarlatinal  inflammation  of  the  mid- 
dle ear,  because  it  so  often  leads  to  permanent  and  serious  disturbances  of 
function.     It  not  infrequently  occurs  in  the  desquamating  period  in  the  form 


48  ACUTE   GENERAL   INFECTIOUS   DISEASES 

of  a  benign  purulent  otitis,  but  may,  on  the  other  hand,  occur  at  the  height 
of  the  disease  in  a  very  serious  form,  with  a  pronounced  tendency  to  necrotic 
degeneration.  This  more  serious  form,  as  in  the  case  of  "  scarlatinal  diph- 
theria," is  a  strejDtococcus  infection  of  a  severe  type.  Sometimes,  however, 
there  is  a  true  aural  diphtheria.  Destruction  of  the  ossicles,  the  mucous  mem- 
brane of  the  middle  ear,  and  the  tympanic  membrane  may  occur  in  a  few 
days.  In  especially  severe  cases  the  necrotic  inflammation  extends  to  the 
mastoid  process,  the  labyrinth,  the  sigmoid  sinus,  etc.,  and  may  even  lead  to  a 
purulent  meningitis.  It  should  be  mentioned  that  this  serious  complication 
nearly  always  commences  without  any  marked  pain.  It  is  therefore  readily 
overlooked  in  the  beginning,  especially  since  the  deafness  of  the  little  patients 
does  not  attract  attention  while  they  are  so  ill.  When  perforation  of  the 
drum  membrane  occurs,  there  is  usually  a  purulent  foul-smelling  discharge. 
If  the  children  recover  from  the  scarlet  fever,  permanent  difficulty  in  hearing 
very  often  remains.  Statistics  have  shown  that  four  or  five  per  cent  of  all 
cases  of  deafness  are  referable  to  an  attack  of  scarlet  fever  in  childhood.  Not 
a  small  percentage  of  cases  of  deaf-mutism  is  due  to  scarlet-fever  otitis. 

We  have  already  spoken  of  the  purulent  or  even  diphtheritic  rhinitis  which 
almost  always  accompanies  the  scarlatinal  sore  throat.  In  rare  cases  there  may 
also  occur  a  purulent  conjunctivitis,  which  is  most  probably  the  result  of  a 
direct  conveyance  of  inflammatory  secretions. 

The  tongue  in  scarlet  fever  deserves  special  mention.  The  first  coating 
cleans  off,  and  then  the  tongue  usually  presents  a  very  characteristic  appear- 
ance. It  is  diffusely  reddened  and  covered  with  little  elevations  corresponding 
to  swollen  papillae  (strawberry  or  raspberry  tongue,  scarlatinal  tongue). 

4.  The  Skin. — The  characteristic  eruption,  as  developed  in  the  great  ma- 
jority of  cases,  has  been  described  above.  It  remains  to  describe  certain  varia- 
tions from  the  usual  appearances. 

First,  the  eruption  may  be  rudimentary.  It  is  then  not  pronounced,  and 
visible  only  on  a  limited  portion  of  the  body  (face,  trunk,  or  extremities). 

Variations  from  the  type  are  not  rare;  sometimes  the  papules  are  more 
strongly  developed  (scarlatina  papulosa)  ;  very  frequently  there  are  little  vesi- 
cles (scarlatina  miliaris).  This  latter  form  of  the  eruption  appears  by  pref- 
erence upon  the  trunk,  but  it  may  come  also  upon  the  extremities,  and  is  often 
brought  out  by  excessive  perspiration,  or  by  wrapping  up  the  patient  too 
warmly.  Many  epidemics  are  noticeable  from  the  frequent  appearance  of  this 
miliary  form.  More  rarely  the  rash  has  a  spotted  look,  resembling  the  erup- 
tion of  measles  (scarlatina  variegata).  There  may  be  minute  ecchymoses, 
which  are  not  very  rare  and  not  ominous.  Well-developed  cases  of  hemor- 
rhagic scarlatina  are,  however,  very  dangerous,  because  here  the  general  in- 
fection of  the  system  is  almost  always  exceedingly  severe,  and  probably  due  to 
secondary  sepsis;  and  there  is  besides,  as  a  rule,  a  general  hemorrhagic  di- 
athesis. Other  cutaneous  lesions,  especially  herpes  and  urticaria,  are  not  so 
very  unusual  in  connection  with  the  scarlatinal  eruption.  Furunculosis  has 
been  repeatedly  observed  after  the  rash  fades. 

Desquamation  generally  begins  as  soon  as  the  rash  has  completely  disap- 
peared, but  it  may  not  occur  till  a  few  days  or  even  one  or  two  weeks  later. 
Its  extent  corresponds  in  general  to  the  severity  of  the  eruption,  although 
extensive  desquamation  may  follow  a  rudimentary   eruption.     It  is  seldom 


SCARLET   FEVER  49 

bran-like  or  furfuraceous,  as  in  measles.    The  rule  is  for  ii  to  be  in  lamella-, 
so  that,  as  we  have  slated,  quite  large  stripe  of  epidermis  may  be  detached 

entire 

In  rare  eases  an  oedema  of  (lie  skin  appears  alter  scarlel  fever,  which  can- 
not be  shown  to  depend  upon  nephritis  (vide  infra),  but  which  may  perhaps 
be  due  to  an  abnormal  permeability  of  the  walls  of  the  cutaneous  blood  vessels 
following  the  eruption  (hydrops  scarlatinosus  sine  nephritide). 

5.  The  Kidneys. — Next  to  the  severer  forms  of  tbroat  trouble,  the  most  im- 
portant and  dangerous  complications  are  located  in  the  kidneys.  They  may 
appear  as  early  as  the  acme  of  the  disease,  as  in  many  other  infectious  diseases. 
The  urine  has  a  trace  of  albumen.  In  rare  cases  the  amount  of  albumen  may 
be  considerable.  The  appearance  of  the  urine  is  generally  not  much  changed, 
and  the  microscope  reveals  but  few  abnormal  constituents.  There  are  some 
white  and  red  blood  globules,  a  few  hyaline  casts,  sometimes  one  or  two  renal 
epithelial  cells.     This  initial  albuminuria  very  rarely  gives  cause  for  alarm. 

The  genuine  scarlatinal  nephritis  scarcely  ever  develops  much  before  the 
end  of  the  second  or  the  beginning  of  the  third  week.  Sometimes  it  comes 
even  later.  In  one  case  under  our  own  observation  it  did  not  begin  till  the 
thirty-third  day  of  the  disease.  It  may  therefore  be  regarded  to  a  certain 
degree  as  a  localized  relapse.  It  may  be  so  mild  as  to  cause  no  subjective  symp- 
toms whatever,  so  that  it  would  be  unnoticed  if  the  urine  were  not  carefully 
examined.  On  the  other  hand,  it  may  be  accompanied  by  the  gravest  symp- 
toms, and  may  soon  terminate  fatally.  It  may  follow  either  severe  cases  or 
the  mildest,  so  that  the  rule  should  be  to  examine  the  urine  in  every  case  of 
convalescence  from  scarlet  fever  as  often  and  as  carefully  as  possible.  Xo 
exact  statement  can  be  made  as  to  the  frequency  of  this  complication,  for  it 
is  much  more  common  in  some  epidemics  than  in  others. 

The  development  of  nephritis  is  often  marked  by  a  fresh  rise  of  tempera- 
ture. The  elevation  may  be  slight  or  it  may  reach  104°  F.  (40°  C).  Accord- 
ing to  our  own  experience,  the  fever  often  comes  a  day  or  two  earlier  than  the 
changes  in  the  urine.  As  the  nephritis  goes  on,  it  is  very  often  accompanied 
by  a  moderate  fever  with  remissions.  This  fever  may  be  almost  wholly  absent, 
especially  in  mild  cases.  The  pulse  generally  becomes  harder,  and  is  some- 
times quickened ;  but  in  many  cases  it  will  be  slow,  and  it  is  sometimes  irregu- 
lar. Among  other  objective  symptoms,  the  first  to  excite  notice  is  generally  a 
slight  puffiness  of  the  face,  which  is  usually  pale.  The  eyelids,  particularly, 
present  an  evident  oedema.  In  the  milder  cases  this  oedema  remains  limited, 
while  in  others  it  gradually  increases  in  extent  and  degree,  involving  first, 
as  a  rule,  the  dependent  parts  of  the  trunk,  and  later  the  extremities.  Severe 
cases  develop  a  pronounced  anasarca.  There  are  then,  usually,  effusions  into 
the  serous  cavities,  especially  ascites  and  hydrothorax.  The  latter  is  dangerous 
chiefly  through  disturbance  of  the  respiration,  particularly  if  it  be  associated 
with  severe  bronchitis  or  pneumonia  (vide  infra).  Although,  in  general,  the 
development  of  a  universal  dropsy  is  characteristic  of  scarlatinal  nephritis, 
there  may  sometimes  be  no  oedema.  On  the  other  hand,  it  is  noteworthy  that 
the  oedema  may  occasionally  show  a  peculiar  localization,  especially  in  the 
mucous  membranes  (oedema  of  the  conjunctivae,  oedema  of  the  aryepiglottic 
folds  with  symptoms  of  laryngeal  stenosis,  oedema  of  the  uvula  and  soft 
palate,  etc.). 


50  ACUTE   GENERAL   INFECTIOUS   DISEASES 

The  urine  exhibits  the  most  important  changes  (vide  the  section  on  renal 
diseases).  These  may  be  insignificant  in  the  milder  cases,  but  they  are  very 
pronounced  in  the  severe  ones.  The  amount  is  much  diminished.  Sometimes 
there  will  be  for  several  days  almost  complete  anuria.  In  cases  of  any  severity 
the  urine  is  turbid,  dark,  often  evidently  bloody,  with  increased  specific  gravity 
(about  1.015  to  1.025),  and  containing  a  large  amount  of  albumen.  The  sedi- 
ment is  generally  abundant,  and  exhibits  numerous  hyaline  casts  of  various 
lengths  and  diameters.  To  these  may  be  attached  red  or  white  blood  corpuscles, 
detritus,  granules  of  haematoidin,  or  bacteria.  In  cases  of  some  duration  the 
casts  are  often  moderately  fatty.  Very  frequently  there  are  found  noticeably 
long  and  broad  waxy  [fibrinous]  casts,  which  are  opaque  and  yellow.  In  many 
cases  of  scarlatinal  nephritis  the  urine  is  peculiar  in  having  very  many  white 
blood  corpuscles,  either  isolated  or  adhering  to  the  casts.  These  undoubtedly 
originate  for  the  most  part  in  the  kidneys.  Eed  globules,  some  of  them  in 
the  form  of  colorless  rings,  are  found.  They  are  usually  present  in  small  num- 
bers, but  may  become  more  abundant,  especially  for  a  day  at  a  time.  We 
have  seen  a  very  hemorrhagic  urine  after  the  special  albuminuria  had  disap- 
peared. Renal  epithelium  is  frequently  seen,  but  not  invariably  nor  in  very 
large  amount. 

Ursemic  symptoms  often  develop  in  scarlatinal  nephritis.  They  may  be  of 
all  degrees  of  severity.  They  will  be  described  in  detail  under  diseases  of  the 
kidney  (vide  infra).  The  uraemia  may  be  so  severe  as  to  cause  convulsions, 
coma,  and  death ;  but  it  is  remarkable  how  often  children  recover  from  what 
seems  to  be  the  most  pronounced  uraemia. 

The  duration  of  scarlatinal  nephritis  varies  greatly  according  to  its  sever- 
ity. In  cases  which  run  a  favorable  course,  the  urine  is  generally  abnormal 
for  two  to  four  weeks,  or  even  longer.  There  is  sometimes  a  very  slight  albu- 
minuria present  for  months  without  causing  any  symptoms.  Death  may  be 
due  to  uraemia  or  more  frequently  it  may  come  on  with  severe  dyspnoea.  The 
latter  is  due  partly  to  dropsical  conditions  (hydrothorax,  ascites),  or  often  to 
a  severe  diffuse  bronchitis  or  pneumonia  accompanying  the  nephritis.  Cardiac 
insufficiency  also  may  be  the  cause  of  death.  The  transition  of  acute  scarla- 
tinal nephritis  into  chronic  nephritis,  especially  into  chronic  contracted  kid- 
ney, is  rare,  but  it  has  certainly  been  seen  both  by  ourselves  and  others.  It  is 
worthy  of  note  that,  after  the  nephritis  has  lasted  some  four  to  six  weeks, 
beginning  hypertrophy  of  the  left  ventricle  can  be  detected  by  the  displacement 
and  strengthening  of  the  apex  beat.  Friedlander  has  demonstrated  this  early 
hypertrophy  at  autopsy. 

The  anatomical  changes  of  scarlatinal  nephritis  can  be  mentioned  only 
briefly  here.  The  forms  vary.  We  often  find  the  "  large  white  kidney  " — 
that  is,  a  diffuse  acute  nephritis  with  fatty  degeneration  of  the  epithelium — 
and  usually  also  more  or  less  numerous  hemorrhages.  In  other  cases  the 
kidneys  macroscopically  are  apparently  little  altered,  but  we  see  in  the  cortex 
the  gray,  prominent,  bloodless  glomeruli,  in  which  the  microscope  shows  very 
marked  changes  ("  glomerulo-nephritis  "  of  Klebs  and  others). 

6.  The  Joints. — When  desquamation  begins,  or  even  earlier,  pain  and 
swelling  may  attack  a  certain  number  of  the  joints.  This  trouble  was  for- 
merly called  scarlatinal  rheumatism,  but  now  it  is  usually  known  as  scarla- 
tinal synovitis.     It  is  generally  mild  and  quite  temporary,  but,  exceptionally, 


SCARLET    FEVER  51 

it  may  be  severe  and  even  puruleriT.    Then  it  ie  usually  a  part  of  a  secondary 
sepsis,  as  evinced  I > \  such  other  lesions  as  empyema,  subcutaneous  ab 
jaundice,  splenic  tumor,  nephritis,  etc.;  and  they  all  seem  to  be  caused  by  a 

secondary  infection  with  streptococci,  etc. 

We  have  seen  a  few  instances  of  excessive  pain  in  the  muscles  of  the  thighs, 
accompanied  by  a  moderate,  diffuse  swelling. 

7.  Other  Complications. — Another  important  complication  of  scarlet  fever 
is  pneumonia.  In  severe  cases  lobular  pneumonia  sometimes  appears  as  early 
as  the  first  stage  of  the  disease;  but  it  occurs  more  frequently  in  connection 
with  the  nephritis,  when  it  may  have  the  significance  of  so-called  nephritic 
pneumonia  (vide  infra).  The  respiration  may  be  very  serious] v  einharrassed 
by  it.  Inflammations  of  serous  memhranes  in  the  chest — viz.,  endocarditis, 
pericarditis,  and  pleurisy — are  more  rare.  They  may  or  may  not  be  accom- 
panied by  disturbances  in  the  joints  (vide  supra).  Pericarditis,  endocarditis, 
and  myocarditis  sometimes  develop  during  scarlet  fever,  but  it  is  usually  hard 
to  decide  whether  they  are  due  to  the  direct  action  of  the  scarlatinal  poison 
itself  or  to  secondary  septic  complications.  We  refer  the  tendency  to  tachy- 
cardia or  bradycardia,  irregularity  of  the  heart  beat,  etc.  (which  sometimes 
lasts  long  after  the  scarlet  fever),  to  myocarditic  changes.  Endocarditis  may 
result  in  permanent  valvular  disease.  Quite  severe  intestinal  symptoms,  such 
as  diarrhea,  may  appear.  These  are  generally  the  result  of  a  catarrhal  in- 
flammation of  the  intestinal  follicles.  Dysentery  is  less  frequent.  The 
enlargement  of  the  spleen  has  been  already  mentioned.  The  liver  is  sometimes 
found  to  be  considerably  enlarged.  A  general  moderate  swelling  of  the  lymph- 
glands  (neck,  axillae,  groins)  is  usually  present  in  scarlet  fever  at  the  time  of 
the  eruption.  We  usually  find  in  the  blood  a  pronounced  leucocytosis  which 
sometimes  lasts  long  after  the  other  morbid  symptoms. 

The  marked  increase  in  the  eosinophile  cells  (up  to  fifteen  to  twenty  per 
cent  of  all  the  white  cells)  is  a  very  striking  condition  that  is  almost  regu- 
larly present;  it  usually  appears  about  the  third  clay  of  the  disease. 

Variations  in  the  Course  of  the  Disease. — The  diversities  of  the  clinical  pic- 
ture in  different  cases  of  scarlatina  will  be  understood  when  we  consider  the 
variety  and  number  of  the  disturbances  thus  far  cited.  It  is  to  be  added  that 
the  general  course  of  the  disease  may  exhibit  numerous  peculiarities,  of  which 
it  is  hardly  possible  to  give  an  exhaustive  presentation.  We  will  content  our- 
selves with  a  cursory  statement  of  the  most  important  deviations  from  the 
typical  course. 

1.  Rudimentary  Forms. — To  this  class,  in  which  the  disease  does  not  reach 
a  perfect  development,  belong  first  the  cases  of  simple  sore  throat  with  no 
eruption,  or  at  most  an  extremely  faint  and  partial  one  (scarlatina  sine  exan- 
themate).  Sometimes  even  the  sore  throat  is  hardly  to  be  seen,  and  there  is 
nothing  but  a  brief  and  slight  fever  with  mild  symptoms  of  general  disturb- 
ance. The  recognition  of  these  cases  as  scarlatinal  is  possible  only  when  we 
consider  their  aetiological  relation  to  other  undoubted  cases  of  scarlet  fever. 
We  had  an  excellent  opportunity  to  observe  them  when  the  disease  broke  out 
in  the  children's  wards  of  the  hospital  at  Leipsic.  The  diagnosis  is  sometimes 
confirmed  by  a  slight  though  evident  desquamation,  affecting  the  hands, 
feet,  legs,  and  back,  or  by  an  acute  nephritis,  which  may  follow  the  mild- 
est attacks  of  this  sort.     Many  cases  of  acute  nephritis,  though  apparently 


52  ACUTE   GENERAL   INFECTIOUS   DISEASES 

wholly   spontaneous   and   primary,   must   be   regarded   as   setiologically   scar- 
latinal. 

2.  Rudimentary  hut  Pernicious  Forms. — Under  this  head  belong  those 
attacks  of  scarlet  fever  in  which  the  erujDtion  is  scanty  or  absent,  while  from 
the  very  start  the  most  violent  general  symptoms  appear.  There  is  a  very  high 
fever,  excessively  rapid  pulse,  and  delirium.  Such  cases  must  be  the  result 
of  an  uncommonly  severe  general  infection.  They  usually  end  in  speedy  death. 
Other  cases,  ending  fatally  in  a  few  days,  have  a  well-developed  rash  without 
other  localized  disturbances. 

3.  Severe  Forms  with  a  more  Protracted  Course. — In  these  cases  the  long 
duration  is  not  the  exclusive  result  of  especial  complications,  but  is  likewise 
due  to  the  severity  of  the  intoxication.  One  variety  is  the  so-called  typhoidal 
form  of  scarlatina,  with  persistent  high  fever  and  severe  constitutional  symp- 
toms. Another  variety  is  the  hemorrhagic  form  briefly  mentioned  above,  in 
which  there  are  extensive  hemorrhages  into  the  skin  and  into  the  mucous  and 
serous  membranes.  This  form  may  run  an  extremely  acute  course.  Further, 
in  all  pernicious  forms,  there  may  be  severe  local  complications,  particularly 
diphtheritic  or  gangrenous  sore  throat,  inflammations  of  serous  membranes, 
etc.  Attacks  of  this  sort  are  often  not  produced  by  the  poison  of  scarlet  fever 
alone,  but  by  secondary  complicating  infections  {vide  supra). 

4.  Relapses. — In  extremety  rare  cases  relapses  occur.  After  the  first  ill- 
ness a  fresh  eruption  breaks  out  with  all  the  other  symptoms  of  scarlet  fever. 
In  anomalous  cases  running  a  severe  course,  there  is  sometimes,  at  an  ad- 
vanced stage,  a  fresh,  imperfect  eruption  (generally  in  spots),  which  Thomas 
has  termed  a  pseudo-relapse.     Probably  this  is  usually  a  septic  eruption. 

Diagnosis. — The  diagnosis  of  scarlet  fever  is  made  in  most  cases  from  the 
characteristic  eruption  taken  in  connection  with  the  other  symptoms.  "We 
should,  however,  bear  in  mind  that  exceptionally  other  eruptions  appear  which 
exhibit  the  closest  resemblance  to  that  of  scarlet  fever.  1.  After  the  use  of 
certain  drugs,  especially  atropin  (belladonna),  quinin,  antipyrin,  morphin, 
chloral,  etc. ;  more  rarely  after  the  ingestion  of  crabs,  fish,  etc. ;  and  sometimes 
after  the  injection  of  antitoxic  sera.  2.  As  a  symptom  of  other  infectious 
diseases,  such  as  typhoid  fever,  smallpox;  and,  above  all,  in  septic  diseases 
(vide  infra).  In  an  uncertain  or  anomalous  case,  factors  of  importance  for 
diagnosis  are  the  aetiology  (connection  with  other  well-defined  cases),  the 
initial  sore  throat,  and  the  eventual  occurrence  of  desquamation  or  of  a  sec- 
ondar}'  nephritis. 

Prognosis. — The  prognosis  must  in  every  case  be  guarded.  From  what  has 
been  said  of  the  course  of  the  disease,  it  is  evident  that,  even  in  cases  which 
are  at  first  apparently  the  most  favorable,  dangerous  complications  may  appear. 
The  commonest  dangerous  complication  during  the  height  of  the  disease  is 
scarlatinal  diphtheria,  the  commonest  dangerous  sequel  is  nephritis. 

Treatment. — The  majority  of  those  cases  of  scarlet  fever  which  take  a  typi- 
cal course  will  recover  completely  without  our  aid.  In  these  the  task  of  the 
physician,  so  far  as  treatment  is  concerned,  consists  in  arranging  the  details 
of  hygiene  and  the  general  care  of  the  patient.  The  sick-room  should  be  cool 
and  well  ventilated  and  the  diet  rather  strict,  consisting  mainly  of  milk. 
Broths  and  eggs  may  also  be  allowed.  We  should  see  that  the  skin  and  the 
mouth  are  kept  clean.     To  change  the  linen  frequently,  if  done  with  proper 


SCARLET   FEVER  53 

precaution,  is  not  only  permissible,  but  very  desirable.  Rubbing  the  skin  wii.li 
olive  oil,  vaselin,  etc.,  lias  some  merit,  and  is  especially  to  be  recommended 
if  the  skin  be  harsh  and  dry  after  the  eruption  has  faded. 

[From  the  moment  that  the  disease  is  declared,  the  patienl  should  be  thor- 
oughly anointed  daily  with  carbolized  vaselin,  lard,  or  the  like;  and  this  should 
be  kept  up  until  desquamation  has  ceased.  Xot  only  is  the  comfort  of  the 
patient  promoted,  but  the  danger  of  the  spread  of  the  infection  is  thereby 
greatly  lessened.] 

The  scarlatinal  disease  of  the  throat  must  be  treated  with  the  greatest  at- 
tention, the  main  duty  of  the  physician  in  this  regard  being  to  prevent,  if 
possible,  the  ingress  of  the  above-mentioned  secondary  infection.  It  is  there- 
fore our  opinion  that  in  every  case  of  scarlet  fever  the  greatest  pains  should 
be  taken  from  the  very  commencement  of  the  disease  to  maintain  complete 
disinfection  of  the  mouth  and  throat.  Larger  children  may  use  a  gargle  of 
chlorate  of  potash,  hydrogen  peroxid,  borax,  permanganate  of  potash,  sage  tea, 
etc.  Inhalations  of  hydrogen  peroxid,  boric  acid,  etc.,  are  also  to  be  recom- 
mended where  practicable.  If  there  is  prostration,  or  if  the  child  be  young 
or  willful,  we  may  frequently  cleanse  the  mouth  and  throat  by  means  of  a 
spray  apparatus.  Sometimes  it  is  a  good  plan  to  let  the  patient  swallow  slowly 
a  half  teaspoonful  of  a  solution  of  potassium  chlorate  (about  1  to  40),  every 
half  hour  or  oftener,  with  the  object  of  contributing  to  the  local  disinfection 
of  the  throat.  If  scarlatinal  diphtheria  nevertheless  develops  and  the  cervical 
lymph-glands  begin  to  increase  further  in  size,  there  is  reason  to  hope, 
according  to  the  experience  of  Taube  and  Heubner,  that  parenchymatous  in- 
jections into  the  tissue  of  the  tonsils  or  the  palatine  arches  may  yet  check 
the  spread  of  the  secondary  infection.  About  6  minims  (a  Pravaz  syringe 
half  full)  of  a  three-per-cent  solution  of  carbolic  acid  may  be  injected  twice 
daily  upon  each  side  by  means  of  a  long  hollow  needle  and  a  subcutaneous 
syringe.  Catti  recommends  painting  the  affected  parts  with  a  1  to  1,000  solu- 
tion of  corrosive  sublimate.  Of  the  many  other  remedies  advised,  we  may 
add  that  the  insufflation  or  dusting  of  the  tonsils  with  powdered  sugar  is  of 
advantage.  In  ordinary  scarlatinal  diphtheria  we  can  expect  no  benefit  from 
Behring's  serum  therapy,  but  if  there  is  a  complication  with  true  diphtheria 
a  serum  injection  is  most  advisable. 

Numerous  attempts  have  recently  been  made  by  Moser  and  others  to  treat 
the  serious  secondary  streptococcus  infections  with  an  antistreptococcus  serum 
("  scarlet-fever  serum  of  the  Hochster  Farbwerke  ").  Although  good  observers 
(Escherich)  have  reported  favorable  results,  a  definite  conclusion  is  not  at  the 
present  time  possible.  At  any  rate,  it  is  justifiable  to  try  the  serum  treatment 
in  severe  cases. 

If  the  nose  be  likewise  affected,  the  chief  thing  to  do  is  frequent  cleansing 
and  syringing  while  the  head  is  bent  forward.  We  should  be  on  the  watch 
for  the  possible  occurrence  of  otitis.  In  this  particular  the  physician  is  often 
guilty  of  sins  of  omission.  We  would  particularly  emphasize  the  importance 
of  careful  watching  of  the  drum  membrane  and  the  mastoid  process  in  every 
case  of  scarlet  fever,  because  timely  interference  (paracentesis  of  the  drum 
membrane,  etc.)  may  at  least  prevent  a  great  deal  of  mischief.  The  treatment 
of  the  purulent  ear  discharge  (irrigations,  etc.)  must  be  carried  out  according 
to  general  otological  principles. 


54  ACUTE   GENERAL   INFECTIOUS   DISEASES 

Inflammation  of  the  glands  in  the  neck,  if  severe,  is  prone  to  pass  on  to 
suppuration,  and  it  must  then  be  treated  surgically.  Ice  is  generally  not  so 
well  borne  as  warm  applications  (poultices  or  warm  bran  cushions). 

If  there  be  continuous  high  fever,  accompanied  by  rather  severe  consti- 
tutional symptoms,  a  moderate  employment  of  the  cold-water  treatment  in 
scarlet  fever  is  to  be  strongly  recommended.  The  baths  seldom  need  to  be 
cooler  than  81°  to  88°  F.  (27°  to  30°  C),  and  are  to  be  employed  two  or 
three  times  daily.  If  the  nervous  disturbance  be  serious,  or  if  the  respiration 
be  impaired,  the  patient  should  be  douched  with  cold  water  during  the  bath. 
Instead  of  baths,  wet  packs  may  be  used  to  advantage.  Internal  antipyretics, 
such  as  antipyrin,  may  usually  be  dispensed  with,  although  in  private  practice 
we  may  be  obliged  to  employ  them. 

We  must  watch  the  condition  of  the  heart  carefully.  When  the  pulse  is 
very  rapid  we  may  use  an  ice  bag  on  the  heart.  When  the  heart  begins  to 
grow  weak  we  may  prescribe  caffein,  tincture  of  strophanthus,  wine,  etc.,  and 
the  most  efficient  remedy  for  threatening  collapse  is  injections  of  camphor. 
With  mild  scarlatinal  arthritis  salicylate  of  sodium  and  antipyrin  act  well  as 
palliatives,  but  in  severe  cases  they,  of  course,  do  little  good. 

We  know  of  no  means  to  avert  scarlatinal  nephritis.  In  justice  to  him- 
self, the  physician  must  always  at  the  start  point  out  the  possibility  of  its 
occurrence,  and  must  avoid  as  far  as  possible  errors  in  diet  or  exposure  to  cold 
on  the  part  of  his  patient.  He  may  thus  escape  blame.  The  treatment  of  the 
nephritis  and  its  results  are  fully  described  in  the  section  on  renal  diseases 
(Vol.  II).  The  most  important  remedies  are  a  suitable  (milk)  diet  and  the 
use  of  warm  or  possibly  hot  baths  and  packs. 

The  patient  must,  as  a  rule,  keep  his  bed  three  or  four  weeks,  even  if  con- 
valescence be  uninterrupted. 

[This  injunction  is  rather  extreme.  Nephritis  is  as  likely  to  follow  a  mild 
as  a  severe  case,  and  occurs  sometimes  in  spite  of  every  precaution.  The 
physician  should  use  his  discretion  as  to  the  length  of  time  the  patient  is 
kept  in  bed,  carefully  guarding  against  exposure  to  cold  and  imprudence 
in  diet.] 

After  desquamation  is  completed  the  skin  should  be  thoroughly  cleansed  by 
warm  baths.  The  disease  is  so  dangerous  that,  whenever  a  case  occurs  in  a 
family,  isolation  is  absolutely  demanded,  and,  if  possible,  all  the  other  children 
should  be  sent  away.  If  this  advice  be  disregarded,  we  can  reject  all  respon- 
sibility for  any  further  cases  and  their  results. 

According  to  the  laws  almost  universal  in  Germany  at  the  present  time, 
brothers  and  sisters  of  the  patient  may  not  attend  school  for  at  least  six 
weeks.  Everything  that  has  come  in  contact  with  the  patient  (linens, 
clothes,  toys)  should  either  be  destroyed  or  thoroughly  fumigated.  The 
sick-room  should  be  cleansed,  aired,  and  disinfected  at  the  termination  of 
the  disease. 

[Scarlet  fever  is  a  disease  at  once  so  bighly  contagious  and  so  common  that 
it  may  be  taken  as  the  type  of  its  class.  Its  hygienic  treatment  and  the 
measures  needful  to  prevent  its  spread  consequently  deserve  more  minute 
detail. 

The  sick-room  should  be  at  the  top  of  the  house,  if  possible,  and  exposed 
to  the  south ;  every  unnecessary  article  of  furniture  and  all  ornaments  should 


MEASLES  55 

be  removed  beforehand,  carpets,  curtains,  and  stuffed  or  upholstered  furniture 
being  included.  A  window  should  be  kept  open  constantly,  top  and  bottom; 
in  cool  weather  a  fire  should  be  burning;  in  warm  weather  ventilation  is  fur- 
thered by  placing  a  gas  burner  or  large  kerosene  lamp  near  the  throal  of  thi 
chimney.  Outside  the  door  of  the  sick-room  a  sheel  moistened  with  a  disin- 
fectant solution  should  be  carefully  hung.  Only  those  whose  presence  is  abso- 
lutely necessary  are  to  be  allowed  in  the  sick-room,  and  the  physician,  when  his 
visit  is  completed,  should  pass  directly  out  of  the  house. 

A  convalescent  should  he  kept  away  from  all  who  are  liable  to  contract  or 
convey  the  disease  until  desquamation  has  entirely  ceased.  Several  warm  soap 
baths  should  be  given  before  the  child  emerges  into  everyday  life,  and  it 
should  finally  he  dressed  in  uncontaminated  clothing.] 


CHAPTER    V 

MEASLES 

(Morbilli) 


etiology. — In  contrast  with  the  malignancy  of  scarlet  fever  is  the  compara- 
tively benign  nature  of  measles,  a  disease  of  childhood  which  is  but  little 
feared  even  by  mothers.  It  is  so  widespread,  and  the  susceptibility  to  it  is  so 
universal,  that  measles  passes  for  an  almost  unavoidable  but  comparatively 
insignificant  annoyance.  Indeed,  few  escape  it;  and  probably  the  reason  why 
adults  have  measles  so  much  less  frequently  than  children  is  simply  that  most 
adults  have  already  suffered  from  it  in  childhood.  A  second  attack  of  measles 
in  the  same  individual  may  occur,  but  it  is  certainly  rare. 

[In  highly  civilized  countries  measles  has  prevailed  so  long  that  it  would 
seem  that  a  relative  resistance  against  the  poison  has  been  acquired.  The 
frightful  ravages  of  the  disease  when  it  was  planted  in  virgin  soil,  as  among 
the  Fiji  Islanders  not  many  years  ago,  apparently  bear  out  this  view.] 

Measles  generally  comes  in  epidemics.  Sporadic  cases  are  exceptional.  In 
this  respect  measles  differs  decidedly  from  scarlet  fever.  The  rapid  spread  of 
the  disease  when  it  has  once  broken  out  is  a  result  of  its  great  contagiousness. 
If  one  child  in  a  family  is  attacked,  the  others  almost  always  take  the  disease. 
The  infection  may  be  transmitted  even  by  well  persons  and  by  means  of  arti- 
cles with  which  the  sick  have  come  in  contact,  although  this  is  not  often  the 
case.  We  are  not  yet  acquainted  with  the  specific  poison  of  measles — although 
its  existence  is  to  be  taken  for  granted — nor  with  the  details  of  its  trans- 
mission. Still,  it  seems  most  probable  that  the  poison  is  inhaled  through  the 
mouth  and  nose,  and  that  this  is  the  reason  why  its  effects  are  usually  first 
developed  in  the  respiratory  passages  (vide  infra).  The  disease  can  be  arti- 
ficially produced  by  the  inoculation  of  healthy  children  with  the  blood  or 
liquid  secretions  of  those  suffering  from  it. 

Clinical  History. — The  length  of  the  stage  of  incubation  is  tolerably  uni- 
form. It  is  ten  days  to  the  beginning  of  the  first  symptoms,  and  thirteen  or 
fourteen  days  to  the  breaking  out  of  the  eruption.    These  figures  have  been 


56  ACUTE   GENERAL   INFECTIOUS   DISEASES 

established  by  the  observations  of  Panum,  the  opportunity  having  been  af- 
forded upon  the  first  introduction  of  the  disease  into  the  Faroe  Islands.  As 
a  rule,  there  are  no  especial  prodromata  during  the  period  of  incubation  except 
some  slight  elevations  of  temperature.  At  the  end  of  ten  days  the  initial  stage  x 
begins,  generally  suddenly,  and  with  an  abrupt  rise  of  temperature  to  102° 
or  104°  F.  (39°  to  40°  C).  At  the  same  time  the  characteristic  catarrhal  symp- 
toms appear:  nasal  catarrh  (coryza),  to  be  recognized  by  the  abundant  nasal 
secretion,  the  frequent  sneezing,  and  sometimes  also  by  nosebleed ;  more  or 
less  severe  conjunctivitis,  characterized  by  photophobia,  reddening  of  the  eyes, 
and  increased  flow  of  tears,  and,  lastly,  symptoms  of  a  catarrh  of  the  upper 
part  of  the  respiratory  tract,  usually  moderate,  but  nevertheless  causing  hoarse- 
ness and  a  slight  cough.  With  all  this  the  general  condition  is  disturbed,  the 
children  are  restless,  have  headache,  and  eat  little.  Symptoms  of  a  mild  sore 
throat  are  not  infrequent,  but  are  very  far  from  being  so  prominent  as  in 
scarlet  fever. 

The  smaller  children  are  greatly  annoyed  by  mucus  collecting  in  the  nose 
or  nasopharynx.  In  most  cases,  on  the  second  or  third  day  of  the  disease,  the 
characteristic  initial  mucous  membrane  exanthem  appears.  It  occurs  on  the 
mucous  membrane  of  the  soft  and  hard  palate  in  the  form  of  irregular  red 
macules,  the  size  of  a  lentil  or  even  larger.  About  the  same  time,  or  even 
earlier,  punctate,  white,  scale-like  spots,  often  surrounded  by  a  red  areola,  ap- 
pear on  the  buccal  mucous  membrane  opposite  the  molar  teeth  (the  so-called 
Koplik's  spots). 

These  initial  symptoms  last,  as  we  have  said,  three  or  four  days.  Then  the 
eruption  begins  (stage  of  eruption).  The  true  eruption  of  measles  begins 
almost  always  in  the  face,  on  the  cheeks,  forehead,  and  around  the  mouth  (con- 
trasting with  the  characteristic  pallor  of  the  chin  in  scarlet  fever),  and  spreads 
from  there  rapidly  downward  over  all  the  rest  of  the  body.  The  eruption  con- 
sists at  first  of  little  papilla?,  corresponding  to  the  follicles.  These  are  soon 
surrounded  by  a  pale-red,  slightly  elevated  border,  and  in  many  cases  become 
confluent.  Perfectly  flat  elevations,  of  various  sizes  and  of  extremely  irregu- 
lar, dentated,  roundish,  or  angular  shape,  develop.  They  are  often  so  thickly 
crowded  together  as  to  touch  one  another,  but  usually  limited  portions  of 
normal  skin  intervene  between  them.  Within  each  raised  spot  the  little  fol- 
licular papilla?  remain  visible. 

With  the  beginning  of  the  eruption  the  fever  rises,  having  been,  as  a  rule, 
slight  during  the  last  days  of  the  initial  stage.  It  attains  about  104°  or  105° 
F.  (40°  to  40.5°  C).  In  thirty-six  to  forty-eight  hours  the  eruption  reaches 
its  full  development  and  its  greatest  extent.  The  fever  and  the  catarrhal 
symptoms  also  persist  for  the  same  length  of  time.  Sometimes  we  find  a  slight 
swelling  of  all  the  lymph-glands.  Then  follows  a  decline  in  the  fever,  usually 
rapid,  and  indeed  almost  by  crisis,  while  the  eruption  after  a  short  period  of 
full  development  begins  gradually  to  fade  during  the  two  or  three  days  follow- 
ing. At  the  same  time  the  catarrhal  symptoms  diminish.  A  more  or  less  ex- 
tensive desquamation  of  the  epidermis  begins,  scarcely  ever  in  large  pieces,  as 


1  We  consider  the  term  "initial  stage"  more  correct  than  "prodromal  stage."  The  "pro- 
dromal symptoms"  are  the  first  slight  symptoms  which  occur  during  the  time  of  incubation  of  an 
infectious  disease,  while  the  symptoms  presented  by  measles  before  the  breaking  out  of  the 
eruption  are  a  part  of  the  already  developed  disease. 


MEASLES 


57 


Initial  Fever. 


Eruptive  Fever. 
Eruption. 


Fig.  8.- 


Example  of  the  temperature  curve  in 
measles. 


in  scarlet  fever,  but  in  little  scales  like  bran.     In  eight  or  ten  'lays,  if  the 
disease  runs  a  normal  course,  the  patient  is  fully  convalescent. 

After  this  brief  description  of  the  usual  course,  we  must  consider  more 
closely  some  of  tbe  symptoms  and  possible  complications. 

The  fever  (see  Fig.  8)  of  measles  exhibits,  as  lias  been  already  implied,  a 
tolerably  typical  course.  It  begins  with  a  rather  marked  and  rapid  rise  upoo 
the  commencement  of  tbe  disease.  On 
the  morning  of  tbe  second  day  there 
is  usually  a  marked  remission,  often 
to  normal.  In  the  last  two  days  of 
the  initial  stage  the  fever  is  moderate, 
very  rarely  being  so  high  as  at  the  be- 
ginning. With  the  eruption  there  is 
a  new,  rapid  rise,  usually  higher  than 
the  initial  one,  so  that  we  may  well 
divide  the  fever  into  two  periods — the 
prodromal  fever  and  the  eruptive  fever. 
This  latter  is  but  brief  and  does  not 
persist,  as  in  scarlet  fever,  during  the 
entire  duration  of  the  eruption.  It 
falls  by  crisis  when  the  rash  has  at- 
tained full  development.  There  may, 
to  be  sure,  be  slight  elevations  of  tem- 
perature during  the  next  day  or  two; 
but,  if  the  fever  is  considerable  and 
persistent,  it  is  always  a  sign  that  complications  have  arisen,  probably  in  the 
respiratory  apparatus. 

The  eruption  usually  assumes  the  form  described  above,  but  may  present 
manifold  varieties.  Sometimes  its  development  is  rudimentary.  Sometimes 
it  does  not  begin  on  the  face,  but  on  some  other  part  of  the  body.  This  is 
generally  regarded  as  a  sign  that  the  case  will  be  anomalous  in  other  ways  as 
well.  The  individual  spots  may  be  smaller  than  usual,  and  may  remain  en- 
tirely separate  from  each  other  {morbilli  papulosi).  In  other  cases  the  erup- 
tion is  so  confluent  (morbilli  confluentes)  that  it  resembles  the  eruption  of 
scarlatina.  The  formation  of  vesicles  (morbilli  vesiculosi)  also  occurs,  but 
much  more  rarely  than  in  scarlet  fever.  Hemorrhagic  measles  is  also  observed, 
but  usually  only  in  the  form  of  small,  capillary  bleeding,  and  in  cases  that 
otherwise  run  a  perfectly  favorable  course.  Very  rare  cases  have  indeed  been 
described,  with  a  general  hemorrhagic  diathesis  and  severe  symptoms,  resem- 
bling hemorrhagic  scarlatina  (so-called  "  black  measles  ").  In  addition  to  the 
proper  eruption  of  measles,  other  eruptions  sometimes  develop — such  as  vesi- 
cles, wheals,  and  pustules. 

The  pulse  is  generally  not  so  rapid  in  measles  as  in  scarlet  fever.  En- 
largement of  the  spleen  can  be  made  out  only  to  a  slight  degree,  if  at  all. 
As  a  rule,  we  find  no  pronounced  leucocytosis  in  the  blood.  Indeed,  in 
striking  contrast  to  scarlet  fever  (q.v.),  there  is  usually  a  pronounced 
leucopenia  at  the  height  of  the  disease.  It  is  only  in  the  period  of  incuba- 
tion and  with  the  advent  of  complications  (pneumonia,  etc.)  that  leucocytosis 
is  present. 


58  ACUTE   GENERAL   INFECTIOUS   DISEASES 

Complications. — The  complications  of  measles  are  for  the  most  part  exag- 
gerations or  abnormal  varieties  and  extensions  of  those  troubles  which  are 
observed  during  the  usual  mild  course  of  the  fever.  As  in  scarlet  fever  (vide, 
supra),  we  often  have  to  deal  with  the  effects  not  of  the  original,  but  of  sec- 
ondary infections.  Compared  with  the  great  majority  of  mild  attacks  taking 
the  typical  course,  cases  presenting  complications  of  any  severity  are  rare,  and 
much  less  frequent  than  in  scarlet  fever.  Epidemics  are  only  now  and  then 
distinguished  by  unusual  severity. 

Often  quite  serious  eye  diseases  are  developed,  particularly  blennorrhagic 
conjunctivitis,  keratitis,  and  iritis. 

Marked  inflammation  of  the  mucous  membrane  of  the  nose,  throat,  and 
larynx  may  prolong  the  course  of  the  disease.  This  is  often  merely  an  exag- 
geration of  the  usual  catarrh.  Otitis  media  likewise  sometimes  occurs.  A 
laryngitis  of  marked  intensity,  with  considerable  swelling  of  the  parts  in- 
volved, may  produce  much  discomfort,  or  even  symptoms  of  stenosis  ("false 
croup").  Actual  croupous  and  diphtheritic  lesions  of  the  throat  and  larynx 
also  occur  (diphtheria  of  measles).  This  last  is  indeed  much  rarer  than  scar- 
latinal diphtheria,  but  it  may  have  the  same  unhappy  termination.  It  is 
worth  mentioning  that  sometimes  genuine  laryngeal  croup  is  observed  in 
measles,  unaccompanied  by  lesions  of  the  pharynx. 

It  is,  however,  in  the  lungs  that  the  most  frequent  and  important  of  all 
complications  in  measles  occur.  The  usual  mild  bronchitis  becomes  very  in- 
tense, extends  into  the  bronchioles  (capillary  bronchitis),  and  then  results,  for 
the  most  part,  in  a  more  or  less  extensive,  lobular,  catarrhal  pneumonia  (q.  v.). 
According  to  Koster,  measles  pneumonia  rises  from  an  inflammatory  prolifer- 
ation of  nuclei  about  the  small  bronchi,  and  it  usually  invades  the  neighbor- 
ing alveoli  by  continuity  along  the  small  branches  of  the  pulmonary  artery. 
It  is  then  a  "  small  nodular,"  but  not  strictly  a  lobular  pneumonia.  Measles 
pneumonia  is  to  be  diagnosticated  when  moist  rales  are  heard  in  abundance 
over  a  large  part  of  the  chest,  and  when  there  is  at  the  same  time  persistent 
fever  and  pronounced  difficulty  in  respiration,  with  cough,  dyspnoea,  or  cya- 
nosis. We  get  decided  dullness  on  percussion  only  when  the  separate  centers 
of  infiltration  are  more  than  usually  confluent.  Genuine  lobar,  croupous  pneu- 
monia appears  much  less  often  than  the  lobular  variety.  It  attacks  one  lobe, 
or  several,  is  attended  by  high  fever,  and  may  end  with  a  well-marked 
crisis. 

The  foregoing  pulmonary  symptoms  usually  appear  at  the  height  of  the 
disease,  and  persist  after  the  eruption  fades.  .  They  may  delay  convalescence 
for  weeks.  In  other  cases  measles  will  be  seen  at  the  start  to  run  a  normal 
course,  temperature  will  have  already  fallen,  and  then  come  new  fever  and  the 
appearance  of  decided  pulmonary  disturbance.  This  is  always  to  be  regarded 
as  a  grave  complication ;  and  especially  in  feeble  children  it  may  lead  to  death, 
with  the  symptoms  of  impaired  respiration  or  of  constitutional  exhaustion. 
At  present  we  cannot  definitely  state  how  far  in  measles  pneumonia  we  have 
to  do  with  the  direct  action  of  the  measles  poison  itself  or  with  secondary 
infection  (streptococci,  diplococci,  etc.). 

Marked  intestinal  symptoms  sometimes  appear,  particularly  an  excessive 
diarrhea,  due  to  intestinal  catarrh.  It  is  characteristic  of  measles  that  in 
severe  cases  such  a  diarrhea  may  assume  a  pronounced  dysenteric  character, 


MEASLES  59 

indicated  by  Mood  and  slime  in  the-dejections,  symptoms  which  usually  depend 
upon  the  development  of  follicular  colitis  wit  1 1  ulcerations. 

Now  and  then  still  other  complications  may  preset  themselves,  of  which 
a  full  enumeration  is  impossible.  Nephritis  does  occur,  but  far  less  often  than 
in  scarlet  fever.  A  simple  albuminuria  during  the  acme  of  the  disease  is  not 
infrequent,  but,  as  a  rule,  it  has  no  especial  clinical  significance.  We  should 
mention  gangrene  of  the  cheek,  the  so-called  noma,  as  a  complication,  which 
is  very  rare  but  apparently  characteristic. 

Peculiarities  in  the  Course  of  the  Disease. — Peculiarities  in  the  course  of  the 
disease  are  much  rarer  in  measles  than  in  scarlet  fever.  Yet  we  see,  on  the  one 
hand,  unusually  mild  or  rudimentary  cases,  in  which  either  the  rash  or  the  other 
local  symptoms  are  remarkably  slight,  and,  on  the  other  hand,  abnormally 
severe  cases.  These  latter  are  distinguished  by  the  unusual  height  or  persist- 
ence of  the  fever,  by  the  severe  constitutional  and  nervous  symptoms,  and  fur- 
ther by  the  early  appearance  of  complications.  Such  cases  have  been  termed 
"  typhoid  measles."  We  have  already  mentioned  the  severe  form  of  hemor- 
rhagic measles. 

We  should  notice  the  clinical  relation  which  measles  bears  to  two  other  in- 
fectious diseases — to  whooping  cough  and  tuberculosis.  Measles  and  pertu  — 
(q.  v.)  may  follow  each  other  in  the  same  individual  at  a  short  interval,  some- 
times one  and  sometimes  the  other  taking  the  initiative ;  epidemics  of  the  two 
diseases  prevail  with  comparative  frequency  at  the  same  time.  Tuberculosis  is 
likewise  to  be  mentioned  as  an  important  sequela  of  measles.  In  these  cases  it 
is  probable  that  the  children  have  a  tuberculous  focus  smoldering  somewhere  in 
the  body  (lymph-glands,  lungs)  before  the  attack  of  measles  which  kindles  it 
and  aids  its  further  extension.  The  measles  may  also,  of  course,  excite  a  pre- 
disposition to  infection  with  tubercle  bacilli. 

Diagnosis. — The  diagnosis  of  measles,  as  of  the  other  acute  exanthematous 
diseases,  is  based  chiefly  upon  the  eruption,  but  we  must  also  regard,  of  course, 
other  symptoms  which  may  be  present  (fever,  catarrhal  symptoms).  Personal 
experience  does  more  to  sharpen  the  perception  than  can  the  fullest  descriptions. 
We  can  merely  suspect  the  disease  during  the  initial  stage  unless  an  epidemic 
prevails.  If,  besides  the  characteristic  catarrhal  symptoms,  the  above-men- 
tioned eruption  on  the  mucous  membrane  of  the  jjalate  exists,  or  if  Koplik's 
spots  are  present  on  the  buccal  mucous  membrane,  the  diagnosis  becomes  tol- 
erably certain.  We  should  consider  that  eruptions  similar  to  that  of  measles 
appear  in  other  diseases,  more  especially  in  German  measles,  scarlet  fever, 
typhus  fever,  in  the  beginning  of  smallpox,  and  in  secondary  syphilis  (rose- 
ola). Furthermore,  we  need  to  exclude  eruptions  which  are  due  to  drugs, 
especially  antipyrin,  and  also  turpentine,  balsam  of  copaiba,  etc.  In  cases 
which  are  doubtful  we  shall  be  enabled  to  form  a  decided  opinion  by  a 
consideration  of  the  other  symptoms,  and,  above  all,  by  the  further  course 
of  the  disease. 

The  difference  in  the  blood  picture  in  scarlet  fever  and  measles  is  of  value 
in  their  differential  diagnosis — leucocytosis  and  eosinophilia  in  scarlet  fever, 
leucopenia  in  measles. 

Prognosis. — We  have  already  remarked  how  favorable  in  general  the  prog- 
nosis is,  but  we  must  here  repeat  that  all  epidemics  do  not  exhibit  the  same 
benign  character,  and  that  in  every  case  the  physician  must  bear  in  mind  the 


60  ACUTE   GENERAL   INFECTIOUS   DISEASES 

possibility  of  complications,  and  particularly  the  danger  of  severe  pulmonary 
disturbances. 

It  should  be  mentioned  that  measles  frequently  seems  to  run  a  severer 
course  in  adults  than  in  children. 

Treatment. — The  patient  should  in  general  be  kept  somewhat  warmer  than 
in  scarlet  fever.  Even  in  what  seem  to  be  the  mildest  cases  the  child  should 
be  kept  in  bed  till  desquamation  is  over.  The  sick-chamber  is  to  be  somewhat 
darkened,  on  account  of  the  photophobia  which  usually  exists  at  first.  In  this 
way,  normal  cases  run  on  favorably  without  any  especial  therapeutic  interposi- 
tion. The  catarrhal  symptoms,  however,  should  always  be  heeded,  since  to 
disregard  them  may  lead  to  their  becoming  aggravated.  The  chief  requisite 
is  cleanliness.  At  regular  intervals  the  eyes,  the  nasal  cavity,  and  the  mouth 
should  be  washed  out  and  douched  with  lukewarm  water. 

If,  despite  all  this,  certain  disturbances  appear  in  a  worse  form  than  usual, 
or  if  complications  develop,  these  must  receive  especial  attention.  Severe  eye 
troubles  should  be  treated  according  to  the  usual  ophthalmological  practice. 
The  treatment  of  croupous  trouble  in  the  throat  or  larynx  will  be  fully  de- 
scribed in  a  later  chapter.  For  the  pulmonary  complications,  lukewarm  baths, 
combined  if  need  be  with  rather  cool  douches,  constitute  the  most  effectual 
remedy.  Cold  packs  are  also  very  efficient.  These  we  shall  speak  of  later  in 
more  detail  in  the  chapter  on  catarrhal  pneumonia.  The  chief  task  of  the 
physician  in  the  treatment  of  measles  is,  however,  to  hinder  as  far  as  possible 
the  appearance  of  complications.  We  are  not  acquainted  with  any  internal 
remedies  for  the  lung  troubles  which  are  at  all  trustworthy.  In  rare  instances 
the  excessive  accumulation  of  mucus  in  the  bronchi  requires  the  administra- 
tion of  an  emetic.  As  expectorants  we  may  try  ipecac,  liquor  ammonii  ani- 
satus,  etc.  If  considerable  intestinal  disturbance  arises,  we  must  employ  small 
doses  of  opium,  calomel,  tannalbin,  or  subnitrate  of  bismuth.  We  hardly  need 
to  say  that,  whatever  else  is  done,  the  strength  of  the  patient  should  be  kept 
up  as  much  as  possible  by  giving  wine,  broths,  milk,  eggs,  etc.  For  at  least 
two  or  three  weeks  after  the  disease  has  ended,  the  child  must  be  very  carefully 
watched. 

As  the  disease  is  usually  so  mild,  prophylaxis  is  not  very  strenuously  at- 
tempted. If  one  child  in  a  family  is  attacked,  it  is  probably  already  too  late  to 
isolate  the  others,  and  it  is  even  an  advantage  to  the  family  to  have  all  the 
children  finish  at  once  what  they  will  hardly  be  able  eventually  to  avoid.  We 
would  make  an  exception  in  favor  of  isolation  if  the  disease  prevailed  in  a 
severe  form. 

[It  is  not  customary  with  us  to  insist  so  strongly  upon  isolation  and  thor- 
ough disinfection  as  in  scarlet  fever,  but  the  tendency  of  the  present  day  is 
toward  a  wide  application  of  the  principles  of  preventive  medicine.  It  is  cer- 
tainly of  no  advantage  to  a  child  to  contract  measles.  Delicate  children,  espe- 
cially those  with  tuberculous  predisposition,  should  be  carefully  guarded  against 
it;  and,  even  if  it  is  decided  that  it  is  not  worth  while  to  attempt  to  confine 
the  disease  to  one  member  of  a  family,  every  precaution  should  be  taken  against 
infecting  other  families.  Under  suspicious  circumstances,  consequently,  chil- 
dren are  to  be  kept  away  from  school  and  from  contact  with  others. 

If  there  is  any  reason  to  fear  the  development  of  tuberculosis,  every  possible 
hygienic  means  should  be  employed  in  order  that  full  vigor  may  be  regained.] 


SMALLPOX  61 


CHAPTER    VI 


ROTHELN 

{German  Measles.     Rubella) 

Rotheln  is  a  disease  similar  to  measles,  but  distinct  from  it,  although 
formerly  often  confounded  with  it,  and  perhaps  with  scarlet  fever  as  well.  The 
observations  of  Steiner,  Thomas,  and  others  leave  now  no  room  to  doubt  thai 
these  diseases  are  distinct,  for  epidemics  occur  in  which  all  cases  present  the 
characteristic  peculiarities  ascribed  to  rotheln.  But  the  best  proof  is  that  chil- 
dren who  have  had  rotheln  are  not  infrequently  attacked  by  genuine  measles 
later.  It  may  indeed  be  very  difficult  in  an  individual  case  to  decide  which 
disease  is  present;  but  that  rotheln  does  exist,  as  an  independent  form  of  dis- 
ease, can  be  denied  by  those  alone  who  have  never  seen  it. 

After  an  incubation  of  about  two  or  three  weeks  the  disease  begins  with 
the  appearance  of  the  eruption,  which  is  usually  noticed  first  in  the  face. 
Initial  symptoms  (cough,  sneezing,  etc.),  preceding  the  eruption,  either  are 
wholly  absent  or  at  most  last  for  half  a  day.  The  eruption  is  decidedly  like 
that  of  measles,  but  its  individual  spots  are  smaller.  They  are  seldom  larger 
than  small  peas  and  circular,  being  only  exceptionally  as  dentated  and  irregu- 
lar in  outline  as  are  the  maculae  of  measles.  They  appear  on  the  whole  face, 
the  head,  the  trunk,  and  the  extremities,  are  pale  reel  (sometimes  deep  red), 
only  slightly  elevated,  and  are  not  apt  to  become  confluent.  In  rare  instances, 
small  vesicles  develop  upon  the  macules.  The  soft  palate  sometimes  exhibits, 
as  in  measles,  a  faint  macular  eruption  at  the  beginning  of  the  disease.  After 
three  to  four  days  the  eruption  fades.  There  is  usually  no  decided  desqua- 
mation. 

Other  symptoms  of  disease  than  this  eruption  are  slight.  Fever  in  many 
cases  appears  to  be  entirely  absent.  As  a  rule,  there  is  for  a  day  or  two  a  little 
elevation  of  temperature,  reaching  102°  F.  (39°  C.)  at  most.  Tokens  of  a 
moderate  catarrh  of  the  conjunctiva,  the  nasal  mucous  membrane,  the  throat, 
and  the  larynx  are  also  observed — viz.,  photophobia,  nasal  discharge,  and 
cough.  Often,  the  cervical  lymph-glands  are  more  or  less  swollen.  The  con- 
stitutional disturbance  is  generally  so  slight  that  the  child  can  hardly  be  kept 
in  bed.     Important  complications  hardly  ever  occur. 

The  prognosis  of  rotheln  is  therefore  perfectly  favorable,  and  the  employ- 
ment of  any  special  treatment  is  needless. 


CHAPTER    VII 

SMALLPOX 

(Variola.     Varioloid) 

Etiology. — Smallpox  has  been  known  for  centuries,   although  formerly 
often  confounded  with  other  diseases.1     It  is  one  of  the  most  dreaded  acute 

1  The  very  name  smallpox  (petite  verole)  is  significant  of  its  confusion  with  syphilis,  which  was 
termed  the  "great  pox." 


62  ACUTE   GENERAL   INFECTIOUS   DISEASES 

infectious  diseases,  and  in  earlier  times  it  has  destroyed  thousands  in  its  pesti- 
lential progress.  It  was  the  discovery  of  the  possibility  of  prophylactic  inocu- 
lation, and  the  ever-increasing  spread  of  this  precautionary  measure,  which 
first  robbed  the  disease  of  some  portion  of  its  terrors. 

Despite  numerous  studies  (L.  Pfeiffer,  G-uarnieri,  Wasilewski,  and  others), 
the  specific  agent  of  smallpox  is  not  known.  The  so-called  Guarnieri  vaccine 
bodies — small,  round  bodies  found  in  the  cells  of  smallpox  and  vaccine  pus- 
tules, that  stain  deeply  and  have  nucleus-like  centers — do  not  appear  to  be  pro-, 
tozoa,  but  rather  extruded  nuclei.  Their  presence  is,  however,  so  characteristic 
of  smallpox  that  they  may  serve  in  the  differentiation  of  that  disease  from 
other  pustular  affections,  more  especially  varicella  (vide  infra).  The  Guar- 
nieri bodies  are  most  easily  found  in  the  characteristic  pustules  that  appear 
on  the  rabbit's  cornea  after  the  latter  has  been  inoculated  with  the  contents 
of  a  smallpox  pustule  (Jtirgens). 

[Councilman  and  his  colaborers  have  described  the  whole  life  history  of  a 
protozoon  in  the  skin  lesions,  with  confirmation  by  Calkins  and  by  Howard 
and  Perkins.] 

Predisposition  to  variola,  except  as  diminished  by  vaccination  (vide  infra), 
is  universal.  The  disease  may  appear  at  any  age,  even  in  utero.  Women  are 
believed  to  be  especially  liable  to  it  during  pregnancy  and  child-bed.  It  is  said 
that  persons  ill  with  another  acute  infectious  disease,  such  as  scarlet  fever, 
measles,  or  typhoid  fever,  are,  for  the  time  being,  tolerably  secure  from  infec- 
tion with  smallpox;  but  this  rule  certainly  has  exceptions.  The  explanation 
of  the  fact  that  the  most  widespread  epidemics  of  smallpox  generally  occur 
in  winter  is  to  be  found  in  the  closer  living  quarters  of  humanity  in  the  cold 
season.    The  same  individual  rarely  takes  the  disease  a  second  time. 

A  case  of  variola  is  always  the  result  of  transmission  of  the  poison  to  a 
healthy  person  from  one  who  is  already  ill  with  it.  The  specific  poison  is  most 
abundant  in  the  diseased  portions  of  the  body  and  in  the  pus  of  the  suppu- 
rating pocks,  as  well  as  the  crusts  and  scales  which  are  left  when  these  have 
dried  up.  Owing  to  the  presence  of  pustules  in  the  mucous  membranes,  the 
dejecta  and  the  nasal  mucus  of  a  patient  may  also  contain  the  contagium. 
But  the  disease  is  also  contagious  in  its  earlier  stages,  before  the  pustules 
develop,  and  even,  according  to  a  few  observations,  during  the  stage  of  incu- 
bation. The  variolous  poison  is  certainly  very  volatile — that  is,  it  is  prone  to 
disseminate  itself  through  the  air  in  the  neighborhood  of  the  patient  in  the 
form  of  small  drojDS  or  of  fine  dry  particles  of  dust.  For,  in  order  to  catch  the 
disease,  it  is  not  necessary  to  touch  the  patient,  but  merely  to  remain  in  his 
vicinity.  In  many  cases  we  cannot,  however,  determine  with  exactness  the 
mode  of  transmission,  since  the  contagion  may  either  be  direct  or  by  means  of 
objects  and  utensils  with  which  a  patient  has  come  in  contact — for  example, 
the  soiled  linen.  The  dead  body  also  is  capable  of  transmitting  the  disease. 
In  general,  numerous  instances  point  to  a  considerable  "  tenacity  "  in  the  poi- 
son. The  precise  manner  of  infection  is  not  yet  known.  It  is  most  probable 
that  the  poison  is  drawn  into  the  lungs  with  the  inspired  air. 

It  has  been  demonstrated  that  the  disease  can  be  transmitted  to  healthy 
persons  by  direct  inoculation  of  the  contents  of  the  variolous  pustules.  It  is 
stated  that  monkeys  and  other  animals  may  be  successfully  inoculated  in  the 
same  way.    Whether  inoculations  with  the  blood  of  the  sick  will  reproduce  the 


SMALLPOX  63 

disease  is  not  yet  settled.  The  secretions  (saliva,  sweat,  urine,  and  milk)  do 
not  apparently  contain  the  infectious  matter. 

Course  of  the  Disease.  Variola  and  Varioloid. — The  stage  of  incubation 
lasts,  as  a  rule,  thirteen  to  fourteen  days,  sometimes  a  somewhat  shorter  time. 
During  this  period  prodromal  symptoms  are  absent  or  insignificant. 

The  disease  itself  begins  suddenly  with  what  are  usually  very  character- 
istic initial  symptoms — rigor,  fever,  headache,  and  intense  pain  in  the  loins. 
It  is  only  in  comparatively  few  cases  that  one  or  another  of  these  symptom-  is 
slight  or  wanting.  The  constitutional  symptoms  may  he  very  severe — a  dry 
tongue,  stupor,  wakefulness,  delirium.  The  fever  continues  intense  for  some 
days.  The  pulse  is  much  quickened.  There  is  almost  total  anorexia,  and 
often  there  is  vomiting.  There  is  constipation,  or,  more  rarely,  diarrhea. 
Frequently  there  is  a  slight  sore  throat,  and  sometimes  a  slight  bronchitis. 
The  spleen  is  enlarged  in  most  of  the  severe  cases,  and  the  urine  often  has  a 
trace  of  albumen.  In  women,  menstruation  occurs  in  a  remarkably  large  num- 
ber of  cases.  The  proper  variolous  eruption  does  not  at  once  appear,  but  from 
the  second  day  other  characteristic  efflorescences  are  not  rare.  These  are 
termed  the  initial  rash  of  smallpox.  We  may  find  either  a  diffuse  or  macular 
erythema,  extending  in  varying  degree  over  the  trunk  and  extremities  (espe- 
cially on  the  extensor  surface),  or  a  hemorrhagic  eruption  with  small  spots, 
appearing  by  preference  upon  the  hypogastrium  and  the  inner  surface  of  the 
thighs  (in  the  so-called  femoral  triangle  of  Simon)  or  on  the  lateral  surface 
of  the  trunk  and  on  the  upper  arm.  The  erythema  soon  disappears,  but  the 
hemorrhagic  spots  can  be  seen  longer.  Both  forms  of  the  initial  eruption 
may  be  combined. 

The  initial  stage,  just  pictured,  lasts  usually  three  days.  Severe  symptoms 
occurring  at  this  time  do  not  exclude  the  possibility  that  the  further  course  of 
the  disease  may  prove  favorable,  while  mild  symptoms  are  of  good  omen. 

At  the  end  of  the  third  or  on  the  fourth  day  the  temperature  makes  a  de- 
cided fall,  and  the  regular  variolous  eruption  begins  to  be  developed  upon  the 
skin — the  stadium  eruptionis.  During  this  period  an  evident  difference  among 
the  separate  cases  becomes  manifest.  This  distinction  cannot  indeed  be 
always  drawn  with  a  narrow  line,  but  it  is  noticeable  enough  to  justify  the 
establishment  of  two  types  of  variolous  disease.  We  refer  to  the  division  into 
a  severe  form  (variola  vera),  and  another,  mild  form  (varioloid).  The  vari- 
ola proper  has  a  well-developed  eruption  with  many  pustules,  and,  as  a  result 
of  this,  a  second  stage  of  fever  (stadium  suppurationis).  Varioloid  has  a 
much  more  scanty  eruption,  and  little  or  no  suppurative  fever.  We  must  now 
discuss  these  two  forms  separately. 

Variola  Vera. — The  eruption  almost  always  begins  in  the  face  and  upon 
the  hairy  scalp,  appearing  somewhat  later  on  the  trunk  and  arms,  and  last 
of  all  upon  the  legs.  It  begins  in  the  form  of  little  red  dots  and  spots,  which 
develop  in  about  two  days  to  small  papules  (stadium  floritionis) .  If  the  hand 
be  passed  over  thickly  set  and  well-developed  papules  of  variola,  a  peculiar  soft, 
satin-like  feeling  is  perceived.  On  the  points  of  these  papillae  a  little  vesicle 
forms.  This  keeps  growing  larger  and  larger,  its  contents  becoming  turbid 
and  purulent,  till  at  last,  on  the  sixth  clay  of  the  eruption  and  the  ninth  of 
the  disease,  the  development  of  the  genuine  pustule  of  variola  is  complete 
(stadium  suppurationis).     The  pustule  usually  presents  upon  its  summit  a 


64  ACUTE   GENERAL   INFECTIOUS   DISEASES 

little  dimple  (umbilication),  and  is  surrounded  by  a  red  border  or  "halo." 
Where  the  pocks  are  especially  close  together,  as  in  the  face,  the  skin  between 
them  is  diffusely  swollen,  and  the  consequent  burning  and  pain  are  excessive. 
The  countenance  becomes  much  disfigured.  Often  the  eyes  cannot  be  opened 
because  of  the  oedema.  The  hands  also  are  apt  to  be  intensely  affected,  espe- 
cially the  backs  of  the  hands,  and  also  all  parts  which  have  previously  been 
injured  in  any  way  (pressure  or  friction  of  clothing,  etc.).  On  the  trunk  the 
pustules  are  very  rarely  as  close  together  as  on  the  face  and  hands.  It  is 
worthy  of  note  that  often  new  eruptions  of  pustules  keep  appearing  for  two  or 
three  days. 

At  the  same  time  with  the  eruption  upon  the  skin,  or  even  somewhat  earlier, 
a  perfectty  analogous  efflorescence  develops  upon  the  mucous  membranes.  The 
chief  places  for  its  appearance  are  the  mouth  and  throat,  the  tongue,  the  soft 
palate,  the  nasal  cavity,  also  the  larynx,  the  trachea,  and  the  upper  part  of  the 
oesophagus.  In  the  vagina  and  rectum  it  is  rare  and  scanty.  In  this  mucous 
efflorescence,  however,  there  are  no  proper  pustules,  but  small,  superficial 
ulcers.  These  result  from  the  maceration  of  the  uppermost  layers  of  the  mu- 
cous membrane.  They  sometimes  become  confluent.  The  annoyance  produced 
by  this  eruption  in  the  mouth  and  throat  is,  of  course,  very  great.  The  pocks 
in  the  larynx  manifest  themselves  by  hoarseness,  and  occasionally  by  symptoms 
of  stenosis. 

As  we  have  said,  the  beginning  of  the  eruption  is  the  signal  for  a  notice- 
able fall  in  the  temperature;  but  in  true  variola  the  fall  does  not  reach  the 
normal,  or  only  temporarily.  The  other  symptoms  likewise  remit,  especially 
the  headache  and  lumbar  pain.  When,  however,  the  suppuration  begins,  the 
fever  rises  once  more,  and  there  are  fresh  symptoms  of  constitutional  disturb- 
ance. This  is  the  time  for  the  dreaded  attacks  of  delirium,  during  which  the 
patient  must  be  vigilantly  watched  lest  some  untoward  event  happen.  Now, 
too,  complications  may  arise  (vide  infra). 

On  the  twelfth  or  thirteenth  day  of  the  disease  the  pustules  begin  to  dry  up 
(stadium  exsiccationis) .  The  purulent  contents  of  the  pustules,  part  of  which 
have  burst,  form  yellow  crusts,  the  swelling  of  the  skin  subsides,  and,  a  few 
days  later,  the  crusts  and  scabs  begin  to  fall  off.  With  the  beginning  of  desic- 
cation, the  fever  declines,  the  local  as  well  as  the  constitutional  symptoms 
become  daily  slighter,  and  convalescence  follows.  The  healing  of  the  pustules 
is  frequently  accompanied  by  an  extremely  troublesome  itching.  After  the 
scabs  have  been  cast  off,  the  skin  presents  pigmented  spots,  which  persist  for 
months.  Wherever  the  cutis  vera  has  itself  been  destroyed  by  the  suppuration, 
a  scar  is  inevitable.  Thus  arise  the  familiar  scars  (pitting)  of  smallpox, 
which  continue  visible  through  life.  Very  often,  after  the  end  of  the  disease, 
there  is  almost  complete  alopecia.    The  hair  often  grows  again,  but  not  always. 

Varioloid. — The  distinction  between  varioloid  and  variola  vera  is  not  in 
kind,  but  in  degree.  Varioloid  is  only  a  milder  form  of  variola.  There  is,  as 
we  have  already  said,  no  sharp  boundary  line  between  the  two.  Varioloid  is 
most  often  observed  in  those  whose  susceptibility  to  the  variolous  poison  has 
been  diminished  b}^  vaccination  (vide  infra). 

As  above  mentioned,  the  behavior  of  the  disease  during  its  initial  stage  does 
not  permit  us  to  decide  positively  whether  variola  or  varioloid  will  be  devel- 
oped.    It  is  true  that  if  the  symptoms  be  especially  mild,  we  may  guess  that  it 


SMALLPOX 


65 


will  bo  varioloid ;  and,  likewise,  the  appearance  of  the  initial  erythema  already 
spoken  of  is  regarded  as  a  favorable  omen. 

Shortly  after  the  pocks  begin  to  appear,  the  decision  can  almost  always  be 
made  with  certainty.  In  varioloid  the  eruption  is  rather  scanty.  It  i-  often 
irregular,  and  does  not  by  any  means  always  begin,  like  that  of  variola,  in  the 
face,  but  often  on  the  trunk.  The  individual  pocks  are  in  no  way  different  from 
those  of  variola;  but  it  often  happens  that  they  do  not  pass  through  all  the 
regular  stages  to  full  suppuration,  but  undergo  resolution  before  this  occurs. 
Such  cases,  in  which  there  is  nothing  beyond  papilla?  or  vesicles,  are  sometimes 
spoken  of  as  variolois  verrucosa  seu  miliaria.  The  scantiness  of  the  eruption 
and  the  limited  amount  of  suppuration  have  for  their  corollary  an  absence,  or 
at  least  a  very  slight  development,  of  the  suppurative  fever. 

When  the  eruption  appears  the  temperature  usually  falls  by  crisis  to  the 
normal  level  and  remains  there.  The  desiccation  may  begin  as  earlv  as  the 
eighth  or  tenth  day  of  the  disease,  so  that  the  whole  duration  of  varioloid  is 
considerably  shorter  than  that  of  variola.  Grave  complications  are  very  excep- 
tional. The  pocks  may  develop  upon  the  mucous  membranes,  but  here,  too, 
they  are  scanty  and  not  very  vigorous. 

Course  of  the  Fever,  Symptoms  presented  by  Separate  Organs,  and  Compli- 
cations.— 1.  Fever  (vide  Fig.  9). — In  the  initial  stage,  as  we  have  said,  the 
temperature  rises  rapidly,  as  a  rule,  with  a  pronounced  rigor;  and  during  the 
first  days  it  very  often  reaches  104°  to  106°  F.  (40°  to  41°  C).     It  sinks  on 


2         3         4         5 


9        10        11       12        13        14        15        16        17        18 


40.0« 


39.0C 


38.0° 


37.0° 


Initial  Fever 

Eruption. 


Suppurative  Fever. 
Fig.  9. — Example  of  the  temperature  curve  in  true  smallpox. 


the  third  to  the  sixth  day,  when  the  first  papillae  develop,  and  then,  in  the 
case  of  varioloid,  falls  rapidly  to  normal,  and  remains  there.  In  variola  the 
decline  is  slower  and  less  complete ;  and  with  the  beginning  of  suppuration  the 
temperature  begins  to  rise  again.  The  violence  of  this  suppurative  fever  is 
usually  in  direct  proportion  to  the  severity  of  the  eruption.  It  has  manifold 
fluctuations,  but  seldom  lasts,  in  severe  cases,  less  than  a  week.  Temperatures 
of  104°  F.  (40°  C.)  and  higher  are  common.  The  fever  declines  by  lysis.  In 
case  of  approaching  death,  the  temperature  may  be  extremely  high,  even  reach- 
ing 108°  or  109°  F.  (42°  to  43°  C). 

2.  The  Skin. — We  have  already  described  the  macroscopic  appearance  of 
the  eruption.    It  remains  to  mention  briefly  the  histological  phenomena.    The 


66  ACUTE   GENERAL   INFECTIOUS   DISEASES 

first  demonstrable  changes  are  in  the  cells  of  the  deeper  layers  of  the  rete  Mal- 
pighii.  As  a  result  of  the  variolous  infection,  the  cells  perish,  are  swollen  by 
the  lymph  which  escapes  from  the  papillary  blood  vessels,  and  transformed 
into  flaky,  homogeneous  masses  without  nuclei  ("coagulation  necrosis"  of 
Weigert).  The  lymph  becomes  more  and  more  abundant,  and  crowds  the  cells 
farther  and  farther  apart.  These  are  thereby  finally  changed  into  threads  and 
membranes,  forming  a  distinct  network  in  the  vesicle.  This  explains  why,  if 
such  a  vesicle  be  pricked,  its  entire  contents  are  never  discharged  at  once. 
Great  numbers  of  white  corpuscles  escape,  along  with  the  lymph,  from  the 
blood  vessels,  and  finally  render  the  contents  of  the  original  vesicle  purulent. 
Proliferative  processes  occur  in  the  surrounding  epithelial  cells,  which  are  still 
intact,  and  thus  the  margin  of  the  vesicle  becomes  elevated,  while  the  dead 
portion  in  the  center  sinks  in.  Thus  the  pock  becomes  umbilicated.  If  a 
portion  of  the  papilla  itself  suppurates,  a  scar  must  be  left  on  healing.  If 
the  process  remains  limited  to  the  epithelium,  complete  regeneration  takes 
place,  and  the  skin  reassumes  its  normal  appearance. 

Certain  secondary  complications,  which  sometimes  attack  the  skin,  remain 
to  be  mentioned :  abscess,  phlegmon,  erysipelas,  gangrene,  and  bedsores. 
1ST  one  of  these  are  due  directly  to  the  specific  variolous  intoxication. 

3.  Respiratory  Organs. — The  disturbances  here  are  in  part  symptoms  of 
the  specific  process  of  the  disease,  and  in  part  secondary.  The  frequent  occur- 
rence of  secondary  symptoms  in  smallpox  is  easy  to  understand  (compare  the 
chapter  on  lobular  pneumonia).  Of  the  primary  symptoms,  we  should  men- 
tion genuine  pocks  in  the  larynx,  the  trachea,  and  the  larger  bronchi.  As 
sequels  to  these,  more  or  less  severe  secondary  disorders  are  very  frequent : 
laryngeal  ulcerations,  which  may  even  lead  to  laryngeal  perichondritis  and 
cedema  of  the  glottis;  diffuse  bronchitis;  lobular  pneumonia,  often  of  great 
extent,  due  to  the  inhalation  of  solid  matter  into  the  lungs,  and  frequently 
accompanied  by  pleurisy.  It  should  be  especially  noticed  that  lobar,  croupous 
pneumonia  is  not  rare.  Whether  this  be  likewise  secondary,  or  a  direct  result 
of  the  variolous  poison,  is  not  yet  known. 

4.  Digestive  System. — The  genuine  pocks  often  develop,  as  stated,  in  the 
mouth  and  pharynx,  and  likewise  in  the  upper  part  of  the  oesophagus.  They 
are  not  observed  in  the  mucous  membrane  of  the  stomach  or  intestines.  The 
active  diarrhea  sometimes  seen  depends  upon  catarrh  of  the  intestine.  Dysen- 
tery is  rare.  The  eruption  in  the  mouth  and  throat  may  result  in  severe  sec- 
ondary troubles,  purulent  otitis,  parotitis,  pharyngeal  diphtheria,  etc.  The 
spleen  is  almost  always  considerably  enlarged,  and  often  the  liver  also,  but  in 
a  less  degree. 

5.  Circulatory  System. — Pathological  changes  in  the  heart  are  rare,  if  we 
except  slight  parenchymatous  degeneration.  Sometimes  there  is  a  slight  endo- 
carditis ( q.  v. ) ,  which  is  probably  secondary.  Pericarditis  is  rather  more 
frequent. 

The  blood  shows  a  pronounced  leucocytosis,  mainly  affecting  the  large 
mononuclear  leucocytes,  but  neutrophilic  and  eosinophilic  myelocytes  are  also 
present;  the  lymphocytes,  however,  are  only  slightly  increased. 

6.  Organs  of  Special  Sense. — Genuine  variolous  pustules  occur  upon  the 
eyelids  and  the  conjunctiva.  Later  in  the  disease  there  may  be  keratitis,  iritis, 
or  choroiditis. 


SMALLPOX  ()7 

Wo  have  already  mentioned  the  relative  frequency  of  aural  disturbances, 

particularly  purulent  otitis  media. 

7.  The  Joints. — Articular  swelling  may  appear  in  the  suppurative  stage. 
The  shoulders  and  knees  are  most  apt  to  be  attacked.     Periostitis  also  occurs. 

8.  Nervous  System. — We  find  no  pathological  changes  corresponding  to  tin- 
severe  nervous  derangements  manifested  during  the  disease.  After  the  small- 
pox is  over,  spinal  diseases  sometimes  occur,  with  either  paralysis  or  ataxia. 
Westphal  has  shown  that  they  are  caused,  in  some  cases,  hy  numerous  dissemi- 
nated centers  of  inflammation  in  the  spinal  cord.  Encephalitis  processes  I 
also  heen  observed  in  smallpox,  and  in  some  cases  neuritic  paralysis. 

9.  The  Kidneys. — Albuminuria  is  quite  common  in  severe  attacks,  but 
genuine  nephritis  is  a  very  rare  complication. 

In  pregnant  women  attacked  by  smallpox  abortion  or  premature  labor  is 
very  apt  to  occur.    If  a  living  child  be  born,  it  usually  dies  soon  after  birth. 

Anomalies. — Anomalies  in  the  course  of  the  disease  are  manifold.  We  will 
not  speak  of  the  two  typical  forms  already  considered.  There  are  abnormally 
mild  cases,  with  scarcely  any  initial  symptoms,  or  with  an  obscure  eruption,  or 
with  no  eruption  at  all  (febris  variolosa  sine  exanthemate) .  In  such  cases  a  cor- 
rect diagnosis  is  possible  only  at  the  time  an  epidemic  prevails,  and  by  the  aid 
of  the  attendant  aatiological  circumstances.  There  are  also  abortive  cases  in 
which  the  first  symptoms  are  severe,  but  which  recover  with  remarkable 
rapidity. 

The  abnormally  severe  cases  are  more  important.  First,  there  is  the  con- 
fluent variety.  This  is  merely  the  typical  process  in  its  completest  develop- 
ment. The  initial  symptoms  are  themselves  generally  very  severe,  and  are 
followed,  without  any  considerable  remission  of  the  fever,  by  the  eruption  of 
hundreds  of  pustules.  The  skin  of  the  face  and  hands  is  one  continuous  area 
of  suppuration.  The  local  discomfort  is  extreme,  as  is  also  the  intensity  of  the 
fever  and  of  the  constitutional  symptoms.  The  nervous  system  suffers  most. 
There  is  at  the  same  time  an  unusually  abundant  eruption  upon  the  mucous 
membranes.  The  occurrence  of  the  above-mentioned  complications  affecting 
the  various  organs  of  the  body  is  frequent.  Death  is  a  common  result;  or, 
if  recovery  takes  place,  it  may  be  delayed  by  tedious  sequelae. 

Hemorrhagic  smallpox  is  the  worst  anomalous  form.  The  name  is  applied 
to  several  different  varieties.  In  the  first  place,  any  variolous  eruption  may 
become  more  or  less  hemorrhagic,  and  yet  the  general  course  of  the  disease 
not  be  essentially  altered.  Such  cases  are  more  common  among  elderly  peo- 
ple, cachectic  persons,  and  drunkards.  Secondly,  there  is  a  very  severe  form 
of  smallpox  which  is  generally  fatal.  The  initial  stage  is  marked  by  the 
unusual  severity  of  the  symptoms.  The  abundant  eruption  soon  becomes 
hemorrhagic,  and  there  are  also  ecchymoses  in  the  mucous  membranes  and 
the  internal  organs.  This  has  been  called  black  smallpox,  and  by  Cursch- 
mann  variola  licemorrhagica  pustulosa. 

There  is  another  form  of  hemorrhagic  variola,  different  from  these  but 
linked  to  them  by  transitional  varieties.  In  it  the  acute  hemorrhagic  diathesis 
develops  during  the  initial  stage.  Death  almost  always  occurs  before  the  regu- 
lar variolous  eruption.  This  most  frightful  form  is  usually  termed  purpura 
variolosa.  That  it  is  smallpox  is  proved  by  its  etiological  relations  alone. 
Otherwise  it  would  be  impossible  to  distinguish  it  from  certain  other  acute 
6 


68  ACUTE  GENERAL  INFECTIOUS  DISEASES 

septic  disorders.  It  is  prone  to  attack  the  youthful  and  vigorous.  Chills, 
headache,  and  i:>ain  in  the  loins  are  the  first  symptoms,  just  as  in  ordinary 
cases.  Cutaneous  ecchymoses  appear  as  early  as  the  second  or  third  day.  They 
increase  in  area  so  rapidly  that  one  can  almost  see  them  grow.  They  are 
most  extensive  in  the  hypogastric  region.  There  are  also  ecchymoses  in  the 
eyelids,  the  conjunctiva,  the  mouth  and  pharynx,  and,  as  the  autopsy  dis- 
closes, many  in  the  internal  viscera.  The  constitutional  symptoms  are  most 
severe,  and  the  patient  seldom  survives  the  fifth  or  sixth  day  of  the  disease. 

Diagnosis. — The  certainty  with  which  we  can  make  the  diagnosis  of  small- 
pox in  any  well-developed  case  is  equaled  by  the  difficulty  of  deciding  about  it 
during  the  beginning  of  the  disease,  or  even  during  the  beginning  of  the 
eruption.  At  this  period  diagnosis  may  be  impossible.  When  the  variolous 
eruption  is  in  process  of  development,  it  may  be  confounded  with  typhus 
fever,  with  that  form  of  measles  in  which  the  papilla?  are  prominent,  with 
syphilitic  eruptions,  and  with  certain  forms  of  beginning  erythema  exsu- 
dativum.  In  doubtful  cases  one  must  consider  not  only  the  cutaneous  manifes- 
tations but  also  the  other  symptoms,  for  the  diagnosis  can  often  only  be  made 
with  certainty  after  continued  observation.  It  will  require  further  study  to 
determine  the  diagnostic  value  of  the  inoculation  of  the  rabbit's  cornea,  and 
of  the  demonstration  of  the  Guarnieri  bodies   (vide  supra). 

Prognosis. — The  facts  which  are  of  greatest  weight  in  prognosis  have  al- 
ready been  emphasized.  We  may  repeat  that  during  the  initial  stage  the 
prognosis  of  any  individual  case  can  seldom  be  determined.  If  the  first  symp- 
toms are  mild,  or  if  the  initial  erythema  appears,  the  case  is  regarded  hope- 
fully. The  abundance  of  the  eruption  has  an  influence  upon  the  severity  of 
the  disease.  Circumstances  peculiar  to  the  individual  are  also  important — 
e.  g.,  age,  constitution,  or  alcoholic  habits.  We  have  already  called  attention  to 
the  danger  of  confluent  smallpox,  and  to  the  almost  absolutely  fatal  prognosis 
in  the  genuine  hemorrhagic  variety.  The  mortality  varies  greatly  in  different 
epidemics;  on  the  average  it  may  be  taken  at  about  fifteen  to  thirty  per  cent. 
Beyond  doubt,  the  introduction  of  vaccination  has  decidedly  lessened  the 
fatality  of  the  disease  by  diminishing  the  frequency  of  the  severe  forms. 

Treatment. — 1.  Prophylaxis — Vaccination. — As  in  all  contagious  diseases, 
isolation  is  of  little  avail  unless  complete.  This  fact  has  led  to  the  erection  in 
late  years  of  smallpox  hospitals.  All  utensils  used  by  the  patient,  and  his 
clothing,  bedding,  and  the  like,  should  be  most  carefully  disinfected.  The 
best  method  is  to  employ  a  high  degree  of  heat. 

These  precautionary  measures  are  employed  in  many  other  diseases  as 
well,  but  for  smallpox  we  are  acquainted  with  a  special  method  of  prophylaxis. 
It  is  founded  upon  a  fact  which  is  the  most  remarkable  within  the  domain 
of  the  infectious  diseases.  We  refer  to  prophylactic  vaccination.  It  must  long 
ago  have  been  remarked  that  a  person  who  has  had  the  disease  once,  enjoys, 
to  a  large  degree,  immunity  from  any  fresh  infection.  This  suggested  the 
idea  of  exposing  children  purposely  to  contagion,  so  as  to  insure  them  from 
smallpox  for  the  rest  of  their  lives.  The  actual  inoculation  of  smallpox  is 
said  to  have  been  long  practiced  in  India  and  China.  In  the  year  1717  it  was 
employed  by  Lady  Mary  Wortley  Montagu,  of  England,  upon  her  own  son, 
and  with  success.  Unfortunately,  however,  the  inoculated  smallpox  proves 
fatal  in  many  instances;  and,  being  itself  contagious,  it  serves  to  spread  the 


SMALLPOX  69 

disease  still  further.  Then  appeared  an  article  written  by  the  English  sur- 
geon, Edward  Jenner,  in  1798.  This  informed  the  medical  profession  of  a 
fact  already  known  to  the  rural  population  of  his  native  place,  but  which 
Jenner  first  established  scientifically,  and  recognized  in  all  its  Importance. 
There  sometimes  occurs  a  disease  similar  to  smallpox  upon  the  teats  and  adder 
of  the  cow,  called  variola  vaccina.  It  is  apparently  a  local  trouble,  and  it 
can  easily  be  inoculated  upon  the  skin  of  human  beings.  Vaccine  pustules  will 
be  developed  upon  the  spot  inoculated.  These  almost  invariably  heal  without 
any  great  constitutional  disturbance;  but  the  person  vaccinated  possesses  the 
same  immunity  from  smallpox  as  if  he  had  had  smallpox  itself.  This  statement 
of  Jenner's  was  soon  confirmed  upon  every  side.  The  result  is  the  continually 
spreading  custom  of  prophylactic  vaccination. 

In  some  countries,  especially  in  Germany,  universal  vaccination  (compul- 
sory vaccination)  is  enforced  by  law;  it  can  be  opposed  only  by  ignorance  or 
lamentable  prejudice.  The  discovery  of  vaccination  was  the  foundation  for  all 
the  subsequent  remarkable  discoveries  in  immunity  and  in  serum  investiga- 
tion. It  has  been  definitely  proved  by  Fischer  and  others  that  vaccinia  is, 
in  fact,  only  a  form  of  smallpox  rendered  milder  and  modified  by  transmission 
to  animals.  If  we  inoculate  a  calf  with  the  contents  of  a  fresh  smallpox 
vesicle  from  man,  typical  vaccinia  is  produced.  With  the  contents  of  this 
vaccine  vesicle  children  can  be  inoculated  without  any  danger,  and  they  are 
no  longer  susceptible  either  to  vaccinia  or  smallpox. 

We  can  mention  only  the  most  important  of  the  details  relating  to  vaccina- 
tion and  the  method  of  its  performance.  Only  exceptionally  do  we  vaccinate 
with  the  contents  of  a  human  vaccine  vesicle  ("humanized  lymph"),  but  we 
almost  invariably  use  animal  lymph  from  vaccine  vesicles  of  calves.  This  is 
now  obtained  in  large  quantities  and  put  on  the  market.  The  process  of  vac- 
cination is  to  make  three  shallow  incisions,  3  or  4  cm.  apart,  in  the  skin  of 
the  upper  arm,  and  to  introduce  the  vaccine  lymph  into  them.  The  surround- 
ing tissue  becomes  swollen  in  three  or  four  days.  In  seven  or  eight  days  the 
vaccine  vesicles  are  well  developed,  if  the  disease  takes  its  normal  course. 
Next  they  become  purulent,  and  then  dry  up,  and  finally,  on  healing,  leave 
the  familiar  scar  behind.  The  whole  process  occupies  about  three  weeks.  If 
the  vaccination  fails,  or  is  but  partially  successful,  it  must  be  repeated  after  a 
few  months.  The  protective  power  of  vaccination  does  not  last  indefinitely, 
and  therefore  revaccination  is  necessary  every  five  or  six  years.  The  first 
vaccination  of  children  usually  takes  place  when  they  are  three  or  four  months 
old.    If  they  are  feeble  we  wait  longer,  unless  smallpox  is  prevalent. 

According  to  the  vaccination  laws  of  Germany  every  child  must  be  vacci- 
nated before  the  end  of  his  first  year  of  life,-  and  all  school  children  must 
be  revaccinated  during  their  twelfth  year. 

It  must  be  confessed  that  vaccination  is  not  without  its  dangers.  The  little 
cutaneous  wound  made  by  it  may  lead,  like  any  other,  to  sepsis,  or  to  ery- 
sipelas. The  latter  has  been  called  vaccination-erysipelas.  But  such  misfor- 
tunes are  extremely  rare.  The  not  uncommon  "  vaccine  roseola  "  deserves  es- 
pecial mention.  It  appears  first  upon  the  arm  vaccinated,  and  spreads  over 
the  rest  of  the  body ;  but  it  is  not  a  serious  matter.  It  is,  of  course,  possible, 
by  especially  bad  luck  in  the  use  of  human  lymph,  that  other  diseases,  among 
which  syphilis  is  of  chief  importance,  may  be  inoculated  along  with  vaccinia ; 


70  ACUTE   GENERAL  INFECTIOUS   DISEASES 

but  this  is  a  very  rare  occurrence — much  more  so  than  the  enemies  of  vac- 
cination pretend.  If  the  physician  exercise  proper  care  in  the  selection  of  the 
person  from  whom  to  take  humanized  virus,  it  can  be  entirely  avoided. 

Impetigo  contagiosa  and  favus  have  been  observed  as  the  result  of  trans- 
mission by  vaccination,  but  they  have  no  serious  significance. 

[The  incubation  stage  of  vaccinia  being  shorter  than  that  of  smallpox,  the 
prompt  vaccination  of  an  unprotected  individual  who  has  been  exposed  to 
infection  should  always  be  practiced,  if  possible;  oftentimes  the  severe  disease 
may  thus  be  prevented.] 

2.  Symptomatic  Treatment. — The  treatment  of  smallpox  is  purely  symp- 
tomatic. When  the  disease  has  once  begun  it  is  too  late  for  vaccination  to 
have  any  influence  upon  its  further  course.  During  the  initial  period  we  may 
advantageously  employ  cool  baths  to  diminish  the  fever  and  alleviate  the  con- 
stitutional symptoms.  An  ice  bag  will  relieve  the  headache.  We  must  not 
let  the  lumbar  pains  lead  us  to  any  but  a  cautious  use  of  local  irritants,  for 
the  pocks  come  out  in  greater  abundance  upon  such  portions  of  the  skin  as 
have  been  in  any  way  irritated.  If  the  disease  proves,  during  the  stage  of 
eruption,  to  be  varioloid,  there  will  be  no  further  need  of  special  treatment. 
Good  nursing  and  proper  food  will  suffice. 

The  true  smallpox,  on  the  other  hand,  demands  the  interposition  of  the 
physician.  He  must  strive  to  guard  the  regular  course  of  the  disease  in  the 
skin  and  in  those  portions  of  the  mucous  membrane  which  are  accessible  from 
being  disturbed  by  secondary  inflammations;  for  we  have  no  doubt  that  the 
ruptured  pustules  furnish  a  most  easy  ingress  to  septic  impurities  from  the 
surrounding  atmosphere,  so  that  later,  when  there  is  extensive  suppuration  of 
the  skin,  or  analogous  and  severe  disturbance  in  the  mucous  membrane,  it  is 
impossible  to  discriminate  between  the  effects  of  the  smallpox  itself  and  those 
due  to  the  secondary  suppuration.  If  we  were  able  to  have  the  whole  process 
go  on  "  aseptically  "  we  should  certainly  have  made  an  important  advance  in 
therapeutics.  It  is  very  doubtful  if  this  is  to  be  attained  by  means  of  externally 
applied  disinfectants,  such  as  the  paste  recommended  by  Schwimmer  (acidi 
carbol.,  4  to  10  parts;  olei  olivarum,  40  parts;  cretas  opt.  trit.,  60  parts;  to 
be  spread  on  linen  and  applied  to  the  affected  surfaces).  Many  physicians, 
therefore,  confine  themselves  to  the  use  of  cold  applications,  Priessnitz  packs, 
simple  salves  and  oils.  Under  Hebra,  in  Vienna,  continuous  warm  baths  were 
employed  in  severe  cases  with  great  success.  The  recent  claims  of  various  ob- 
servers that  the  red-light  treatment  (i  e.,  the  sick-room  so  arranged  that  only 
red  light  can  enter)  has  a  decidedly  limiting  effect  upon  the  suppuration  re- 
quires further  substantiation. 

The  treatment  of  the  affected  mucous  membrane  in  smallpox  must  also 
meet  the  indication  above  mentioned.  The  most  thorough  disinfection  of  the 
mouth  and  pharynx  must  be  aimed  at.  The  means  to  be  used  are  careful 
washing  and  gargling  with  solutions  of  chlorate  of  potash  (1  to  30),  borax, 
permanganate  of  potash,  hydrogen  peroxid,  etc.  The  eyes,  if  they  need  it, 
must  also  be  appropriately  treated.  As  to  all  other  complications,  cool  baths 
are  relatively  the  most  useful  remedy.  They  can  be  given  without  difficulty. 
The  chief  indications  for  them  are  severe  pulmonary  or  nervous  symptoms, 
or  continuous  high  fever.  Internal  antipyretics,  such  as  quinin  or  antipyrin, 
are  also  employed.    Violent  nervous  disturbances,  such  as  delirium,  sometimes 


VARICELLA  71 

require  the  cautious  use  of  narcotics.  There  ie  aothing  to  add  ae  to  the  treat- 
ment of  malignant  hemorrhagic  smallpox,  for,  ae  we  have  said,  such  cases  are 
unfortunately  almost  hopeL 


CHAPTEE    VTTT 

VARICELLA 
(Chicken  Pox) 

Varicella  is  truly  one  of  the  diseases  of  childhood.     Adults  very  rarely 

have  it.     It  is  contagious,  and  often  comes  in  epidemic. 

The  stage  of  incubation  does  not  last  over  thirteen  to  seventeen  days.  The 
disease  begins  with  the  appearance  of  vesicles,  the  size  of  a  pea  or  a  little 

larger,  usually  having  a  small  red  areola,  and  varying  from  ten  to  one  hun- 
dred or  more.  The  trunk  usually  bears  the  greater  part  of  the  vesicles,  while 
the  extremities  have  few.  The  face  is  frequently  the  seat  of  a  considerable 
number,  and  there  are  often  a  few  upon  the  hairy  scalp.  There  may  be  a 
vesicle  here  and  there  upon  the  mucous  membrane  of  the  mouth  or  palate. 
There  are  seldom  any  prodromata.  Slight  symptoms  of  fever  may  attend  the 
eruption  itself.  The  full  eruption  does  not  appear  at  one  time.  Successive 
crops  of  vesicles  develop  over  a  period  of  several  days  or  of  even  almost  one 
week.  For  this  reason  one  sees,  at  one  and  the  same  time,  early,  fully  devel- 
oped, and  healing  vesicles.  The  contents  of  the  vesicles  always  become 
slightly  cloudy  (purulent),  but  the  cutaneous  tissue  is  almost  never  deeply 
involved  as  in  smallpox.  The  course  of  the  disease  is  generally  completed  in 
from  one  to  two  weeks.  Most  children  feel  perfectly  well  the  whole  time, 
although  in  rare  cases  there  may  be  pain  in  the  limbs,  anorexia,  and  a  slight 
coryza.  Severe  complications  are  seen  very  exceptionally,  the  most  frequent 
one  being  a  mild  nephritis. 

Exceptionally,  the  disease  may  be  rudimentary,  with  a  varicelloid  roseola 
and  no  formation  of  vesicles.  On  the  other  hand,  some  cases  present  quite 
severe  constitutional  symptoms  and  a  high  fever,  even  reaching  105°  F.  (41° 
C.)  temporarily.  In  most  cases,  however,  as  we  have  said,  the  child  is  so 
slightly  disturbed  that  a  physician  is  hardly  thought  necessary. 

Diagnosis. — The  diagnosis  is  almost  always  easy.  Formerly  varicella  was 
often  confounded  with  smallpox,  and  for  a  long  time  the  followers  of  Hebra, 
in  Vienna,  for  some  inconceivable  reason,  maintained  the  identity  of  the  two. 
That  they  are  essentially  distinct  is  shown  (1)  by  the  epidemics  of  the  two 
appearing  entirely  separate  from  each  other,  (2)  by  the  fact  that  having  one 
does  not  give  immunity  from  the  other,  and  (3)  by  the  uniform  failure  of 
attempts  to  produce  variola  by  inoculating  varicella,  or  vice  versa. 

Prognosis. — The  prognosis  is  perfectly  good.  There  is  usually  no  special 
treatment  necessary,  but  young  children  and  those  having  fever  should  be 
kept  in  bed  till  the  eruption  has  dried  up. 


72 


ACUTE   GENERAL   INFECTIOUS   DISEASES 


CHAPTER   IX 


ERYSIPELAS 
(St.  Anthony's  Fire) 

iEtiology. — Erysipelas  is  a  peculiar  inflammation  of  the  skin,  recognized 
by  redness,  swelling,  and  pain.  It  has  the  peculiarity  of  spreading  gradually, 
by  direct  extension,  from  its  point  of  origin  over  a  larger  or  smaller  portion 
of  the  body.  The  cause  of  this  inflammation,  as  was  first  shown  by  Eehleisen, 
is  a  local  infection  by  the  streptococcus  pyogenes  and  its  further  extension  in 
the  skin.  The  exciting  agent  of  erysipelas  is  then  bacteriologically  identical 
with  the  streptococcus  which  is  the  cause  of  phlegmonous  suppuration,  severe 
septic  infection,  etc.  The  reason  why  in  the  individual  case  erysipelas  de- 
velops, and  not  some  other  streptococcus  disease,  is  the  special  variety  of  in- 
fection and  the  further  spread  of  the  streptococci  in  the  deeper  lymphatics  of 
the  skin,  and  in  part  perhaps  the  special  "  virulence  "  of  the  infecting  germs. 

The  former  distinction  between  "  traumatic  "  and  "  idiopathic  "  or  "  ex- 
anthematic  "  erysipelas  can  no  longer  be  rigidly  maintained.    Every  erysipelas 

is   in  a   certain   sense   traumatic,   since   in- 

^A-jWiftAWf^yi^-         fection     with     streptococci     cannot     occur 

^MM' //' //  4aE§&-       through  the  unbroken  skin.     The  so-called 

P^nJpJB  "  idiopathic "  erysipelas  is  distinguished 
from  "wound  erysipelas"  (in  which,  of 
course,  we  include  puerperal  erysipelas,  ery- 
sipelas of  the  newborn  starting  from  the 
umbilical  wound,  etc.)  only  by  the  fact  that 
in  the  former  the  infection  takes  place  in 
small,  insignificant  wounds  of  the  skin 
which  are  easily  overlooked.  Such  an  ery- 
sipelas occurs  chiefly  in  the  face  and  head, 
and  the  following  description  of  the  symp- 
toms refers  chiefly  to  this  facial  erysipelas. 
Most  of  these  cases  of  erysipelas  arise  from 
little  excoriations,  cracks,  and  scratches 
Fig.  10.  — The  cocci  of  erysipelas.  aljout  the  noge  or  eargj  or  more  rarely  about 
X700.     Section  through  a  lymph-  ,,  ,        P  ,,       ->  ■,  . 

vessel  in  the  skin.  other  parts  of  the  face  or  scalp.     A  previous 

coryza,  by  the  accompanying  slight  erosions 
about  the  nose,  sometimes  gives  the  opportunity  for  an  attack  of  erysipelas, 
but  sometimes  the  infection  occurs  in  the  mucous  membrane  of  the  nose  or 
pharynx;  then  we  have  a  primary  erysipelas  of  the  mucous  membrane,  which 
extends  through  the  nasal  passages  and  finally  appears  on  the  external  sur- 
face of  the  nose. 

Facial  erysipelas  is  most  apt  to  attack  the  young,  and  seems  to  be  some- 
what more  frequent  in  women  than  in  men.  The  laity  erroneously  regard 
catching  cold  and  getting  frightened  as  frequent  causes  of  the  disease.  If  we 
except  the  predisposing  causes  above  mentioned — viz.,  coryza,  slight  scratches, 
cuts,  etc. — we  usually  find  no  cause  of  which  we  can  feel  certain.     Often 


ERYSIPELAS  73 

endemic  influences  are  important.  It  lias  been  long  known  that  traumatic 
erysipelas  can  get  so  secure  a  footing  in  particular  hospitals  or  wards  that 
every  wounded  person  treated  in  them  is  in  danger  of  this  disease;  but  the 
apparently  idiopathic  variety  is  sometimes  remarkably  frequenl  in  particular 

places  (barracks,  etc.).  Several  members  of  one  family  may  likewise  have 
facial  erysipelas  simultaneously.  In  nearly  all  such  cases  the  sufferers  are  in- 
fected from  some  common  source,  for  direct  contagion  is  certainly  exceptional; 
but  patients  with  open  wounds  should  never  be  put  near  erysipelas  cases,  be- 
cause here  the  risk  of  infection  cannot  be  wholly  excluded.  Direct  inoculation 
can,  however,  as  has  been  proved,  convey  the  disease  from  a  patient  to  other 
persons  or  to  animals. 

In  contrast  with  the  behavior  of  many  other  infectious  diseases  (typhoid 
fever,  measles,  scarlet  fever,  smallpox,  etc.),  erysipelas  is  peculiarly  apt  to 
attack  the  same  individual  over  and  over  again.  There  are  persons  who  have 
facial  erysipelas  about  every  one  or  two  years,  and  ten  to  fifteen  times.  Often 
the  explanation  of  this  apparently  lies  in  some  chronic  disease — e.  g.,  chronic 
ozasna,  chronic  eczema  of  the  nostrils  or  ears — which  makes  infection  easy, 
but  in  other  cases  no  cause  can  be  discovered.  Of  course  when  e^sipelas 
afflicts  the  same  person  a  number  of  times  the  individual  attacks  gradually  be- 
come milder.  Marasmus  seems  to  predispose  to  erysipelas.  At  least  we  have 
observed  that  erysipelas  occurred  with  relative  frequency,  in  the  Leipsic  hos- 
pital, in  patients  suffering  from  the  last  stages  of  phthisis  or  cancer,  or  similar 
diseases. 

Clinical  History. — The  incubation  period  of  erysipelas  is  short,  generally 
lasting  but  from  one  to  three  days.  In  many  cases  the  first  subjective  symp- 
toms are  simultaneous  with  the  cutaneous  swelling,  and  these  are  chiefly  local. 
There  is  pain  and  a  sense  of  tension  in  the  skin.  Soon  subjective  symptoms  of 
fever  also  appear,  such  as  general  malaise,  anorexia,  headache,  and  sometimes 
vomiting.  In  other  cases  the  disease  starts  with  more  violent  constitutional 
symptoms :  there  is  an  initial  rigor,  with  violent  headache  and  great  languor. 
The  local  erysipelatous  swelling  appears  almost  at  the  same  time  with  these 
general  symptoms,  or  sometimes  a  few  days  later,  either  because  the  local  in- 
flammation is  at  first  slight  or  because  it  is  not  noticed,  as  in  the  scalp  when 
the  hair  is  very  thick.  In  rare  instances  the  disease  begins  with  sore  throat. 
We  saw  three  almost  simultaneous  cases  of  facial  erysipelas  in  one  family, 
in  which  a  severe  sore  throat  lasted  for  four  or  five  days  preceding  the  appear- 
ance of  the  cutaneous  disorder.  We  have  seen  a  number  of  similar  cases  since, 
and  believe  that  they  are  due  to  a  true  erysipelatous  sore  throat — that  is,  to  an 
erysipelas  of  the  soft  palate  which  extends  through  the  nostrils  to  the  external 
skin.  In  cases  of  erysipelas  which  follow  a  coryza  we  may  assume,  as  stated 
above,  that  there  sometimes  is  an  erysipelas  of  the  nasal  mucous  membrane 
preceding  the  erysipelas  of  the  skin. 

The  erysipelatous  process  in  the  skin  is  almost  always  circumscribed  at 
first.  It  usually  starts  on  the  nose,  less  often  upon  the  cheek,  the  ears,  or  the 
hairy  scalp.  The  skin  becomes  considerably  swollen,  grows  red,  smooth,  and 
shiny,  and  feels  hot.  The  redness  and  swelling  keep  spreading.  There  is 
usually  a  sharp,  elevated  ridge,  perceptible  to  sight  ancl  touch,  separating  the 
diseased  from  the  still  healthy  portion  of  the  skin.  As  long  as  the  erysipelas 
is  spreading,  we  see  stretching  out  from  its  border,  or  somewhat  removed  from 


74  ACUTE   GENERAL   INFECTIOUS   DISEASES 

it,  small  red  streaks  and  spots  which  gradually  increase  in  area  and  intensity, 
and  finally  coalesce.  Any  decided  fold  in  the  skin  may  hinder  for  a  time  the 
extension  of  the  disease.  The  nasolabial  folds  are  particularly  apt  to  limit 
it.  The  border  of  the  hairy  scalp  frequently  forms  a  terminal  line;  but  the 
whole  scalp  may  be  attacked,  the  inflammation  stopping  only  when  it  reaches 
the  nape  of  the  neck.  The  boundary  of  the  erysipelas  in  the  hairy  scalp 
can  usually  be  quite  accurately  determined  by  palpation  (swelling  and  local 
tenderness). 

It  is  only  in  a  relatively  small  number  of  cases  that  it  spreads  farther  yet, 
attacking  the  back,  the  arms,  and  the  anterior  surface  of  the  trunk,  or  even 
extending  to  the  feet.  This  is  known  as  erysipelas  migrans.  The  facial  ery- 
sipelas may  be  healed  long  before  the  disease  ceases  to  extend  over  the  other 
parts  of  the  body.  When  the  spreading  process  is  about  to  cease,  the  inflam- 
mation usually  becomes  decidedly  milder,  appears  only  in  isolated  spots,  and 
finally  stops  completely.  In  most  cases,  only  the  face,  the  ears,  and  a  part  of 
the  scalp  are  attacked. 

It  is  not  a  rare  thing  for  vesicles  or  bulla?  to  form  in  the  portions  of  skin 
attacked.  Such  cases  are  called  erysipelas  vesiculosum  or  erysipelas  bullosum. 
The  serum  may  change  to  pus  in  these  blisters,  and  then  we  have  erysipelas 
pustulositm.  Exceptionally  the  infiltration  of  the  skin  becomes  so  intense  as 
to  result  in  a  localized  necrosis  or  gangrene — erysipelas  gangrenosum.  The 
parts  most  apt  to  be  attacked  by  this  are  the  eyelids,  where  abscesses  sometimes 
form. 

Microscopic  examination  of  the  skin  shows  a  marked  hyperemia  of  all  the 
blood  vessels  and  a  very  considerable  infiltration  of  both  the  skin  and  the  sub- 
cutaneous connective  tissue  with  serum  and  cells.  In  those  parts  where  vesi- 
cles are  formed  there  are  many  dead  and  disintegrated  epithelial  cells  in  the 
rete  Malpighii.  In  the  parts  where  most  streptococci  develop  there  may  also 
be  necrosis  of  the  deeper  la}rers  of  the  skin.  We  have  already  said  that  there 
may  be  many  streptococci  in  the  lymphatics  of  the  skin,  but  they  are  found 
only  in  the  first  fresh  stages  of  the  inflammation.  When  the  inflammatory 
exudation  has  reached  its  full  height,  the  streptococci  have  usually  wholly 
disappeared.  As  a  rule,  we  find  only  a  few  or  no  streptococci  in  the  contents 
of  erysipelas  vesicles. 

The  inflammation  in  any  one  spot  usually  ends  four  or  five  days  after  it 
has  made  its  appearance  there.  There  is  apt  to  be  much  attendant  desqua- 
mation.   The  face  is  often  left  with  a  finer  complexion  than  it  had  before. 

The  other  symptoms,  of  which  the  constitutional  disturbance  and  the  fever 
are  chief,  correspond  pretty  closely  to  the  severity  and  extent  of  the  cutaneous 
lesion.     It  is  comparatively  seldom  that  this  correspondence  does  not  exist. 

The  fever  in  facial  erysipelas  usually  rises  rapidly  at  first,  and  to  a  con- 
siderable height.  We  have  seen  but  few  cases  where  the  high  fever  was  de- 
layed till  a  day  or  two  after  the  skin  was  attacked.  The  temperatures  observed 
in  erysipelas  are  often  extreme:  106°  F.  (61°  C.)  is  not  at  all  rare.  The 
highest  we  ever  saw  was  107.2°  F.  (41.8°  C).  While  the  erysipelas  continues 
or  is  spreading,  the  fever  is  seldom  continuous,  nor  are  the  remissions  insig- 
nificant. Pronounced  intermissions,  even  down  to  normal,  are  very  frequent, 
but  are  followed  again  by  a  rapid  and  great  rise  of  temperature.  The  fever 
may  terminate  with  a  genuine  crisis  (see  Fig.  11).     In  intense  cases  of  con- 


KI.'YSII'HLAS 


75 


40.5' 


38.5° 


38.0° 


37.5° 


37.0° 


36.5° 


mm 


siderable  extent,  or  in  erysipelas  migrans,  the  termination  is  more  apl  to  be 
by  ;i  more  or  less  gradual  Lysis.  We  have  seen  the  cutaneous  inflammation  in 
erysipelas  migrans  still  extend  itself  ;i  little,  in  a  rudimentary  form,  after  the 
fever  had  completely  ceased. 

The  headache  is  often  intense,  and  Beems  to  result  nut  merely  from  the 
inflammation  of  the  scalp  but  from  disturbances  of  the  circulation  in  the 
underlying  parts,  or  more;  probably  from  the  action  of  a  toxin.  Other 
severe  cerebral  symptoms 
are  also  relatively  fre- 
quent. The  patient  may 
be  very  restless,  excited, 
and  wakeful.  At  night 
there  may  be  mild  or  even 
violent  delirium;  or  there 
may  be  decided  stupor. 
All  these  symptoms  are  in 
chief  part  due  to  the  gen- 
eral intoxication  caused  by 
the  infection ;  but  they 
also  justify  a  surmise,  as 
we  have  said,  that  there  is 
a  circulatory  derangement 
in  the  meninges  and  the 
brain  itself,  resulting  from 
the  inflammation  of  the 
scalp.  In  drunkards,  de- 
lirium tremens  is  not  in- 
frequent. 

One  of  the  most  constant  symptoms  in  facial  erysipelas  is  gastric  and  in- 
testinal disturbance.  There  is  usually  complete  anorexia.  The  tongue  is 
thickly  coated.  Vomiting  is  frequent,  not  only  at  the  beginning  but  during 
the  course  of  the  disase.  There  is  constipation,  or  there  may  be  quite  severe 
diarrhea.    The  spleen  is  usually  moderately  swollen. 

In  almost  all  severe  cases  the  urine  contains  albumen,  some  casts  and  white 
blood  cells.  In  most  cases  we  find  in  the  blood  a  pronounced  leucocytosis 
(16,000  to  18,000  leucocytes  in  a  cubic  millimeter).  Streptococci  are  not 
usually  found  in  the  blood. 

The  entire  duration  of  the  disease  varies  greatly  in  different  cases.  A  very 
light  case  may  get  well  in  a  few  days.  Most  cases  of  average  severity  last  a 
week  or  ten  days.  Erysipelas  migrans  may  continue  for  many  weeks.  We  have 
several  times  seen  a  relapse  come  on  after  a  number  of  days  of  complete 
apyrexia.  Either  the  face  would  be  once  more  attacked,  or  some  portion  of 
the  skin  which  had  previously  escaped. 

Complications. — Local  complications  are  comparatively  rare  and  insignifi- 
cant in  erysipelas.  The  lymphatic  glands  of  the  throat  and  back  of  the  neck 
are  very  frequently  somewhat  swollen,  but  seldom  attain  great  size.  Bron- 
chitis and  lobular  pneumonia  may  develop  in  severe  cases,  but  are  not  at  all 
characteristic.  Some  observers  call  attention  to  the  occurrence  of  pleurisy, 
endocarditis,   and   pericarditis;   but  these  complications   also   are  very  rare. 


Fig.  11.  —  Example  of  the  fever  curve  of  a  case  of  severe 
facial  erysipelas  (Erlangen  Medical  Clinic). 


76  ACUTE   GENERAL   INFECTIOUS   DISEASES 

Sometimes  there  is  an  icteroid  hue.  As  stated  above,  the  urine  frequently 
contains  a  small  amount  of  albumen,  and  in  severe  cases  of  erysipelas  acute 
hemorrhagic  nephritis  is  not  so  very  rare,  but  it  almost  always  disappears 
entirety.  The  albuminuria  usually  disappears  a  few  days  after  the  fever. 
Swelling  of  the  joints  has  been  repeatedly  observed.  It  is  more  frequent  in 
the  severe  surgical  forms  of  erysipelas,  which  are  combined  with  universal 
septic  and  pyasmic  conditions  of  the  system.  Purulent  meningitis  may  com- 
plicate an  erysipelas  located  in  the  head,  but  it  is  very  rare.  We  should  be 
exceedingly  cautious  about  asserting  its  existence  even  when  the  cerebral  symp- 
toms are  very  pronounced. 

Cutaneous  complications  are  relatively  frequent.  We  have  seen  herpes 
labialis  quite  often,  and  a  number  of  cases  of  urticaria.  Of  much  greater  im- 
portance are  the  cutaneous  abscesses  which  occur  in  severe  cases.  These  are  due 
to  a  phlegmonous  or  even  gangrenous  inflammation  of  the  connective  tissue. 
Their  most  frequent  seat  in  the  face  is  the  eyelids,  as  already  stated ;  and  in  that 
case  the  eye  may  itself  be  endangered.  At  the  close  of  severe  cases  of  ery- 
sipelas migrans,  numerous  abscesses  may  develop  in  the  skin  of  the  trunk 
and  extremities,  delaying  convalescence.  Since,  as  we  have  said,  the  strepto- 
coccus of  erysipelas  is  absolutely  identical  with  the  streptococcus  pyogenes, 
all  purulent  inflammatory  complications  of  erysipelas  are  to  be  referred  to 
the  local  or  metastatic  action  of  the  original  infectious  germs,  but  erysipel- 
atous nephritis  is  probably  of  purely  toxic  origin. 

Diagnosis. — The  diagnosis  of  erysipelas  is  almost  always  easy  when  once  the 
cutaneous  lesion  has  developed.  Phlegmonous  inflammation  of  the  skin  and 
lymphangitis  are  to  be  eliminated;  but  this  is  always  possible,  with  proper 
care.  After  a  single  examination,  we  may  confound  it  with  acute  facial  eczema 
of  great  severity,  or  even  with  a  marked  urticaria.  Chief  attention  should  be 
paid  to  the  characteristic  border  of  erysipelas  and  to  its  manner  of  extension. 
In  erysipelas  beginning  in  the  hairy  scalp  the  local  inflammation  may  easily 
be  overlooked,  being  completely  masked  by  the  severe  general  symptoms. 

Prognosis. — The  prognosis  of  facial  erysipelas,  when  it  attacks  a  healthy 
person,  is  very  favorable.  In  drunkards  a  severe  case  may  be  complicated  by 
delirium  tremens,  and  the  issue  be  unfavorable.  We  saw  one  case  end  fatally 
because  of  gangrene  of  the  eyelids,  followed  by  purulent  inflammation  of  the 
orbital  connective  tissue.  Erysipelas  migrans  may  so  exhaust  the  powers  of 
feeble  patients  as  to  become  dangerous.  The  prognosis  of  surgical  erysipelas 
is  relatively  more  unfavorable,  but  it  cannot  be  considered  here. 

Treatment. — The  treatment  of  ordinary  erysipelas  of  the  head  and  face, 
which  is  the  main  question  here,  is  purely  symptomatic.  The  large  number  of 
remedies  recommended  (tincture  of  iodin,  nitrate  of  silver,  iodoform,  ichthyol, 
carbolic  acid,  collodion,  etc.)  shows  that  they  cannot  any  of  them  materially 
influence  the  morbid  process.  It  is  easy  to  be  deceived  about  their  efficacy, 
as  most  cases  are  relatively  benign.  We  therefore  usually  content  ourselves 
with  powdering  the  affected  skin  or  covering  it  with  oil  or  vaselin  to  relieve 
the  tension,  and  also  with  putting  on  an  ice  bag  if  the  patient  likes  it.  We 
can  expect  no  specific  action  from  internal  remedies  (Pirogoffs  camphor  cure, 
liquor  ferri  sesquicblorati,  etc.). 

Apart  from  alleviating  the  local  discomfort,  some  other  symptoms  occasion- 
ally demand  special  consideration.    Severe  headache  and  other  severe  nervous 


DIPHTHERIA  77 

symptoms  may  be  relieved  by  the  local  use  of  cold  ot  by  antipyrir  and  similar 
remedies.  With  high  temperature  cool  baths  or  antipyretics  internally  may  be 
used  with  benefit,  but  in  general  the  fever  does  no1  ofteD  demand  energetic 
treatment,  since  in  erysipelas,  as  we  have  said,  considerable  spontaneous  remis- 
sions of  temperature  often  occur.  When  there  are  marked  gastro-intestinal 
symptoms  we  may  prescribe  hydrochloric  acid,  opium,  etc. 

Only  when  there  is  a  true  migrating  erysipelas  and  the  disease  spreads  over 
the  body  should  we  try  more  energetic  methods.  Strips  of  adhesive  plaster, 
firmly  applied  at  the  border  line  of  the  lesion,  may  be  tried ;  thereby  the 
lymph  vessels  may  be  compressed,  and  the  spread  of  the  inflammation  thus 
interfered  with.  Hueter  recommended  subcutaneous  injections  of  a  two-per- 
cent solution  of  carbolic  acid  a  little  way  from  the  edge  of  the  erysipelas.  We 
have  seldom  seen  great  benefit  from  any  of  these  methods.  Better  results  are 
promised  from  the  plan  recently  advanced  to  scarify  the  erysipelatous  area,  and 
then  apply  a  sublimate  lotion.  Many  attempts  have  been  made  to  produce  an 
effective  antistreptococcic  serum,  and  sanguine  therapeutists  believe  they  have 
obtained  curative  results  from  the  injection  of  some  such  sera.  I  do  not  wish 
to  advise  against  such  attempts  being  made,  but  proof  of  the  effectiveness  of 
the  serum  treatment  of  this  disease  is  entirely  wanting.  [Johnson,  of  Toronto, 
reports  favorable  results  from  vaccination  with  devitalized  cultures  of  strepto- 
coccus erysipelatis.]  In  the  severe  cases  the  main  point,  after  all,  is  to  main- 
tain the  patient's  strength  by  nursing  and  food.  If  cutaneous  abscesses  form, 
they  should  be  opened  promptly,  when  they  usually  soon  heal. 


CHAPTER    X 

DIPHTHERIA 

(Diphtheritis.     Croup.     Cynanche  contagiosa) 

iEtiology  and  General  Pathology. — Clinically,  "  diphtheria  "  means  a  cer- 
tain well-characterized,  specific,  acute,  infectious  disease,  the  chief  visible 
lesion  of  which  is  a  croupous-diphtheritic  inflammation  of  the  pharynx  and 
upper  air-passages.  In  a  purely  pathological  sense,  however,  the  terms 
"  croupous  "  and  "  diphtheritic  "  have  a  broader  meaning.  They  denote  a  cer- 
tain form  of  inflammation  which  may  occur  in  the  mucous  membrane  of 
almost  any  part  of  the  body.  It  is  frequent  in  the  intestine  and  bladder. 
There  is  great  diversity  in  the  causes  which  may  produce  it. 

The  pathological  characteristic  of  every  croupous-diphtheritic  inflamma- 
tion consists  in  the  formation  of  a  fibrinous  exudation.  This  may  either  be  a 
croupous  membrane,  which  is  grayish  white,  rather  firm  and  elastic,  and  which 
can  be  lifted  off  with  comparative  ease  from  the  mucous  membrane  upon  which 
it  rests,  or  it  may  be  a  diphtheritic  infiltration  with  necrosis  of  the  tissues. 
Here  the  exudation  is  more  or  less  deeply  imbedded  within  the  proper  struc- 
ture of  the  mucous  membrane  itself.  There  is  no  essential  difference  between 
croup  and  diphtheria;  diphtheritic  inflammation  is  the  severer  form  of  the 
disease,  croupous  inflammation  the  milder.     In  diphtheria  the  fibrinous  exu- 


78  '        ACUTE   GENERAL   INFECTIOUS   DISEASES 

dation  is  preceded  by  a  necrosis  of  the  epithelium  and  of  the  underlying  tis- 
sues of  the  mucous  membrane  as  well,  while  in  the  case  of  croupous  exudation 
the  necrosis  is  limited  to  the  epithelium.  The  croupous  membrane  never  rests 
upon  an  intact  mucous  surface,  but  replaces  the  epithelium,  which  has  already 
been  totally  or  in  very  large  part  destroyed.  Flaky  remnants  of  the  epithe- 
lium, no  longer  nucleated,  are  sometimes  found  in  the  meshes  of  the  fibrin. 
The  preceding  destruction  of  the  epithelium  is  essential  to  the  occurrence  of 
fibrinous,  croupous  inflammation.  The  fibrinous  exudation  can  be  formed  in 
those  places  only  where  the  cause  which  excites  the  inflammation  kills  the  epi- 
thelium at  the  same  time.  It  is  still  undecided  whether  or  in  what  degree  the 
epithelium  takes  part  in  the  formation  of  the  croupous  membrane.  Most 
pathologists  hold  that  the  material  for  the  fibrin  comes  from  the  fibrinogen 
of  the  inflammatory  matter  which  transudes  through  the  walls  of  the  vessels, 
and  also  from  the  disintegrated  migratory  white  blood  globules.  These  last 
are  abundant  throughout  the  deposit  itself,  and  still  more  numerous  in  the 
entire  tissue  of  the  mucous  membrane  beneath  the  croupous  or  diphtheritic 
exudation.  If  recovery  takes  place  in  croup,  all  that  is  needed  after  the  exu- 
dation has  been  cast  off  is  the  renewal  of  the  epithelium,  which  can  be  accom- 
plished through  the  exclusive  agency  of  the  remnants  of  epithelium  left  along 
the  borders  of  the  diseased  spot.  In  diphtheria,  however,  the  entire  necrotic 
portion  of  mucous  membrane  must  slough  off,  a  line  of  demarcation  being 
formed,  and  cicatricial  tissue  replaces  the  necrosed  portion. 

The  above  is  a  bare  outline  of  the  present  views  about  croupous  and  diph- 
theritic inflammations.  They  have  been  reached  gradually  through  the  labors 
of  E.  Wagner,  Weigert,  and  others.  We  have  not  yet  touched  upon  the  setio- 
logical  factors;  but  what  precedes  renders  it  evident  how  manifold  they  may 
be,  for  many  causes  which  destroy  the  epithelial  layer  of  the  mucous  mem- 
brane, and  at  the  same  time  promote  inflammation,  may  excite  croup.  We 
have  mechanical  causes,  such  as  impacted  feces,  gallstones,  renal  calculi; 
chemical  irritants,  caustics,  like  ammonia  and  the  acids;  and,  finally,  a  num- 
ber of  specific,  infectious,  disease-producing  poisons.  Among  these  is  the  spe- 
cific poison  of  diphtheria  proper. 

There  has  been  no  doubt  for  a  considerable  period  that  true  pharyngeal 
diphtheria  could  be  produced  only  by  a  specific  organized  cause.  To  demon- 
strate this,  however,  was  extremely  difficult,  for  in  the  diseased  parts  there  are 
a  great  number  of  diverse  microorganisms,  originating  in  the  mouth  and 
throat,  and  really  secondary  to  the  diphtheritic  process,  that  were  very  hard  to 
distinguish  from  the  diphtheria  bacilli.  It  was  only  in  1883  that  Loftier  was 
able  to  demonstrate  that  the  specific  diphtheria  bacillus  is  a  form  of  bacillus 
characterized  by  a  definite  and  particular  granular  formation,  a  club-like 
swelling  at  the  ends,  and  special  methods  of  growth  on  blood  serum.  (Vide 
under  "Diagnosis.")    Loftier' s  observations  were  substantiated  on  all  sides. 

The  diphtheria  bacilli  are  almost  always  found  only  on  the  diseased  por- 
tion of  the  mucous  membrane  or  the  point  of  inoculation,  and  never  in  the 
blood  or  the  internal  organs.  This  fact  is  of  the  greatest  pathological  sig- 
nificance, and  it  has  been  established  not  only  for  diphtheria  in  man,  but  also 
for  experimental  diphtheria  in  animals.  In  pharyngeal  diphtheria  they  are 
found  chiefly  on  the  under  surface  of  fresh  false  membrane.  The  severe  gen- 
eral symptoms  of  diphtheria,  however,  except  when  due  to  secondary  infection 


DIPJITHKRIA  79 

(vide  infra),  depend  upon  the  poisonous  chemical  action  oi  certain  substai 
produced  by  processes  of  metabolism  in  the  bacilli. 

We  may  accept  it  as  ;i  fad  thai  the  diphtheria  bacilli  almost  alwa 
the  pharyngeal  or  nasal  cavity  directly  through  the  inspired  air  or  in  Bome  other 
way,  and  there,  in  ease  they  attach  themselves  to  the  niueous  membrane  and 
increase,  produce  diphtheria.  In  a  few  rare  eases  they  seem  to  be  inhaled  into 
the  larynx  at  once,  and  to  excite  there  a  "primary  laryngeal  croup"  (vide 
infra).  The  source  of  the  infection  is  always  to  be  referred  ultimately  to  an- 
other case  of  diphtheria,  but  the  way  in  which  the  disease  spreads  cannot 
always  be  traced  in  detail.  In  many  cases,  of  course,  a  direct  ("  contagious  ") 
transmission  of  the  poison  is  evident,  as  from  coughing,  or  the  many  cases 
of  the  disease  in  physicians  and  nurses  from  sucking  the  croupous  membrane 
out  of  the  tracheotomy  tube  in  children,  etc.  If  several  children  in  one  house 
fall  sick,  as  often  happens,  we  may  here  suspect  a  direct  transmission  of  the 
disease,  although  it  is  also  possible  that  in  such  an  event  several  cases  may 
arise  from  the  same  source  of  infection.  It  seems  certain  that  the  infection 
can  be  carried  from  one  person  to  another  by  some  intermediary,  by  clothing, 
linen,  toys,  and  other  objects  to  which  diphtheria  poison  clings.  The  diph- 
theria bacilli  show  considerable  resistance  to  external  influences  (temper- 
ature, drying,  and  the  like)  when  they  have  dried  in  rather  thick  masses  and 
are  shielded  from  light.  For  this  reason,  diphtheria  bacilli  on  the  walls  or 
floors  of  damp  and  unwholesome  dwellings  may  retain  their  virulence  for  a 
long  period.  After  apparently  complete  recovery  from  diphtheria,  virulent 
diphtheria  bacilli  may  be  found  in  the  oral  cavity  for  a  considerable  time. 


'.-i  ,?,»  A 


.*'•'" 
'•.**'*« 


.',tV/\<rw  ;'*"v.;/ ;     ' 

Fig.  12. — Diphtheria  bacilli  (Loffler's  methyl-        Fig.    13. — Diphtheria  bacilli  (Xeisser's  polar 
ene  blue).  body  stain). 

This  is  particularly  to  be  noted  .on  account  of  its  practical  importance.  In- 
deed, diphtheria  bacilli  have  been  found  in  healthy  individuals  who  have  been 
in  contact  with  diphtheria  cases  ("bacillus  carriers").  We  must  mention,  in 
conclusion,  that  attention  has  lately  been  called  to  the  possibility  of  the  trans- 
mission of  diphtheria  from  sick  animals  (hens,  doves,  calves,  [cats] )  to  man, 
since  diseases  resembling  diphtheria  undoubtedly  occur  in  the  domestic  ani- 
mals mentioned.  It  is,  however,  very  unlikely  that  the  disease  can  be  thus 
transmitted,  for,  as  Loftier  has  shown,  the  bacilli  in  hens  and  calves  are 
entirely  different  from  the  human  variety. 

Diphtheria,  as  is  well  known,  is  a  disease  chiefly  of  childhood,  but  some 
cases,  and  even  very  severe  ones,  may  occur  in  adults.  In  advanced  life  the 
disease  is  very  rarely  seen.  In  large  cities  sporadic  cases  occur  from  time  to 
time,  but  the  disease  often  takes  on  an  epidejnic  character. 


80  ACUTE   GENERAL  INFECTIOUS   DISEASES 

[While  it  seems  in  the  highest  degree  probable  that  the  poison  is  usually 
purely  local  at  the  start,  cases  occur  which  suggest  that  constitutional  infection 
through  the  pulmonary  blood  vessels  may  precede  the  local  manifestations.. 
Infection  through  the  alimentary  canal  is  not  probable,  though  its  occurrence 
cannot  be  positively  denied. 

There  are  still  points  in  the  aetiology  and  pathology  of  this  affection  which 
are  involved  in  obscurity.  Much  has  been  said  and  written  in  this  country  and 
in  England  about  the  relations  of  filth  and  diphtheria.  That  filthy  surround- 
ings contribute  a  soil  favorable  to  the  development  of  the  poison,  and  at  the 
same  time  diminish  the  resisting  power  of  the  human  organism,  cannot  be 
doubted;  but,  as  long  as  the  parasitic  theory  of  infectious  diseases  prevails, 
sewer  gas  and  the  like  must  be  classed  among  the  predisposing  or  accessory 
causes. 

Some  of  the  frightfully  virulent  epidemics  of  diphtheria  in  sparsely  settled 
country  districts  and  on  the  Western  plains  are  difficult  to  explain  under  the 
theory  that  each  case  is  mediately  or  immediately  the  result  of  a  previous 
case;  these  difficulties  will,  however,  doubtless  be  cleared  away  in  time.] 

Clinical  History. — The  incubation  is  rather  brief,  seldom  exceeding  two  to 
five  days.  The  disease  itself  almost  always  begins  with  general  malaise,  head- 
ache, fever,  and  pain  on  swallowing.  Little  children,  however,  often  do  not 
complain  of  this  last  symptom,  and  in  older  children  the  sore  throat  may  not 
be  very  troublesome  at  first.  It  is  therefore  a  very  important  rule  for  the 
physician  to  examine  the  throat  carefully  in  every  child  who  presents  ill- 
defined  general  symptoms.  If  diphtheria  is  beginning,  we  find  redness  of  the 
soft  palate,  and  more  or  less  swelling  of  the  tonsils.  Upon  the  inner  surface 
of  the  latter,  and  perhaps  upon  the  arch  of  the  palate  and  the  uvula  also,  are 
spots  covered  with  a  grayish-white  coating,  which  is  quite  firmly  adherent  to 
the  mucous  membrane.  They  are  less  frequent  at  first  upon  the  posterior  wall 
of  the  pharynx  and  the  hard  palate.  Their  extent  varies  greatly  in  different 
cases.  In  the  mildest  they  are  chiefly  confined  to  the  tonsils,  attacking  the 
soft  palate  or  the  tonsillar  surface  of  the  uvula  but  little  if  at  all.  In  severer 
attacks  the  spread  of  the  false  membrane  during  the  first  clays  of  illness  is 
rapid.  Almost  invariably  there  is  a  very  early  and  considerable  swelling  of 
the  lymph-glands  at  the  angle  of  the  jaw.  The  constitutional  symptoms  per- 
sist. The  children  are  restless.  There  is  complete  anorexia,  and  frequently 
vomiting.  The  temperature  curve  is  not  typical.  It  is  irregular,  but  is  often 
rather  elevated.  In  true  diphtheria  such  high  temperature,  104°  to  105°  F. 
(40°  to  41°  C),  as  is  common  in  follicular  tonsillitis,  is  certainly  exceptional. 
On  the  other  hand,  fever  may  be  slight  or  almost  absent,  even  in  the  worst 
cases.  The  pulse  is  very  rapid.  The  urine  may  have  a  trace  of  albumen  and 
sometimes  more.     Herpes  labialis  is  occasionally  present. 

In  mild  cases  the  local  and  constitutional  symptoms  remain  moderate ;  and 
at  the  end  of  a  week  or  ten  days  there  is  decided  improvement,  with  rapid 
convalescence.  In  severe  cases,  however,  dangerous  symptoms  appear,  perhaps 
early;  the  croupous  inflammation  involves  neighboring  organs,  or  a  severe 
constitutional  condition  is  developed. 

The  diphtheria  very  frequently  extends  into  the  nose.  This,  though  not  in 
itself  dangerous,  is  usually  a  sign  that  the  case  is  a  severe  one.  The  inflam- 
mation of  the  nasal  mucous  membrane  may  be  simply  mucopurulent,  but  it 


DIPHTHERIA  81 

may  also  be  croupous.  II.  is  betrayed  by  the  abundant  purulenl  discharge. 
Excoriations  and  superficial  ulcers  are  usually  soon  produced  at  the  edge  of 
the  nostrils.    There  may  be  nosebleed. 

A  much  more  dangerous  complication  is  the  extension  of  the  croupous 
inflammation  into  the  larynx.  This  creates  a  mechanical  hindrance  to  respi- 
ration, which  proves  fatal  in  a  great  many  cases,  as  the  child's  larynx  i 
small.  Formerly  "croup"- — i.e.,  croupous  inflammation  of  the  larynx-  wan 
regarded  as  a  different  disease  from  diphtheria.  Many  specialists  in  children's 
diseases  still  maintain  this  view;  but  it  is  in  direct  opposition  to  all  anatomi- 
cal, clinical,  and  aetiological  Facts.  We  grant  that  there  are  cases  where  the 
pharynx  is  slightly  affected,  while  the  croupous  inflammation  of  the  larynx 
is  extreme;  and  once  in  a  great  while  the  diphtheritic  in  feci  ion  results  in 
croupous  laryngitis  and  tracheitis  alone,  the  pharynx  escaping  disease.  Still, 
the  proposition  that  there  are  two  distinct  diseases,  "croup"  and  "diph- 
theria," is  absolutely  untenable.  In  the  overwhelming  majority  of  cases  the 
throat  is  first  affected  and  then  the  larynx.  "We  should  also  consider  how 
easily  slight  lesions  in  the  pharynx  may  be  overlooked,  especially  if  located 
upon  the  posterior  surface  of  the  soft  palate  or  upon  the  epiglottis.  Cases  of 
what  is  called  "  ascending  croup,"  in  which  the  laryngeal  affection  precedes 
the  appearance  of  the  disease  in  the  pharynx,  are,  to  say  the  least,  very  ex- 
ceptional. 

Hoarseness  is  usually  the  first  indication  that  the  diphtheria  has  attacked 
the  larynx.  Then  follows  the  peculiar,  harsh,  ringing,  "  croupy  cough,"  so 
dreaded  by  the  parents,  and,  finally,  there  are  signs  of  beginning  lar}Tigeal 
stenosis.  Eespiration  is  not  much  accelerated,  but  is  labored,  and  the  acces- 
sory muscles  of  respiration  are  called  more  and  more  into  action.  The  child 
becomes  more  restless  and  anxious.  Its  face  grows  pale  and  livid.  Even  in 
children  who  can  make  no  definite  statement  as  to  their  subjective  sensations 
these  symptoms  which  we  have  mentioned  are  very  noticeable.  The  chief 
cause  of  the  dyspnoea  is  undoubtedly  the  mechanical  stenosis  due  to  the  croup- 
ous deposit.  Paralysis  of  the  laryngeal  muscles  may  perhaps  be  a  factor.  If 
portions  of  the  false  membrane  become  partially  detached,  they  may  act  like 
valves,  being  sucked  in  at  each  inspiration,  and  pushed  aside  by  the  current 
of  expired  air.  If  greater  stenosis  occurs,  respiration  becomes  noisy,  resem- 
bling snoring.  Inspiration,  particularly,  is  prolonged  and  "  sawing,"  and  is 
attended  by  marked  depression  of  the  larynx  toward  the  sternum.  An  impor- 
tant diagnostic  point  is  the  drawing  in  during  inspiration  of  the  suprasternal 
region,  the  epigastrium,  and  the  lower  part  of  the  sides  of  the  thorax.  This 
is  the  direct  result  of  the  obstructed  flow  of  air  into  the  lungs.  As  the  lungs 
do  not  expand  enough  to  correspond  to  the  inspiratory  dilatation  of  the  thorax, 
the  parts  mentioned  are  forced  in  by  atmospheric  pressure.  The  degree  of 
dyspnoea  may  vary  at  different  times.  The  false  membrane  may  be  loosened 
and  coughed  up,  rendering  respiration  easier  for  a  time,  till  fresh  exudations 
or  displacements  of  membrane  cause  renewed  distress.  Spontaneous  recovery 
is  still  possible.  The  membrane  is  expectorated  and  no  more  formed.  In 
most  cases  the  symptoms  of  suffocation  increase  more  and  more,  respiration 
grows  quicker  and  more  superficial,  and  the  child  becomes  more  and  more 
stupefied  by  the  excess  of  carbonic  dioxid  in  the  blood.  The  pulse  gets  very 
small,  rapid,  and  irregular.    There  are  mild  convulsions  and  then  death.    The 


82  ACUTE   GENERAL  INFECTIOUS   DISEASES 

autopsy  in  these  cases 'usually  discloses  that  the  croupous  inflammation  has 
extended  into  the  larger  bronchi  or  even  into  the  smaller.  The  lumen  of  the 
bronchioles  may  be  almost  completely  occluded  by  false  membrane.  This 
croupous  bronchitis  gives  rise  to  no  especial  auscultatory  phenomena  during 
life,  so  that  often  we  suspect  it  rather  than  diagnosticate  it.  Its  clinical  sig- 
nificance, however,  is  very  great,  since,  even  in  adults,  it  may  cause  death  by 
suffocation  without  any  especial  stenosis  of  the  larynx.  If  it  is  present,  res- 
piration may  not  be  materially  relieved  in  spite  of  tracheotomy. 

Besides  the  dangers  attendant  upon  the  local  extension  of  the  diphtheritic 
inflammation,  the  general  intoxication  of  the  body  must  be  regarded  as  the 
second  most  important  circumstance  in  our  general  estimate  of  the  disease. 
As  mentioned  above,  the  diphtheria  bacilli  produce  an  extremely  poisonous 
toxin,  which  enters  the  circulation  and  which  may  give  rise  to  the  severest 
symptoms.  Indeed,  special  attention  must  be  called  to  the  fact  that  the  gen- 
eral symptoms  are  not  infrequently  very  slight,  in  spite  of  extensive  local 
croupous  inflammation.  On  the  other  hand,  where  the  local  disease  is  rela- 
tively slight,  severe  general  symptoms  are  sometimes  to  be  observed  which 
may  justly  be  referred  to  diphtheritic  intoxication.  Among  these  severe  gen- 
eral symptoms  are  somnolence,  which  may  increase  to  complete  sopor,  an 
increase  in  the  pulse  to  120  or  140,  progressive  cardiac  weakness,  and  collapse. 
The  conditions  are  different  in  those  cases  which  are  termed  septic  or  malignant 
diphtheria.  Here  the  local  disease  in  the  pharynx  usually  has  a  special  ap- 
pearance :  instead  of  the  croupous  deposits  we  see  a  deeper-seated  necrotic 
destruction  of  mucous  membrane  covered  with  a  foul-smelling,  greasy,  puru- 
lent deposit  ("gangrenous  diphtheria").  In  such  cases  the  lymph-glands  in 
the  neck  are  almost  always  much  swollen.  The  tongue  is  dry  and  fissured, 
and  a  stinking  secretion  runs  from  the  nose.  The  temperature  is  usually  not 
very  high,  but  the  pulse  is  very  rapid  and  small.  In  some  of  these  cases  there 
is  certainly  a  secondary  septic  infection,  probably  in  most  cases  from  strep- 
tococci, as  in  scarlatinal  diphtheria  (vide  supra). 

It  is  to  be  noted,  however,  that  sometimes  diphtheria  bacilli  with  their 
toxins  are  alone  capable  of  producing  such  septic  clinical  pictures.  In  fact, 
Heubner  and  others  deny  that  mixed  infections  play  any  role  whatsoever  in 
cases  of  septic  or  malignant  diphtheria.  They  believe  that  the  diphtheria 
bacilli  are  alone  responsible  for  every  symptom  present.  In  my  opinion,  this 
viewpoint  is  somewhat  defective. 

Regarding  the  manifestations  in  other  organs  in  diphtheria,  we  have  al- 
ready said  that  the  nose,  larynx,  trachea,  and  bronchi  are  often  involved,  but 
the  dense  squamous  epithelium  of  the  oesophagus  and  the  mucous  membrane 
of  the  stomach,  which  is  protected  by  its  secretion,  are  very  rarely  affected. 
I  have,  however,  seen  two  cases  of  cicatricial  oesophageal  stenosis  following 
diphtheria.  Diphtheria  not  infrequently  extends  to  the  Eustachian  tube  and 
middle  ear;  more  rarely  to  the  oral  cavity,  the  lachrymal  canal,  and  the  con- 
junctiva. The  latter  may  also  be  affected  by  the. direct  conveyance  of  the  in- 
fectious matter  by  the  finger,  etc.  In  a  similar  way  diphtheria  may  sometimes 
involve  the  external  genitals  (in  girls)  or  any  accidental  wounds  or  injuries 
of  the  skin,  such  as  blistered  surfaces,  etc. 

Of  the  internal  organs,  the  lungs,  heart,  and  kidneys  demand  chief  atten- 
tion.   In  the  lungs,  besides  croupous  bronchitis,  pneumonia  often  develops  in 


DIPHTHERIA  83 

severe  cases.  This  is  usually  a  lobular  catarrhal  pneumonia,  more  rarely  lobar 
croupous  pneumonia.  Although  we  cannol  absolutely  deny  thai  the  j »u«;n - 
monia  may  sometimes  be  of  a  true  diphtheritic  nature,  the  majority  of  cases 
of  pneumonia  developing  in  diphtheria  musl  certainly  be  classed  as  second- 
ary affections,  due  to  the  inhalation  and  development  of  secondary  agents 
(probably  streptococci),  which  may  readily  take  place.  After  the  original 
diphtheria  has  disappeared  the  secondary  lobular  pneumonia  may  long  prevent 
recovery  or  even  cause  a  fatal  termination  of  the  illness.  The  condition  of  the 
heart  in  diphtheria  is  of  especial  importance,  because  severe  functional  im- 
pairment, probably  of  toxic  origin,  is  common.  Even  when  the  fever  is  slight 
the  pulse  may  sometimes  be  very  rapid,  small,  and  often  irregular.  An  ab- 
normal slowness  of  beat  is  much  rarer.  It  is  especially  to  be  borne  in  mind 
that  even  in  apparently  mild  cases  there  may  be  very  dangerous  cardiac  weak- 
ness. The  latter  depends  in  part  on  degeneration  of  the  heart  muscle  libers, 
in  part  on  microscopic  focal  areas  of  acute  interstitial  myocarditis.  The  clini- 
cal symptoms  of  this  acute  infectious  myocarditis  (Romberg)  are  arrhythmia, 
inequality,  acceleration  (more  rarely  retardation),  and  weakness  of  the  pulse. 
There  is  often  cardiac  dilatation,  and  as  an  indication  of  beginning  disturbance 
of  circulation,  hepatic  enlargement  and  a  diminished  amount  of  urine.  Some- 
times death  occurs  suddenly  and  unexpectedly  from  cardiac  paralysis.  In 
other  cases  the  manifestations  of  cardiac  weakness  last  several  days  or  even 
weeks,  either  to  end  fatally  or  to  clear  up  slowly.  The  blood  often  shows  a 
distinct  leucocytosis. 

Since  nephritis  is  especially  common  in  septic  diphtheria,  it  is  hard  to 
decide  whether  it  is  due  to  the  primary  disease  or  is  to  be  considered  a  sec- 
ondary complication.  Its  clinical  significance  is  not  very  great,  since  it  neither 
materially  modifies  the  general  picture  nor  has  any  definite  bearing  on  the 
result  of  the'  disease.  (Edema,  uraemia,  etc.,  are  only  rarely  seen  in  diph- 
theritic nephritis.  The  macroscopic  changes  in  the  kidney  are  usually  very 
slight.  Microscopically  we  find  the  various  degenerative  conditions  of  acute 
nephritis. 

The  Nervous  Sequelae  of  Diphtheria. — The  convalescent  from  diphtheria  is 
liable  to  be  attacked  by  certain  nervous  sequelae.  Of  these,  diphtheritic  pa- 
ralysis is  the  most  important.  It  appears  about  one  or  two  weeks  after  the 
throat  trouble  ceases,  or  perhaps  earlier,  and  it  is  quite  as  likely  to  follow 
mild  cases  as  severe  ones.  It  attacks  the  soft  palate  by  preference.  The  voice 
becomes  nasal  and  deglutition  difficult.  The  nasopharynx  is  imperfectly  cut 
off  during  the  act  of  swallowing,  and  with  each  attempt  liquid  regurgitates 
through  the  nose.  Usually  the  pharyngeal  mucous  membrane  is  hypoaesthetic 
at  the  same  time,  and  deprived  of  its  reflex  excitability.  There  may  also  be 
paralysis  of  the  vocal  cords  upon  one  or  both  sides,  and  this  again  is  frequently 
combined  with  anaesthesia  of  the  mucous  membrane  of  the  throat.  There 
may  be  paralysis  of  the  ocular  muscles,  of  which  those  controlling  accommo- 
dation are  most  apt  to  be  affected,  rendering  the  vision  for  near  objects  im- 
perfect. Paralysis  of  the  muscles  of  the  trunk  and  extremities  is  least  fre- 
quent, but  it  may  be  very  extensive.  Sometimes  several  of  these  parts  are 
paralyzed  simultaneously.  Thus  we  see  quite  often  paralysis  of  the  soft  palate 
and  of  the  muscles  of  accommodation  combined.  In  some  cases  there  is  well- 
marked  ataxia  of  the  lower  limbs  with  or  without  paresis.     This  renders  the 


84  ACUTE   GENERAL   INFECTIOUS   DISEASES 

gait  very  uncertain  and  tottering,  the  tendon  reflex  is  almost  always  abolished, 
while  sensation  is  affected  slightly  if  at  all.  Very  rarely  diphtheria  is  fol- 
lowed by  contracture  of  the  hands  or  other  parts,  by  difficulty  in  articulation 
and  paresis  of  the  bladder.  A  paralysis  of  the  pharynx  is  sometimes  left  be- 
hind, so  that  the  children  have  to  be  fed  for  weeks  through  an  oesophageal 
tube.  It  is  a  remarkable  fact  that  not  only  in  almost  every  case  of  the  nervous 
disorders  which  we  have  mentioned,  but  often  also  in  individuals  who  have 
entirely  escaped  them,  there  may  be  no  patellar  reflex  after  diphtheria  for 
weeks  or  even  months.  With  regard  to  the  pathological  state,  it  is  probably 
a  degenerative  condition  of  the  corresponding  peripheral  nerves,  not  only  in 
the  post-diphtheritic  paralysis,  but  also  in  the  cases  of  post-diphtheritic  ataxia 
(see  the  chapter  on  primary  multiple  neuritis  in  Vol.  II).  These  degenera- 
tions are  probably  due  to  the  poisonous  chemical  action  of  the  diphtheria 
toxins.  It  is  of  great  interest  to  note  that  paralysis  has  also  been  produced 
experimentally  in  animals  by  the  action  of  diphtheritic  toxin  by  Koux  and 
Yersin  and  others.  The  prognosis  of  all  the  nervous  sequelae  of  diphtheria- is 
very  favorable,  and  even  in  severe  cases  complete  recovery  usually  takes  place 
in  the  course  of  a  few  weeks  or  months.  This  is  in  harmony  with  the  periph- 
eral nature  of  the  disease.  Only  the  rarer  paralyses  of  the  respiratory  muscles 
(diaphragm)  and  of  the  heart  (vide  supra)  are  really  very  dangerous. 

Diagnosis. — Errors  in  the  diagnosis  of  diphtheria  may  be  made  in  two 
ways.  In  the  first  place,  a  simple  lacunar  and  necrotic  angina  may  not  infre- 
quently be  pronounced  a  diphtheria,  and  the  parents  and  relatives  of  the 
patient  thereby  unnecessarily  frightened.  The  second  error  arises  through  a 
failure  to  properly  recognize  milder  grades  of  the  disease,  and,  in  conse- 
quence, necessary  precautionary  measures  are  not  taken.  In  very  many  cases 
the  trained  physician  can  differentiate  between  diphtheria  and  follicular  ton- 
sillitis by  a  purely  clinical  examination,  above  all  by  an  examination  of  the 
throat.  A  positive  differentiation  cannot,  however,  be  made  in  all  cases.  The 
diagnosis  of  diphtheria  is  almost  certain  if  there  is  a  true  membrano-croupous 
exudate  or  patch  that  extends  beyond  the  tonsils  to  the  soft  palate  or  the 
uvula.  Follicular  tonsillitis,  on  the  other  hand,  is  readily  recognized  where 
punctate  follicular  plugs  are  present.  The  innumerable  bacteriological  exami- 
nations of  the  past  few  years  have  alone  made  it  possible  definitely  to  establish 
the  fact  that  true  diphtheria  sometimes  manifests  itself  as  a  mild  suppurative 
catarrhal  or  follicular  inflammation.  In  such  cases  the  diagnosis  can  only  be 
made  by  the  demonstration  of  the  bacilli.  If  such  examination  be  impossible, 
one  should  be  on  his  guard,  particularly  if  the  patients  are  children. 

The  bacteriological  diagnosis  of  diphtheria  should  at  first  be  attempted 
with  a  smear  stained  with  Loffler's  alkaline  methylene  blue.  The  younger 
diphtheria  bacilli  (vide  Figs.  12  and  13)  present  the  characteristic  club-  or 
wedge-shaped  thickenings  at  their  ends.  They  are  in  addition  often  slightly 
bent,  diverge  from  one  another  and  lie  irregularly  crossed,  and  frequently 
they  are  grouped  in  small  clumps  or  "  nests."  The  older  bacilli  are  somewhat 
longer,  their  ends  are  more  thickened,  and  they  often  show  a  segmental  de- 
generation. The  diphtheria  bacillus  is  nonmotile,  and  reveals  no  spore  for- 
mation. The  growth  of  the  bacilli  on  Loffler's  blood  serum  is  a  further  means 
of  differentiation.  The  growth  consists  of  small,  wax-white  colonies  that 
present  a  characteristic  appearance  under  the  low  power  of  the  microscope.    A 


DIPHTHERIA  85 

definite    differentiation    between    true    diphtheria    bacilli    and   the    so-called 
pseudo-diphtheria  bacilli  is  obtained  by  staining  the  bacilli  from  a  fresh  cul- 
ture according  to  M.  Neisser's  method  (double  stain  with  methylene  blue  and 
Bismarck  brown).     With  this  the   bacilli  are 
colored  brown  and  the  granules  at  their  ends 
blue  (vide  Fig.  13). 

[When  the  membranes  are  confined  to 
the  nose,  the  diagnosis  may  be  more  or  less 
difficult;  but  it  is  especially  in  cases  in  which 
the  nasal  mucous  membrane  is  involved  that 
we  encounter  great  swelling  of  the  glands  at 

the  angles  of  the  jaw.     There  is  also  apt  to  be      _       ,     _.  ,  ,     .  ,     ....    „ 

, ,  .  °  •  i      ,  i       i  i      .      -i  •  Fig-  I4- — Diphtheria  bacilli.   Smear 

a    thm,    acrid,    bloody,    or   sero-purulent    dis-  from  the  tonsil. 

charge. 

Jacobi  states  that  while  diffuse  pharyngeal  injection  may  or  may  not  point 
to  imminent  diphtheria,  marked  local  congestion  is  either  traumatic  or  diph- 
theritic. An  examination  of  the  urine  should  never  be  neglected  in  doubtful 
cases;  in  diphtheria  a  trace  of  albumen  is  very  common ;  in  simple  or  follicular 
sore  throat  albumen  is  very  rare,  if  indeed  it  occurs  at  all.] 

Prognosis. — The  dubious  prognosis  of  true  diphtheria  is  universally  known, 
even  by  the  laity.  The  very  fact  that  the  best-developed  and  healthiest  chil- 
dren so  often  fall  victims  to  it  associates  the  name  diphtheria  with  the  saddest 
memories.  There  are  indeed  many  mild  cases  which  recover  in  a  week  or  two, 
and  severer  ones  which  end  happily  in  three  or  four  weeks ;  but  in  most  cases, 
where  the  process  extends  into  the  larynx,  or  the  s)rmptoms  of  a  severe  con- 
stitutional infection  occur,  the  prognosis  must  be  regarded  as  very  serious. 
Becently,  however,  since,,  the  introduction  of  the  serum  treatment,  the  prog- 
nosis even  of  severe  diphtheria  has  become  considerably  more  favorable.  For- 
merly, before  the  serum  treatment,  it  was  regarded  as  a  relatively  favorable 
result  if  one  half  of  the  children  with  diphtheria  in  the  hospitals,  on  whom 
tracheotomy  was  done,  recovered !  Often  sixty  or  seventy  per  cent  of  the  chil- 
dren operated  on  died.  At  present,  however,  the  mortality  of  the  tracheotomy 
cases,  treated  at  the  same  time  with  serum,  has  fallen  to  about  twenty-five 
per  cent,  and  these  are  only  the  severe  cases  in  which  the  serum  treatment 
was  begun  late.  The  improved  prognosis  under  the  serum  treatment  is  much 
more  favorable  if  we  compare  the  whole  number  of  cases  and  the  death-rate 
of  diphtheria  before  and  after  the  introduction  of  this  treatment  (Heubner, 
Widerhofer,  Baginsky,  etc.). 

In  general,  diphtheria  is  to  he  regarded  as  the  more  serious  the  younger  the 
child  is.  In  later  childhood,  after  the  eighth  or  tenth  year,  the  number  of  dan- 
gerous cases  is  much  less.  The  description  of  the  symptoms  shows  sufficiently 
what  the  dangers  of  the  disease  are,  and  how  they  are  to  be  recognized.  We 
would  state  once  more  that,  even  in  apparently  mild  cases,  the  danger  of  sud- 
den paralysis  of  the  heart,  though  fortunately  rare,  always  demands  the  great- 
est caution. 

Treatment. — Up  to  a  [comparatively]  short  time  ago  it  was  impossible  to 
say  anything  in  regard  to  any  generally  recognized  treatment  of  diphtheria 
which  was  really  effective;  but  in  1893  a  method  of  treatment  was  discov- 
ered, chiefly  by  the  important  and  interesting  investigations  of  Behring  and 


86  ACUTE   GENERAL   INFECTIOUS   DISEASES 

Eoux,  which  deserves  to  be  called  an  actual  specific.  Further  observations 
have  established  this  treatment  as  one  of  the  most  brilliant  and  triumphant 
medical  acquisitions. 

Behring  found,  in  continuing  the  important  discoveries  of  Pasteur,  Buch- 
ner,  and  others,  that  certain  protective  matter  ("antitoxin")  was  formed  in 
the  blood  serum  of  those  animals  (sheep,  goats,  horses,  etc.)  which  had  been 
infected  with  artificially  weakened  cultures  of  diphtheria  bacilli.  If  the  ani- 
mal survive  the  milder  infection,  it  is  less  sensitive  to  a  severer  infection,  and, 
finally,  by  continued  inoculation,  it  may  even  become  immune  to  the  severest 
infection.  The  blood  serum  of  such  immune  animals  (horses  are  now  almost  in- 
variably employed  at  the  serum  establishments)  can  now  be  used  in  the  treat- 
ment of  diphtheria  in  man.  In  order  to  have  a  definite  measurement  for  the 
toxins  and  antitoxins,  the  term  toxin  unit  is  employed  to  indicate  the  smallest 
amount  of  poison  which,  in  four  days,  will  kill  a  guinea  pig  weighing  250 
grams;  while  the  term  antitoxin  unit,  or  the  unit  of  immunity  ("  Immu- 
nitatseinheit,"  "I.  E."),  represents  the  amount  of  serum  which  will  prevent 
the  action  of  100  toxin  units.  Certain  theoretical  objections  have,  however, 
been  raised  against  this  method  of  measurement,  but  it  is  still  in  practical  use. 
A  "  simple  serum  "  is  one  in  each  cubic  centimeter  of  which  there  is  the  equiva- 
lent of  one  antitoxin  unit.  Thus,  for  example,  in  a  bottle  of  "  Hochst  Se- 
rum "  containing  5  c.c.  of  a  "  two  hundredfold  serum,"  there  is  contained  the 
equivalent  of  1,000  antitoxin  units. 

The  treatment  is  simple,  and  consists  in  injecting  the  serum  under  the 
skin  of  the  child  who  has  diphtheria  by  means  of  a  carefully  disinfected 
syringe.  The  best  places  for  injection  are  the  anterior  chest  wall  or  the  thigh. 
Since  the  amount  of  serum  to  be  injected  is  usually  about  5  c.c,  we  should 
use  a  special  syringe  which  is  not  too  small.  The  best  are  made  like  a. 
Pravaz  syringe  with  an  asbestos  packing.  It  is  to  be  understood  that  the 
injections  must  be  made  with  the  strictest  aseptic  precautions.  The  syringe 
and  needle  are  sterilized  by  boiling,  and  the  site  of  the  injection  is  care- 
fully cleansed  with  alcohol  and  ether.  There  are  different  preparations 
of  serum  of  equal  reliability  on  the  market.  We  ourselves  have  almost 
exclusively  employed  that  made  by  the  Hochst  Anilin  Dye  Works.  It  is 
put  up  in  three  strengths :  the  curative  dose  of  No.  I  equals  600  antitoxin 
units,  that  of  No.  II  1,000,  and  of  No.  Ill  1,500  units.  In  addition,  a  "  con- 
centrated serum,"  of  dosage  up  to  3,000  units,  has  recently  been  manufactured. 

In  early  and  milder  cases  we  inject  Serum  I  ("  600  units  of  antitoxin  "), 
in  severer  and  more  advanced  cases,  especially  if  there  be  any  signs  of  disease 
in  the  larynx,  we  use  at  once  Serum  II  ("1,000  units  of  antitoxin"),  or, 
even  better,  Serum  III.  According  to  the  severity  of  the  case,  or  according 
to  its  course,  we  repeat  the  same  injection  or  a  weaker  dose  of  the  same  once 
in  the  next  twelve  to  twenty-four  hours.  In  many  cases  of  moderate  severity 
a  single  injection  of  Serum  II  suffices.  In  adults,  one  usually  begins  at  once 
with  Serum  III,  or,  if  the  case  is  severe,  the  "  concentrated  serum,"  in  doses 
of  2,000  to  3,000  units,  may  be  given. 

[These  doses  of  antitoxin  are  smaller  than  is  the  custom  in  America:  for 
a  child  of  one  year,  an  initial  dose  of  2,000  or  3,000  units,  and  in  laryngeal 
cases  3,000  to  5,000  units;  for  an  adult  4,000  to  6,000  units.  If  treatment 
has  been  delayed,  or  if  the  case  is  severe,  larger  doses  are  required.     J.  H. 


DIPHTHERIA  87 

RIdCollom  has  emphasized  the  efficacy  and  the  harmlessnesfi  of  large  dosea  and 
the  need  of  repeating  them  until  Local  and  general  improvement  is  evident. 
The  danger  lies  no!   in  using  too  much  bul   in  using  too  little.] 

The  favorable  action  of  the  serum  is  shown  chiefly  by  the  fad   thai   the 
affection  does  nof  extend  after  the  injection.     The  existing  croupous  depi 
is  thrown,  oil'  in  (lie  course  o!'  ilic  next  lour  or  five  da 

The  serum  injections  have  no  injurious  action.  Urticaria  sometimes  occurs 
after  an  injection,  but  it  lias  no  serious  significance.  Taking  everything  into 
consideration,  it  is  therefore  the  duty  of  the  physician,  in  accordance  with  our 
present  knowledge,  to  use  the  Berum  in  every  case  of  true  diphtheria  in  chil- 
dren. In  suspicions  cases,  too,  it  is  wiser  to  give  an  injection  al  once,  without 
waiting  for  the  substantiation  of  the  bacteriological  examination.  It  is  un- 
questionable that  deaths  from  diphtheria  occur  even  with  serum  treatment. 
These  are  either  cases  in  which  treatment  has  been  begun  too  late,  or  cases 
in  which  there  is  a  septic  mixed  infection.  The  fact  cannot  be  denied  that 
the  results  in  some  severe  epidemics  were  not  as  good  as  were  obtained  at 
other  times.  Nevertheless,  the  vast  majority  of  observations  to  the  present 
time  speak  emphatically  in  favor  of  the  Behring  method.  If  we  survey 
the  discoveries  made  in  the  field  of  serum  studies  as  well  as  in  its  related 
branches,  we  may  truly  hope  that  Ave  physicians  are  standing  on  the  threshold 
of  an  entirely  new  era  in  the  treatment  of  infectious  diseases. 

It  is  of  the  greatest  practical  importance  that  the  serum  treatment  be  be- 
gun as  early  as  possible.  The  most  favorable  results  are  seen  in  children 
treated  on  the  very  first  days  of  the  disease.  In  these  cases  the  development 
of  post-diphtheritic  paralysis  appears  to  be  much  less  commonly  seen.  Local 
treatment  of  the  affected  places  in  the  pharynx  at  the  same  time  is  unnecessary. 
We  would,  however,  emphasize  the  importance  of  a  general  cleansing  and  dis- 
infection of  the  whole  oral  cavity  by  gargling  and  rinsing  with  dilute  solu- 
tions of  potassium  chlorate,  hydrogen  peroxid,  boric  acid,  and  the  like.  Ice 
bags  or  hot  or  Priessnitz  compresses  may  be  applied  externally.  Internal 
medication  (potassium  chlorate,  potassium  iodid,  etc.)  is  entirely  unneces- 
sary. It  is  also  very  important  -to  watch  the  child's  nutrition  carefully  in 
order  to  keep  up  the  strength.  Milk,  eggs,  meat  juice,  small  quantities  of 
wine,  etc.,  are  most  advisable. 

If  the  larynx  is  attacked,  and  if,  in  spite  of  the  serum  treatment,  the  con- 
sequent laryngeal  stenosis  threatens  to  cause  suffocation,  tracheotomy  is  our 
only  resort.  It  is  never  indicated  by  the  disease  itself  nor  by  the  severity  of 
the  case,  but  only  by  persistent  obstruction  of  the  larjmx.  It  is  therefore  not 
invariably  easy  to  decide  whether  tracheotomy  is  called  for  in  any  particular 
case.  If  the  general  condition  be  bad  and  respiration  already  impaired,  it  is 
often  very  difficult  to  determine  whether  laryngeal  stenosis  exists.  Trache- 
otomy will  be  of  no  avail  if  the  croup  has  already  extended  to  the  bronchi,  or 
if  the  dangerous  condition  of  the  patient  is  due  to  the  severity  of  the  consti- 
tutional infection  or  to  incipient  paralysis  of  the  heart.  We  have  already 
said  that,  since  the  introduction  of  the  serum  treatment,  the  prognosis  of 
diphtheria  has  become  better  even  in  the  tracheotomy  cases.  How  tracheotomy 
is  performed,  and  in  what  the  after-treatment  consists,  must  be  learned  in 
the  text-books  on  surgery,  where  we  will  also  find  a  description  of  the  so-called 
intubation  of  the  larynx. 
7 


88  ACUTE   GENERAL  INFECTIOUS   DISEASES 

If  severe  pulmonary  symptoms  occur  in  diphtheria,  we  should  use  first  of 
all  cool  or  hot  packs  of  the  whole  body  or  tepid  baths  with  cool  effusions. 
Such  cutaneous  stimulation  refreshes  and  enlivens  the  whole  nervous  system, 
and  we  should  therefore  try  it  also  in  the  severe  cases  with  secondary  septic 
infection.  In  septic  diphtheria  we  must  also  pay  especial  attention  to  the 
condition  of  the  heart.  So  far  as  is  possible  we  should  try  to  avert  the  threat- 
ening cardiac  paralysis  by  stimulants,  such  as  wine,  camphor,  and  stro- 
phanthus. 

The  greatest  precautions  must  be  taken  in  all  cases  of  diphtheria  in  which 
even  the  slightest  signs  of  cardiac  weakness  and  arrhythmia  appear.  The  chil- 
dren must  be  kept  perfectly  quiet  in  bed  as  long  as  possible,  and  must  be  most 
carefully  nourished  and  looked  after. 

The  nervous  sequela?  of  diphtheria  are  best  treated  with  the  constant  cur- 
rent. As  an  internal  remedy,  iron  is  good,  and  also  nux  vomica  or  strychnin. 
The  last  may  be  given  subcutaneously,  if  desired,  in  doses  of  -fo  to  -gV  gr.  (gm. 
0.001  to  0.002). 

The  prophylaxis  of  diphtheria  demands  that  every  child  with  diphtheria 
be  absolutely  isolated  from  healthy  children.  The  isolation  is  not  to  be  termi- 
nated too  early,  since  virulent  bacilli  may  remain  in  the  mouth  and  throat 
even  weeks  after  recovery.  The  sick-room,  as  well  as  everything  that  has 
come  in  contact  with  the  patient  (bedding,  toys,  etc.),  must  be  carefully  dis- 
infected. According  to  Behring,  a  healthy  child  may  be  positively  protected 
from  infection  by  diphtheria  for  two  or  three  weeks  by  the  injection  of  a 
small  dose  of  serum — the  whole  or  one  half  of  Dose  I — that  is,  about  three 
hundred  units  of  antitoxin.  It  is,  of  course,  very  hard  to  pass  final  judgment 
on  this,  and  for  the  present,  therefore,  it  must  be  left  to  the  discretion  of 
the  physician  in  what  cases  he  will  try  prophylactic  injections  of  serum. 

[Diphtheria  is  a  disease  which  involves  commonly  much  exhaustion,  and 
too  much  stress  can  hardly  be  laid  on  the  importance  of  administering  the 
maximum  amount  of  nourishment  in  the  most  assimilable  and  easily  swallowed 
forms  from  the  start. 

It  is  also  important  to  give  stimulants  early  in  most  cases,  not  waiting  for 
signs  of  exhaustion.  Enormous  quantities  of  brandy  can  often  be  given  to 
small  children  without  the  slightest  toxic  effect.  No  general  rule  can  be  laid 
down;  the  requirements  of  each  case  must  be  studied  and  met. 

When  painful  deglutition  interferes  with  nutrition,  peptonized  milk,  eggs, 
brandy,  and  the  like,  must  be  given  by  the  rectum.  Eectal  alimentation  and 
stimulation  and  feeding  with  the  oesophageal  tube  are  also  to  be  resorted  to  in 
cases  of  post-diphtheritic  paralysis  of  the  oesophagus.] 


CHAPTEE    XI 

INFLUENZA 

(La  Grippe) 

Influenza  is  a  specific,  acute,  infectious  disease  which  is  especially  distin- 
guished by  the  occasional  enormous  extent  of  its  epidemics.    While  often  years 


INFLUENZA  89 

and  decades  pass  without  any  especial  attention  being  called  to- the  disease, 
suddenly  cases  of  it  will  appear  with  such  frequency  that  the  largest  part  of 
the  population  is  attacked,  and  the  disease  may  better  be  described  as  pan- 
demic than  epidemic.  Pandemics  of  influenza  can  be  traced  back  with  certainty 
into  the  sixteenth  century.  In  the  present  century  the  influenza  during  the 
years  1830-33  traversed  almost  all  of  Asia  and  of  Europe,  then  later  i 
appeared  numerous  smaller  epidemics,  but  these  aroused  general  attention  so 
little  that  the  disease,  upon  its  last  pandemic  appearance  in  the  winter  of 
1889-90,  was  almost  unknown  to  many  physicians.  Since  that  time  the  dis- 
ease seems  never  to  have  wholly  disappeared,  as  a  few  cases,  and  occasionally 
small  groups  of  cases,  are  constantly  seen. 

iEtiology. — The  organized  agent  of  influenza  is,   in   all   probability,   the 
"  inliuenza  bacillus  "  discovered  by  R.  Pfeiffer.    It  is  invariably  found  in  the 
bronchial  secretion  of  patients  with  the  "catarrhal  form"  of  influenza   (vide 
infra),  a  definite  form  of  very  small  bacilli  with  rounded  ends  which  stain 
darker  than  the  central  portion.     These  bacilli  either  are  free  in  the  mucus 
or    (especially   in   the   later   stages)    are 
found  in  the  pus  cells.     They  grow  best 
on  jslates   of   agar   smeared   with   blood. 
The    influenza    bacilli    very   soon    die    if 
dried,  and  also  if  put  in  water. 

In    all    probability    the    infection    is 

usually  due  to  inhaling  the  germs.     The 

bacilli  seem  to  appear  at  certain  times 

over  an  immense  territory,  so  that  they 

are  scattered  everywhere  through  a  large    „      ,r     T  a  .     .....    it_  . 

-.,  i  .  Fig.  15. — Influenza  bacilli  in  the  sputum  of 

extent   oi    country.      Many    observations  a  case  of  broncho-pneumonia. 

upon  the   appearance   of   the   disease   in 

isolated  institutions  (convents,  and  the  like)  render  it  very  probable  that  the 

poison  may  also  be  carried  by  a  person  suffering  from  the  influenza  to  another 

in  regions  previously  unaffected.     Nevertheless,   this  contagious  manner  of 

spreading  plays  no  great  role  in  comparison  with  the  indirect  spread  of  the 

disease,  this  latter  mode  being  everywhere  possible  during  an  epidemic   of 

influenza  by  inhalation  of  the  bacteria. 

There  is  scarcely  any  reason  for  speaking  of  especial  predisposing  causes  of 
influenza,  inasmuch  as  at  the  time  of  a  well-marked  ejndemic  the  overwhelm- 
ing majority  of  the  population  are  attacked,  both  the  healthy  and  the  diseased, 
the  vigorous  and  the  feeble.  Sex  certainly  makes  no  difference,  and  age  only 
to  this  extent,  that  the  disease  is  seen  more  rarely  in  little  children  under  one 
year  of  age  than  in  older  children  and  adults.  That  catching  cold  has  no 
special  getiological  significance  is  evident  from  the  fact  that  influenza  often 
appears  in  patients  who  are  already  sick  in  bed. 

It  should  finally  be  mentioned  that  animals  also,  and,  in  particular,  horses, 
may  be  attacked  by  the  influenza;  but,  nevertheless,  it  is  as  yet  a  doubtful 
question  whether  all  the  diseases  in  animals  which  are  described  under  this 
name  are  actually  identical  with  genuine  influenza. 

Symptoms  and  Clinical  History. — The  best  general  idea  of  the  extremely 
manifold  symptoms  of  the  disease  will  be  obtained  if  we  bear  in  mind  that  the 
influenza  causes  both  a  marked  infectious    (or  toxic)   general  constitutional 


90  ACUTE   GENERAL   INFECTIOUS   DISEASES 

disturbance  of  the  body,  and  also  certain  local  lesions  with  local  symptoms. 
The  clinical  picture  therefore  varies  greatly  according  to  the  predominance  of 
one  or  the  other  group  of  symptoms,  and  also  according  to  the  special  form 
of  the  local  disease. 

The  onset  of  influenza  is  generally  rather  sudden.  As  a  rule,  the  marked 
cases  begin  with  rather  high  fever,  ushered  in  with  a  chill,  violent  headache, 
marked  constitutional  depression,  and  usually  considerable  pain  in  the  back 
and  loins.  The  weakness  of  the  patient  may  be  so  great  that,  even  if  a  vigor- 
ous individual,  he  will  at  once  take  to  his  bed.  Severe  nervous  symptoms,  such 
as  stupor  and  delirium,  are  exceptional.  Sometimes,  but  not  very  often,  there 
is  initial  vomiting.  The  backache  is  often  associated  with  pains  in  the  muscles 
and  joints.  Oppressive  pain  in  the  eyes  also  is  quite  characteristic.  This  is 
particularly  felt  upon  moving  the  eyeballs,  and  therefore  is  probably  located 
in  the  external  muscles.  The  spleen  is  occasionally  somewhat  swollen,  but  any 
great  increase  in  its  size  is  exceptional. 

If  the  clinical  symptoms  as  the  case  progresses  are  mainly  limited  to  the 
above-named  constitutional  symptoms — fever,  languor,  headache,  pain  in  the 
muscles — we  may  speak  of  a  "  typhoidal  form  "  of  the  disease.  Usually,  how- 
ever, certain  local  symptoms  put  in  an  early  appearance,  and  it  is  especially 
the  respiratory  apparatus  which  is  attacked.  The  precise  sjanptoms  vary  con- 
siderably in  different  cases.  Sometimes  the  upper  portion  of  the  respiratory 
tract,  the  nose,  larynx,  and  trachea  are  involved;  sometimes,  from  the  start, 
the  smaller  bronchi.  In  the  first  instance  there  is  marked  coryza,  not  infre- 
quently accompanied  by  conjunctivitis;  in  the  other  case  there  is  cough,  due 
to  a  dry  bronchitis,  which  can  be  easily  detected  upon  auscultation,  and  which 
involves  especially  the  lower  portion  of  the  lungs.  If  these  local  symptoms 
outweigh  the  constitutional,  the  case  is  described  as  belonging  to  the  "  catarrhal 
form  "  of  influenza. 

Sometimes  the  influenza  is  localized  in  the  digestive  apparatus.  This  "  gas- 
trointestinal form  "  is  much  rarer  than  the  catarrhal.  In  this  case,  in  addi- 
tion to  the  more  or  less  strongly  characterized  constitutional  symptoms,  there 
is  marked  disturbance  of  the  stomach  and  intestines,  as  shown  particularly  by 
nausea  with  persistent  vomiting,  diarrhea,  abdominal  pain,  etc.  In  one  case 
we  observed  jaundice.  The  frequent  reddening  of  the  anterior  gums  and  the 
swelling  of  the  papillas  at  the  tip  of  the  tongue  (Franke)  should  also  be 
noticed. 

The  pains  in  the  back,  loins,  and  extremities  already  mentioned  may  per- 
sist with  unusual  violence,  and  this  peculiar  form  of  the  disease  is  known  as 
the  "  rheumatoid."  The  muscles  and  the  muscular  attachments  are  probably 
the  chief  seat  of  these  pains,  which  may  be  so  violent  that  the  patient  is 
unable  to  lie  comfortably,  and  sometimes  keeps  up  a  continual  moaning.  The 
loins,  in  particular,  may  be  the  seat  of  most  acute  pain,  also  the  upper  arms, 
the  knees,  the  thighs,  and  the  eyes.  Objective  changes  in  the  painful  pajts, 
such  as  swelling  of  the  joints,  are  scarcely  ever  seen,  nor  are  the  nerve-trunks, 
as  a  rule,  especially  sensitive  to  pressure.  The  painful  muscles  are  usually 
weaker  than  normal. 

The  grouping  of  the  clinical  varieties  of  influenza  under  the  four  forms 
already  named  affords  a  general  idea  of  the  manifold  symptoms  of  the  disease, 
but  this  division  into  separate  forms  must  not  be  carried  out  too  strenuously, 


INFLUENZA 


91 


40! 


39.5° 


8S5!      SWZ 

■III  1IJIHB 


III 

iiiii 


38.0° 


37.5° 


36.5° 


36.0° 


m\nammtsmm 

fHMWiH   HID 

!■!■■■       Ill 

imkwmi       iBHiikii     mi 
Mwmvim        mmftkMM'Mimi 

NMBL1I  aifiBWAilililMI 

-'MWm  HIBinHlMItU 

■I  11'iBlliaMBMII 


for  in  reality  many  cases  of  the  disease  occur  which  presenl  transition  forms 
and  combinations  of  the  various  groups  of  symptoms.  Moreover,  in  all  the 
forms  a  distinction  must  be  made  between  mild  and  severe  attacks,  for  in 
influenza,  just  as  in  most  other  infectious  diseases,  there  are  many  rudimenl 
and  mild  cases  as  well  as  the  fully  developed  one-,  and  some  could  not  be 
properly  interpreted  but  for  the  presence  of  the  epidemic. 

The  duration  of  the  disease  is  best  determined  by  the  duration  of  the 
fever.  In  the  very  mildest  cases  there  may  he  no  fever  whatever,  or  -im- 
ply a  slight  evening  rise 
of  temperature.  As  a 
rule,  there  is  a  mode  rale 
fever,  between  101.5°  and 
103°  F.  (38.5°  and  3!). 5° 
C),  although  higher  tem- 
peratures even  to  104°  F. 
(40°  C.)  and  more  are  not  39.0 
infrequent.  In  the  begin- 
ning  of  every  severe  attack 
the  fever  rises  abruptly. 
After  a  duration  of  several 
days  (four  to  seven)  it 
may  fall  again  in  a  man- 
ner approaching  a  crisis. 
More  frequently,  espe- 
cialty  when  there  exists 
diffuse,  catarrhal  trouble 
in  the  lungs,  the  fever 
ends  by  lysis.  With  com- 
parative frequency  there 
are  found  to  be  noticeable  deviations  in  the  temperature  curve  (see  Fig. 
16)  ;  thus,  for  example,  the  high  fever  of  the  onset  sinks  on  the  second 
or  third  day,  to  be  followed  by  an  almost  afebrile  period  of  one  or  two 
days,  whereupon  a  marked  rise  of  temperature  ensues.  With  this  change 
in  the  temperature  there  are  usually  also  corresponding  variations  in  other 
symptoms. 

The  heart,  in  influenza,  is  frequently  involved  to  a  marked  degree.  The 
pulse  is  usually  proportionately  rapid.  In  individuals  whose  heart  muscle  has 
previously  been  weakened,  and  especially  in  the  aged,  great  cardiac  weakness 
(arrhythmia,  dilatation),  even  endangering  life,  may  occur. 

The  duration  of  simple,  uncomplicated  influenza  is  in  the  mild  cases  about 
three  or  four  days,  in  the  severer  cases  about  seven  to  ten  days.  To  be  sure, 
we  should  also  consider  in  this  connection  that  convalescence  is  often  sur- 
prisingly slow,  so  that  the  after-pains  (as  it  were)  of  the  disease  are  felt  for 
weeks.  These  consist,  for  instance,  in  a  certain  degree  of  debility,  and  in 
myalgia.  Sometimes  also  there  are  complete  relapses,  so  that  directly  or  a 
short  time  after  the  disease  has  ended  the  symptoms  begin  anew.  The  spe- 
cial form  of  the  disease  may  change  in  this  case,  so  that,  for  example,  the 
relapse  of  an  influenza-  with  predominant  constitutional  symptoms  assumes 
the  pronounced  catarrhal  form.     Again,  it  is  not  very  rare  for  a  patient  to 


ssas 


Fig.  16. — Example  of  a  double-pointed  fever  curve  in  influ- 
enza. The  second  elevation  indicates  the  onset  of  a  mild 
catarrhal  pneumonia.     (Erlangen  Medical  Clinic.) 


92  ACUTE   GENERAL   INFECTIOUS   DISEASES 

suffer  from  two  or  even  more  attacks  of  influenza  separated  by  a  considerable 
interval  of  time. 

Complications  and  Sequelae. — While  all  the  symptoms  of  influenza  which  we 
have  thus  far  described  are  the  direct  effects  of  the  original  pathogenic  cause, 
the  majority  of  the  frequent  comjulications  are  undoubtedly  dependent  upon 
the  ingress  of  secondary  infection.  The  system  when  attacked  by  influenza  is 
greatly  exposed  to  these  secondary  influences,  and  almost  all  the  dangerous 
and  tedious  cases  of  influenza  become  such  only  because  of  a  mixed  infection 
of  this  sort.  This  is  particularly  true  of  the  lungs,  in  which  secondary  disease 
occurs  most  frequently — sometimes  even  in  the  first  days  of  illness,  but  also  in 
other  cases  later.  The  conditions  here  are  similar  to  those  seen  in  measles  and 
whooping  cough.  The  simple,  mild  catarrh  belongs  to  the  original  disease ;  the 
severe  pulmonary  affections  are,  however,  invariably  secondary  complications 
occasioned  by  new  pathogenic  influences.  These  influences  are  not  always  the 
same.  According  to  the  investigations  of  Eibbert,  Finkler,  and  others  it  is 
chiefly  the  pneumonia  diplococcus  and  the  streptococcus  which  are  the  true 
excitants  of  the  secondary  pneumonia  seen  in  influenza.  These  cases  of 
pneumonia  are  either  extensive  catarrhal  pneumonia  especially  affecting  the 
lower  lobes,  or  more  rarely  croupous  pneumonia  with  its  characteristic  spu- 
tum. We  must  also  add  that  the  influenza  bacilli  themselves  may  excite  a 
lobular  pneumonia  which  shows  a  marked  purulent  character. 

Quite  often  the  pneumonia  results  in  localized  suppuration  in  the  lungs. 
Influenza  pneumonia  is  not  infrequently  seen  as  a  relapse  in  cases  apj)arently 
recovered  from  influenza.  The  temperature  again  rises,  and  with  it  dangerous 
cardiac  and  general  weakness  is  often  combined. 

If  pneumonia  be  added  to  influenza,  the  former  overshadows  the  whole 
picture.  The  patient  is  oppressed  for  breath,  has  a  severe  cough  with  profuse 
expectoration,  looks  pale  or  cyanotic,  and  suffers  from  high  fever.  These 
symptoms  persist  for  two  or  three  weeks,  and  then  gradually  abate.  It  is  in 
this  way  that  influenza  becomes  dangerous  for  elderly  and  feeble  or  sickly 
persons.  Some  influenza  pneumonias  have  a  more  prolonged  course,  lasting 
from  four  to  six  weeks  and  even  longer.  Such  cases  usually  end  in  recovery. 
It  is  only  exceptionally  that  the  pulmonary  disease  leads  to  atrophy  and 
bronchiectasis,  pulmonary  abscess,  and  similar  conditions. 

Comparatively  often  pleurisy  with  effusion  is  conjoined  with  the  influenza 
pneumonia.  The  exudation  is  generally  serous,  but  exceptionally  it  is 
purulent. 

Of  the  other  complications,  the  frequent  occurrence  of  inflammation  of 
the  middle  ear  should  be  especially  mentioned.  Serious  affections  of  the  eye 
(keratitis)  are  much  more  rarely  seen.  We  have  several  times  observed  acute 
nephritis,  but  this  has  always  pursued  a  mild  course.  Among  cutaneous  erup- 
tions, herpes  labialis  is  a  frequent  phenomenon  in  all  forms  of  influenza,  even 
the  milder.  Other  exanthems,  such  as  urticaria  and  roseola,  are  much  less 
frequent. 

Many  of  the  complications  named  may  continue  even  after  the  fever  and 
all  other  symptoms  have  ceased,  so  that  they  must  be  regarded  as  sequelae. 
This  is  particularly  true  of  the  diseases  of  the  ear  and  eye  and  of  persistent 
bronchitis,  of  pneumonia  assuming  a  chronic  form,  etc.  An  important  and,  for 
the  patient,  a  troublesome  and  painful  sequel  is  furunculosis,  especially  if  some 


INFLUENZA  93 

of  the  boils  are  located  in  the  axilla  or  near  the  anus.     Very  often  neural 
pains  in  the  distribution  of  the  trigeminus  or  in  the  course  of  the  sciatic  or 
oilier  nerves  will  persist  For  a  considerable  time  after  the  influenza  lias  ceased. 

Painful  disturbances  in  the  muscles,  periosteum,  or  in  the  bonee  may  per- 
sist for  a  long  time.    In  a  few  cases re  severe  nervous  sequelae,  such  as  spinal 

symptoms,  psychoses,  and  neurasthenia  have  been  seen  after  influenza.  A 
special  form  of  acute  hemorrhagic  encephalitis  (see  Vol.  II)  -land-  in  rela- 
tionship to  influenza.  Finally,  permanent  disturbance  of  the  heart's  action 
(cardiac  weakness,  instability,  and  irregular  pulse)  is  sometimes  observed  after 
influenza.  Franke  groups  all  these  often  tedious  Bequelae  under  the  term 
"chronic  influenza."     This  diagnostic  term  should   not,  however,  be  abused. 

Diagnosis. — The  diagnosis  of  influenza  is  in  general  no!  difficult  if  one  lias 
to  deal  with  a  well-marked  case  at  the  time  of  an  influenza  epidemic.  The 
characteristic  initial  symptoms  of  fever,  headache,  and  pain  in  the  loins  are 
to  be  considered  first  of  all.  Their  onset  is  much  more  rapid  than,  for  exam- 
ple, in  typhoid  fever.  Later  on  the  pain  in  the  various  muscles  as  well  as  the 
catarrhal  symptoms  are  the  most  characteristic  phenomena. 

Uncertainties  and  errors  in  diagnosis  may  arise  from  the  fact  that,  on  the 
one  hand,  we  are  disposed  at  the  time  of  an  epidemic  to  call  almost  all  the 
catarrhal  and  indefinite  mild  affections  we  see  "  influenza,"  while,  on  the  other 
hand,  when  there  is  no  epidemic,  we  cannot  positively  distinguish  the  sporadic 
"  cases  like  influenza  "  from  the  ordinary  acute  febrile  bronchitis,  etc.  It  is 
indeed  very  possible,  a  priori,  that  different  morbid  agents  may  produce  similar 
mild  acute  diseases  of  the  accessible  mucous  membranes.  In  such  cases,  with 
pronounced  general  symptoms,  high  fever,  etc.,  we  must  often  be  content  with 
the  diagnosis  of  "  infectious  "  laryngitis,  bronchitis,  etc.,  without  being  able 
to  decide  definitely  whether  the  case  is  to  be  classed  serologically  with  in- 
fluenza or  not.  At  any  rate  in  practice  we  should  not  abuse  the  diagnosis  of 
influenza.  An  absolute  diagnosis  can  only  be  made  by  bacteriological  ex- 
amination, although  this,  as  yet,  is  often  quite  a  difficult  matter. 

Prognosis.— For  an  individual  who  is  healthy  and  vigorous,  influenza  is  not 
a  dangerous  disease,  even  in  its  severer  forms;  for  elderly  persons  or  invalids 
it  may,  however,  be  a  serious  affection.  Patients  with  heart  disease  or  pul- 
monary disease,  or  those  suffering  from  chronic  nervous  troubles,  sometimes 
succumb  to  it;  so  that  the  general  mortality  at  the  time  of  a  great  epidemic 
of  influenza  is  always  considerably  increased.  The  above-enumerated  compli- 
cations are  by  far  the  most  dangerous ;  less  often  is  a  fatal  termination  caused 
by  general  or  cardiac  weakness.  The  above-mentioned  sequela?  are  also  to  be 
considered  in  prognosis. 

Treatment. — No  specific  remedy  for  the  disease  is  known.  In  general  we 
must,  therefore,  pursue  a  purely  symptomatic  method  of  treatment.  For  the 
initiatory  fever,  the  headache,  and  the  pain  in  the  loins,  antipyrin  is  some- 
times a  good  remedy,  and  the  same  may  be  said  also  of  phenacetin,  aspirin, 
and  especially  salipyrin.  These  drugs  as  well  as  soothing  liniments  are  also 
prescribed  for  the  persistent  pains  in  the  muscles.  In  many  cases  presenting 
marked  catarrhal  manifestations  diaphoretic  treatment  acts  well.  The  treat- 
ment of  the  pulmonary  complications  is  according  to  the  established  methods. 
Morphin,  codein,  Dover's  powder,  and  similar  drugs  are  used  for  the  trouble- 
some cough.     Apomorphin,  senega,  and  other  expectorants  may  be  employed, 


94 


ACUTE   GENERAL  INFECTIOUS   DISEASES 


and,  if  indicated,  external  remedies  such  as  an  ice  bag,  moist  applications,  or 
dry  cupping.  Stimulants  (champagne,  camphor,  caffein,  strophanthus)  are  in- 
dicated for  beginning  cardiac  weakness.  Inasmuch  as  influenza,  as  already 
stated,  is  not  infrequently  followed  by  a  protracted  state  of  general  weakness, 
the  patient  must  be  urged  to  take  due  care  of  himself  during  the  entire  period 
of  convalescence. 


CHAPTEE    XII 


DYSENTERY 

etiology.- — By  "  dysentery  "  is  meant  a  disease  of  the  colon,  which  appears 
sporadically,  but  more  often  in  epidemics;  it  is  excited  by  infection  with  an 
organized  pathogenic  poison,  about  which  we  have  as  yet  no  definite  knowledge ; 
and  the  infection  is  probably  at  first  a  local  one.  From  the  investigations  of 
various  men,  especially  Kartulis,  it  seems  very  probable  that  a  certain  form  of 
amoeba  must  be  regarded  as  the  cause  of  "  endemic  tropical  dysentery."  At 
least  in  endemic  dysentery  we  almost  invariably  find,  both  in  the  stools  and  in 
the  walls  of  the  dysenteric  intestinal  ulcers  and  in  the  dysenteric  abscesses  of 
the  liver,  many  amoebae  (amoeba  coli),  which  are  never  found  in  any  other 
intestinal  affection.  Dysentery  may  also  be  artificially  produced  in  cats  by 
means  of  feces  containing  amcebge.  In  dysentery  as  it  occurs  in  Germany, 
however,  we  do  not  apparently  find  amoebae  in  the  stools,  as  a  rule,  although 
even  in  Germany  Quincke  and  others  have  described  certain  cases  of  "  acute 

enteritis  "  ("  amoebic  enteritis  ") 
in  which  there  were  a  large  num- 
ber of  amoebae  present.  Most  of 
the  epidemics  in  Germany  have 
been  caused  by  the  Bacillus  dysen- 
terige,  described  by  Kruse,  Shiga, 
and  others.  This  bacillus  resembles 
the  typhoid  bacillus,  but  is  shorter 
and  thicker,  has  no  flagella,  and  is 
therefore  nonmotile. 

The  true  home  of  dysentery  is 
in  warmer  and  tropical  countries, 
where  the  disease  is  much  more 
violent  and  widespread  than  here. 
For  example,  the  mortality  among 
the  soldiers  of  the  Anglo-Indian 
army  due  to  dysentery  is  said  to 
be  at  times  thirty  per  cent  of  the 
entire  number  of  deaths.  In  our 
climate  most  of  the  epidemics  occur 
at  the  end  of  summer  and  in  autumn.  Endemic  influences  are  certainly  im- 
portant. The  special  conditions  in  some  places  are  evidently  very  favorable 
for  the  development  and  dissemination  of  dysenteric  germs,  and  there  are 


Fig.  17. — Amoeba  dysenteries  (after  Roos).  a. 
Amoebae  without  foreign  bodies,  b.  Amoeba 
containing  blood,  c.  Amcebse  showing  vacu- 
oles,    d.  Young  forms,     e.   Encysted  forms. 


DYSENTERY  95 

other  places  equally  unfavorable.  There  can  be  qo  other  explanation  of  the 
immunity  of  some  localities  contrasting  with  the  greai  prevalence  of  the  dis- 
ease in  others.  How  infection  occurs  we  'I"  not  yei  know.  Many  ■ 
tions,  especially  in  southern  countries,  supporl  the  idea  thai  the  germs  may  be 
taken  into  the  system  by  drinking  water.  Ii  is  very  probable  thai  in  addition, 
dysentery  can  be  spread  through  the  medium  of  the  fecal  dejections  of  the 
sick — e.g.,  from  privies,  chamber  vessels,  and  bed  linen.  Many  cases  were 
formerly  referred  to  catching  cold  or  to  some  error  in  diet;  but  we  must,  of 
course,  regard  these  merely  as  predisposing  influence-. 

Pathology. — The  objective  pathological  lesion  of  the  colon,  in  all  severe 
cases,  consists  in  a  pronounced  croupous-diphtheritic  inflammation.  The  re- 
marks as  to  the  general  pathology  of  such  inflammations  made  in  the  section 
on  pharyngeal  and  laryngeal  croup  (p.  77)  are  equally  applicable  to  the 
analogous  dysenteric  inflammation.  In  this  case,  too,  there  is  lirst  a  destruc- 
tion of  the  epithelium  and  then  the  formation  of  a  fibrinous  exudation  occu- 
pying its  place,  and  penetrating  down  into  the  tissue  of  the  mucous  mem- 
brane itself.  At  the  same  time  there  is  an  intense  purulent  infiltration  of  the 
mucous  and  submucous  tissue,  accompanied  by  extensive  ecchymoses.  In  the 
most  virulent  cases  the  macroscopic  appearances  are  marked  thickening  of  the 
whole  wall  of  the  intestine,  congestion  of  the  serous  layer,  and  the  conversion 
of  the  inner  surface  into  a  mottled,  dark-red,  irregularly  roughened  area  of 
ulceration.  The  disease  may  be  confined  to  the  rectum  and  the  sigmoid 
flexure,  but  in  severer  cases  it  involves  the  entire  colon  as  far  as  the  ileo- 
cecal valve,  or  even  extends  to  the  lower  portion  of  the  ileum.  Besides  this 
severe  form  of  diphtheritic  or  even  gangrenous  dysentery,  there  is  a  milder 
variety,  termed  catarrhal  dysentery.  In  this  the  mucous  membrane  is  found 
in  a  state  of  intense  purulent  inflammation,  with  ecchymoses.  Even  here  little 
masses  of  croupous  exudation,  which  can  be  torn  off,  have  replaced  the  epi- 
thelium ;  hut  they  never  form  continuous  layers  of  great  extent.  There  is  no 
sharp  boundary  line  between  the  two  forms,  the  milder  catarrhal-croupous 
and  the  severer  diphtheritic  dysentery.  Numerous  transitional  and  combined 
varieties  exist. 

We  must  remark,  in.  conclusion,  that  precisely  the  same  anatomical  changes 
as  are  presented  in  true  dysentery  may  result  from  other  causes.  Important 
among  these  is  persistent  fecal  impaction  in  the  rectum,  which,  by  a  purely 
mechanical  effect  upon  the  epithelium,  may  excite  a  diphtheritic  inflammation 
in  the  mucous  membrane.  And  any  severe  constitutional  disease  whatsoever, 
such  as  typhoid  fever,  measles,  smallpox,  septicemia,  or  phthisis,  may  he  at- 
tended by  a  so-called  "  secondary  dysentery."  This  is  most  frequent  in  hos- 
pitals.   Whether  it  has  the  same  etiology  as  genuine  dysentery  is  uncertain. 

Clinical  History. — Throughout  the  entire  illness  the  most  prominent  symp- 
toms are  intestinal.  There  may  be  first  of  all  some  slight  irregularity  of  the 
bowels  for  a  few  days,  and  then  appears  a  moderate  diarrhea.  The  stools  are  at 
first  feculent,  although  thin,  and  number  two  to  six  daily.  After  a  few  days 
the  discharges  increase  in  frequency,  and  become  extremely  characteristic. 

The  stools  are  very  frequent,  occurring  ten  to  twenty,  and  even  sixty  or 
more,  times,  in  twenty-four  hours.  In  severe  cases  there  may  he  a  distressing 
and  almost  constant  desire  to  evacuate  the  bowels.  After  every  operation,  and 
to  some  extent  during  it,  there  is  tenesmus  attended  by  intense  burning  pain 


96  ACUTE   GENERAL   INFECTIOUS   DISEASES 

in  the  anus.  The  stools  soon  lose  their  usual  feculent  character  in  great  part 
if  not  entirely.  They  become  scanty,  so  that  not  more  than  about  half  an 
ounce  is  evacuated  each  time.  For  the  most  part  they  usually  consist  of  a 
sero-mueous  fluid,  in  which  are  suspended  numerous  shreds  and  particles  of 
varying  size.  These  are  blood-stained  bits  of  mucus,  little  coagula  of  blood, 
ancl  necrosed  pieces  of  mucous  membrane.  One  or  another  of  these  constituent 
parts  may  predominate,  so  that  there  may  be  slimy,  purulent,  or  bloody  stools, 
or  all  sorts  of  combinations  of  these  varieties.  We  often  find,  besides,  a  few 
small  masses  of  feces,  usually  covered  with  mucus.  We  sometimes  see  numer- 
ous clumps  of  mucus,  resembling  sago  or  frog's  spawn;  they  are  probably 
mucous  casts  of  the  follicles.  Under  the  microscope  the  greater  part  of  the 
ctysenteric  discharge  is  seen  to  consist  of  pus  corpuscles  and  blood.  There  are 
also  cylinder  epithelium  and  an  enormous  amount  of  detritus,  and  the  bacteria 
of  putrefaction.  A  purely  dysenteric  stool  has  no  bad  odor,  except  that  in 
the  worst  cases  of  gangrenous  dysentery  the  discharges  become  blackish  and 
extremely  offensive. 

Besides  the  rectal  tenesmus  there  ma}'  be  a  cramp-like  pain  during  mic- 
turition. There  are  often  violent  attacks  of  colic.  The  abdomen  is  usually 
rather  tense,  and  tender  on  pressure  along  the  line  of  the  colon,  but  without 
tympanites.  The  anus  may  be  red,  inflamed,  and  excoriated.  Gastric  symp- 
toms are  on  the  whole  infrequent,  if  we  except  the  complete  anorexia  which 
exists  in  all  severe  cases.  Sometimes  there  is  repeated  vomiting.  Occasionally 
hiccoughs  prove  distressing.    The  tongue  usually  has  a  dry,  greasy  coating. 

The  symptoms  just  depicted  last  about  a  week  or  ten  days.  If  the  case  is 
of  much  intensity,  the  general  condition  is  also  greatly  affected.  The  patient 
seems  much  collapsed,  and  is  very  languid  and  feeble,  with  a  small  and  rapid 
pulse.  The  skin  becomes  cool  and  rough,  the  voice  weak  and  hoarse.  There  is 
pain  in  the  muscles.  The  patient  wastes  away.  The  temperature  has  little 
that  is  characteristic  or  typical.  In  many  cases  there  is  no  fever  at  all,  and 
the  temperature  may  even  be  subnormal.  In  most  cases,  however,  there  is  an 
irregular  fever  seldom  exceeding  104°  P.  (40°  C),  and  having  remissions. 

In  the  worst  cases  the  general  weakness  may  increase  more  and  more,  and 
death  occur ;  but  with  us  a  favorable  termination  is  much  more  frequent.  The 
distress  gradually  diminishes,  the  stools  assume  more  and  more  of  a  feculent 
character,  the  patient  becomes  stronger,  and  after  one  and  a  half  to  three 
weeks  convalescence  is  established.  It  may  be  a  long  while,  however,  before  a 
patient  completely  recovers  from  a  severe  attack.  A  third  possibility  is  the 
transition  of  the  acute  into  a  chronic  dysentery.  In  this  the  symptoms  of  a 
chronic  colitis,  usually  attended  with  cachexia,  may  persist  for  months  and 
years. 

Mild,  rudimentary  forms  of  dysentery  also  occur,  presenting  no  severe  in- 
testinal symptoms,  and  recovering  at  the  end  of  a  few  days.  In  these  cases, 
too,  great  sensitiveness  of  the  intestine  to  disturbing  influences  frequently  per- 
sists for  quite  a  long  time  after  the  illness.  There  may  be  exacerbations  of 
the  disease,  and  relapses. 

Complications. — Complications  of  dysentery,  localized  in  otber  organs,  are 
rare,  at  least  in  epidemics  here.  In  tropical  dysentery  abscess  of  the  liver  is 
comparatively  common.  It  is  dependent  upon  metastatic  processes  from  the 
portal  radicals.     In  some  cases  abscesses  of  the  lungs  and  of  the  brain  may 


DYSENTERY  97 

follow  abscess  of  the  liver,  [nflammation  of  the  Berous  membranes  or  of  one 
or  more  joints  may  also  occur,  [f  paraplegia  follows  ii  may  be  referred  either 
to  secondary  myelitis  or  to  polyneuritis.  Dysentery  is  also  said  to  occur  in 
connection  with  n  "general  scorbutic  diathesis,"  bul  to  all  appearances  this 
is  usually  a  "septic  "  complication.  The  dysenteric  ulcers  rarely  lead  to 
perforation  and  consequent  peritonitis. 

Diagnosis. — The  clinical  diagnosis  i-  seldom  very  difficult,  ft  is  based  ex- 
clusively upon  the  intestinal  symptoms  and  the  character  of  the  stool-.  It 
is  only  the  cases  of  secondary  dysentery  which  occur  in  the  course  of  other 
severe  diseases  that  are  likely  to  escape  observation. 

The  bacteriological  demonstration  of  the  dysentery  bacilli  in  the  Btoole 
may  be  made  by  means  of  the  Drigalski-Conradi  nutritive  medium.  The 
bacilli  grow  in  colonies  of  a  bluish  color,  as  do  typhoid  bacilli,  but  the  dysen- 
tery bacilli  are  nonmotile,  and  are  agglutinated  by  the  scrum  from  dysentery 
cases.  The  amoebaj  of  dysentery  are  detected  by  microscopical  examinations 
of  the  stools. 

Prognosis. — The  prognosis  is  mainly  influenced  by  the  character  of  the 
epidemic,  which,  as  we  have  said,  is  in  our  climate  usually  benign.  There  may 
be  danger,  particularly  to  elderly  people,  from  bodily  weakness  and  collapse. 

Treatment. — Prophylaxis  demands  that  the  isolation  of  the  patient  and  the 
disinfection  of  the  stools  be  as  complete  as  possible.  The  healthy  must  be  very 
careful  during  an  epidemic  not  to  catch  cold,  and  to  avoid  errors  in  diet,  for 
experience  shows  that  an  opposite  course  predisposes  to  the  disease. 

The  patient  must  be  kept  warm,  and  must  not  leave  his  bed,  even  if  the 
attack  be  mild.  The  diet  must  be  rigorous.  If  the  strength  is  fair,  thin  por- 
ridge, milk,  and  broths  suffice  for  some  days.  To  a  feebler  person  we  should 
give  somewhat  stronger  nourishment  from  the  start,  e.  g.,  eggs,  peptonized 
meat,  and  wine.  Most  patients  bear  liquids  that  are  lukewarm  better  than 
these  which  are  cold. 

As  to  drugs,  the  habit  of  almost  all  experienced  plrysicians  is  to  give  at 
first  a  mild  laxative.  Although  opium  does  not  usually  control  the  diarrhea 
and  tenesmus  at  all,  it  is  the  rule  for  decided  improvement  to  follow  the  ex- 
hibition of  the  laxative.  During  the  first  days,  or,  if  need  be,  later,  we  give 
two  to  four  tablespoonfuls  of  castor  oil  daily.  If  this  medicine  is  very  dis- 
agreeable to  the  patient,  we  can  replace  it  by  a  strong  infusion  of  rhubarb 
(10-to-100).  In  southern  countries  large  doses  of  calomel  (gr.  viij  to  xv,  gm. 
0.5  to  1)  are  customary,  and  are  highly  praised  by  the  physicians  there.  Fur- 
ther on  in  the  disease  we  may  content  ourselves  with  giving  mistura  amygdalae ; 
or  we  may  administer  bismuth  in  the  following  mixture :  Bismuthi  subnit.  vel 
salicylat.,  5j  (gm.  5)  ;  mucilaginois  acacias,  syrupi  simpl.,  aa  ^ss.  (gm.  15)  ; 
aquae  destil.,  120 — to  be  shaken  before  taking.  If  the  disease  should  get 
worse  again,  however,  we  should  always  try  a  laxative. 

Emetics  at  the  beginning  of  the  disease  are  often  employed  in  the  tropics, 
but  seldom  with  us.  Ipecacuanha  (radix  antidysenterica) ,  given  in  large 
doses  of  15  to  30  gr.  (gm.  1  to  2)  is  even  regarded  by  many  as  a  specific. 
Among  antiparasitic  remedies,  naphthalin  (gr.  viij,  gm.  0.5,  thrice  daily)  and 
salol  (1  to  2  drachms,  gm.  4.0  to  8.0,  a  day)  have  been  especially  recom- 
mended. Numerous  attempts  have  been  made  at  local  treatment  by  enemata. 
No  brilliant  results,  however,  can  be  claimed  for  any  of  these  methods  or 


98  ACUTE   GENERAL  INFECTIOUS   DISEASES 

medicines.  A  decided  palliative  effect  can  be  obtained  from  the  injection  of 
thin  starch  to  which  20  or  30  drops  of  laudanum  have  been  added.  Supposi- 
tories of  cocoa  butter  containing  extract  of  opium  often  mitigate  the  tenesmus. 
Other  injections  are  recommended,  each  to  measure  §ij  *to  ivss.  (gm.  60  to 
100),  and  to  contain  either  argenti  nitrat.,  gr.  j  to  vj  (gm.  0.05  to  0.30),  or 
plumbi  acetat.,  gr.  ij  to  viij  (gm.  0.1  to  0.5),  or  potassii  chlorat.,  gr.  xv  to 
xx  (gm.  1  to  1.5),  and  especially  tannin  (three  injections  a  day  of  a  warm  0.5- 
per-cent  solution).  In  severe  cases  we  may  also  try  high  injections  of  solu- 
tions of  tannin  as  in  cholera  (vide  infra).  Many  other  solutions  are  used. 
The  success  of  this  treatment  is,  however,  dubious.  In  all  cases  the  margins 
of  the  anus  must  be  protected  from  inflammation  by  frequently  washing  and 
anointing  the  skin. 

The  treatment  of  weakness  and  collapse  is  by  the  usual  stimulants — wine, 
ether,  camphor,  and  the  like.  In  chronic  dysentery  the  main  point  is  to  per- 
severe in  a  strict  control  of  the  diet.  We  may  exhibit  astringents,  such  as 
tannin,  tannigen,  and  columbo.  Subnitrate  of  bismuth  is  also  given,  and 
nitrate  of  silver  and  acetate  of  lead.  And  in  these  chronic  cases  a  long- 
continued  and  thorough  use  of  rectal  irrigation  with  fluids  containing  some 
mild  astringent  or  disinfectant  may  have  a  good  effect. 

[Sporadic  dysentery  is  a  self -limited  disease,  and,  as  has  been  shown  by 
Flint,  runs  its  course  within  ten  days  without  medication.  Treatment,  how- 
ever, adds  to  the  comfort  of  the  patient  and  shortens  the  course.  It  is  not 
customary  with  us  to  use  daily  laxatives.  If  there  is  any  doubt  as  to  whether 
the  intestines  have  been  emptied,  a  saline  should  be  given,  the  action  of  which 
should  be  followed  by  opium  in  sufficient  doses  to  allay  pain  and  tenesmus. 
Subsequent  action  of  the  bowels  is  best  obtained  by  simple  large  enemata. 
In  weak  persons  castor  oil  is  to  be  preferred  to  salines. 

In  epidemic  dysentery  active  treatment  is  much  more  important.  Laxa- 
tives are  contra-indicated  by  sero-sanguinolent  dejections  or  by  asthenia,  but 
enemata  can  be  freely  used.  Stimulation  is  often  required ;  nutrition  must  be 
carefully  looked  after,  such  articles  being  chosen  as  are  digested  and  absorbed 
by  the  upper  portions  of  the  intestinal  tract,  leaving  as  little  residue  as  pos- 
sible to  pass  on  to  the  inflamed  colon.  Opium  is  often  demanded  and  tolerated 
in  large  doses,  and  astringents,  such  as  the  acetate  of  lead,  gallic  acid,  and  the 
pernitrate  of  iron,  are  of  service. 

In  acute  dysentery  the  patient  should  be  instructed  not  to  yield  to  the 
desire  to  go  to  stool  if  he  can  help  it,  and  tenesmus  can  often  be  much  dimin- 
ished by  simple  irrigation  of  the  lower  bowel  with  water,  which  may  be  warm 
or  cold,  whichever  the  patient  finds  more  agreeable. 

In  chronic  dysentery  medicated  injections  large  enough  to  reach  the  colon 
are  the  best  remedy.  In  amoebic  d}rsentery,  one  or  two  quarts  of  a  solution  of 
quinin  in  water,  1  to  5,000  gradually  strengthened  up  to  1  to  1,000,  may  be 
given  twice  a  day ;  and  in  bacillary  dysentery,  three  to  six  pints  of  a  solution  of 
nitrate  of  silver  containing  12  to  60  gr.  to  the  quart,  once  a  day.  Preliminary 
use  of  cocain  may  be  required  to  lessen  the  sensitiveness  of  the  rectum.] 


CHOLERA  99 


CHAPTER    XIII 

CHOLERA 
(Asiatic  Cholera) 

Historical  Remarks. — The  home  of  genuine  Asiatic  cholera  is  India.  The 
first  epidemic  in  that  country  with  which  we  are  accurately  acquainted  oc- 
curred in  1817.  This  was  very  widespread.  The  disease  was  probably  endemic 
there  at  an  earlier  period.  In  the  next  few  years  the  cholera  extended  in  all 
directions,  and  reached  Astrakhan  by  way  of  Persia.  Between  1830  and  1832 
the  disease  made  its  first  great  epidemic  progress  over  Europe.  Invading  all 
European  Kussia,  it  reached.  Germany  in  1831,  and  France  and  England  in 
1832.  Then  came  many  smaller  epidemics  up  to  1838,  when  there  was  a  com- 
plete cessation  till  1846,  in  which  year  the  disease,  again  starting  from  Asia, 
overspread  Europe.  There  have  in  later  years  been  epidemics  in  many  places, 
but  we  cannot  here  enter  into  the  particulars  of  them.  During  the  war  of 
1866  there  were  many  cases  of  cholera  in  Germany,  and  from  1883  to  1886 
Italy,  France,  and  Spain  were  visited  by  the  disease.  In  August,  1892,  cholera 
broke  out  suddenly  and  very  unexpectedly  in  Hamburg,  where  within  three 
months  about  18,000  persons  were  attacked  by  the  disease,  and  over  7,600  died 
of  it.     [It  has  not  gained  a  foothold  in  the  United  States  since  1873.] 

etiology. — Some  time  ago  it  had  be6ome  evident  that  the  real  cause  of 
cholera  consists  in  the  infection  of  the  system  by  a  specific  microorganism. 
Koch  was,  however,  the  first  to  succeed  in  the  search  for  the  poisonous  agent. 
He  was  in  charge  of  the  scientific  expedition  sent  out  by  the  German  Govern- 
ment in  1883  to  Egypt  and  India  for  the  purpose  of  investigating  the  disease. 
Koch  found  in  the  intestines  of  all  the  victims  of  cholera  whose  bodies  he 
examined  a  certain  kind  of  microorganism  wdiich  he  named  the  comma  bacillus. 
At  present  it  is  often  termed  the  spirillum  or  the  vibrio  of  cholera.  It  is 
shorter  than  the  bacillus  of  tuberculosis,  but  somewhat  thicker,  and  it  is 
usually  bent  in  the  shape  of  a  comma,  or  even  like  a  semicircle  (see  Fig.  18). 
In  pure  cultures  the  comma  bacilli  grow  into  long  spiral  threads,  resembling 
the  spirilla  of  recurrent  fever.  Examined  in  a  liquid,  the  individual  bacilli 
are  seen  to  make  vigorous  movements.  This  mobility  is  dependent  upon  the 
thin,  filiform  fibers  at  the  ends  of  the  comma  bacilli  discovered  by  Loftier. 

The  comma  bacilli  flourish  best  at  a  temperature  between  86°  and  104°  F. 
(30°  and  40°  C).  Below  61°  F.  (16°  C.)  they  cease  to  grow,  but  they  are 
not  killed  even  by  a  greater  degree  of  cold.  The  free  access  of  oxygen  pro- 
motes but  is  not  absolutely  indispensable  to  their  growth.  They  multiply  very 
rapidly  in  liquids — e.  g.,  broth  or  milk — and  they  may,  under  favorable  cir- 
cumstances, retain  their  vitality  for  many  weeks,  while  they  can  be  readily 
destroyed  by  desiccation.  In  this  again  they  resemble  the  genuine  spirilla, 
which  can  maintain  their  existence  only  in  fluids.  On  the  human  hand  the 
comma  bacilli  usually  die  from  desiccation  after  two  hours,  while  on  food 
stuffs  in  moist  storage  they  keep  alive  for  about  eight  days,  and  on  moist 
laundry  even  fourteen  days.  The  characteristic  features  of  pure  cultures  can 
not  be  described  in  detail  here,  but  we  may  observe  that  the  nutrient  gelatin 


100  ACUTE   GENERAL   INFECTIOUS   DISEASES 

is  slowly  liquefied  by  the  bacilli.  If  a  few  drops  of  sulphuric  acid  are  added 
to  a  fresh  bouillon  culture,  a  reddish-violet  coloration  appears,  due  to  the 
indol  formed  from  the  bacilli  and  the  sulphurous  acid. 

There  can  now  be  no  doubt  that  the  sole  cause  of  cholera  is  infection  by 
the  comma  bacilli.  It  has  been  shown  that  in  every  case  of  genuine  Asiatic 
cholera  the  comma  bacilli  are  present  in  the  intestine,  and  that  they  are  never 
found  under  any  other  circumstances.  The  transmission  to  animals  (guinea 
pigs)  is  successful  only  when  the  gastric  juice  has  previously  been  rendered 
alkaline  by  means  of  a  soda  solution.  Injection  of  cholera  cultures  into  the 
peritoneal  cavity  of  guinea  pigs  rapidly  effects  fatal  intoxication  from  the 
bacterial  proteins.  By  slow  preliminary  treatment  with  small,  gradually  in- 
creased doses  of  cholera  cultures,  the  animals  can  ultimately  be  immunized 
against  the  most  powerful  toxin  actions.  The  blood  serum  of  animals,  thus 
immunized,  is  agglutinative  to  the  cholera  vibrios  (see  p.  25)  and,  if  injected 
simultaneously  with  a  fresh  cholera  culture  into  a  guinea  pig's  peritoneal 
cavity,  rapidly  dissolves  the  comma  bacilli. 

Investigation  as  to  the  origin  of  cholera  must,  therefore,  now  meet  this 
culminating  question:  Under  what  circumstances  and  through  what  channel 
do  the  comma  bacilli  penetrate  into  the  human  system,  and  in  what  manner 
do  they  there  excite  the  characteristic  processes  of  the  disease  ?  There  can  be 
no  doubt  that  among  Europeans,  and  probably  everywhere  except  in  India, 
the  cholera  is  invariably  imported.    It  is  equally  certain  that  the  dejections  of 

cholera  patients,  which  are  rich  in  com- 
,  ma  bacilli,  are  the  chief  if  not  the  only 

/  /      I  )  agent    by    which    the    disease    is    spread. 

I    t!iji}'''&"/>>\J>'/l  The  bacilli  which   escape  into  the  outer 

'  ~j?xI,  tfif]  1    A '#'•  ^    world    with    the    stools    find    abundant 

>>  /  <\,y  ^aW  h     i  means  to  prolong  their  existence.     They 

'^"i     \t'»)       ffrT*7   \  /  continue    their    growth    upon    moistened 

|  «}iLV//    ^J'//'^*'//  1 1  bedclothes,  or  in  water  which  contains  a 

h  %'  ~  -,/>    '(///£f   p  1  sufficient   amount   of   organic    substances, 

' wt* -JL"/?/     1/  &\l     ~''\h  or  in  food,  such  as  fruit  or  milk,  or  in 


[Aijfai/i C '  7'))  '4V'|7  moist  earth;  and  the  ways  by  which  they 

'     "*!'' '/':     u,^  *,  \  I  can  in  turn  enter  the  system  of  a  healthy 

»'  >.*?•  a  \  -y  /if.  k    . 


vs-Tit    " 


)    *.  /'  't  f  )  \\  human  being  are  infinite  in  number.     It 


'N  J  //    I  Ivf^l  ii^'  I  ^s  easy  ^°  imc^erstan(i  why  certain  persons 

V       //      r >»   I'll  o    <t      lcmnrlrpaspa   nnrl    nnrsps nrp   mnrfl 


e.  sr.,  laundresses  and  nurses — are  more 


&•> 


liable  to  infection  than  others;  and  it  is 
Fig.  18. — (From  Koch.)  Comma  bacilli    equally  intelligible  that  the  spread  of  the 

from  a  cholera  dejection  which  had  lain     diseage    gh(mld    often    bear    a    relation    to 
for  two  days  on  a  wet  cloth.      1  he  b-  . 

shaped  bacilli  are  at  a.   600  diameters,    certain  outward  circumstances.     1  he  tact 

has  long  been  a  familiar  one,  that  the 
cholera  almost  always  progresses  along  the  world's  most  frequented  highways, 
and  that  it  never  travels  faster  than  the  means  of  human  intercommunication 
render  possible.  This  is  important,  because  it  shows  plainly  that  the  germs  of 
the  disease  are  not  disseminated  by  currents  of  air.  It  is  easy  to  understand 
that  the  distribution  of  the  disease  should  sometimes  correspond  with  that  of 
water  destined  for  personal  use.  The  experience  of  the  last  few  years  has 
again  proved  most  clearly  that  the  drinking  water  is  the  chief,  although,  of 


CHOLERA  101 

course,  not  the  only,  source  dor  the  dissemination  of  cholera,     [f  an  extensive 

Wiitor  supply  is  contaminated  by  comma  bacilli,  as  was  the  case  in  Hamburg 
in  1892,  the  disease  may  suddenly  break  out  with  ^reat  severity.  Sporadic 
cases  usually  arise  from  the  use  of  a  contaminated  stream  which  is  used  for 
drinking  only  by  a  small  number  of  men  (sailors,  etc.).  it  is  also  important 
to  note  that  flies,  which  have  rested  on  the  evacuations  of  cholera  patients,  on 
soiled  linen,  or  the  like,  can  carry  the  infectious  materials  upon  food  stuffs,  etc. 

A  man  falls  sick  with  cholera,  of  course,  not  simply  from  swallowing  the 
cholera  bacilli,  but  because  the  bacilli  remain  in  the  intestine  and  multiply.  It 
is  safe  to  assume  that  many  men  swallow  comma  bacilli  at  the  time  of  a  cholera 
epidemic  without  falling  sick  at  all,  or  without  any  but  the  slightest  disturb- 
ance, because  the  comma  bacilli  are  at  once  destroyed  by  the  acid  gastric  juice 
or  they  develop  in  the  intestine  only  to  a  slight  extent.  Repeatedly,  comma 
bacilli  have  been  found  in  the  solid  stools  of  healthy  men,  who  were  in  close 
contact  with  cases  of  cholera,  and  also  in  the  stools  of  men  who  had  a  very  mild 
"  cholera  diarrhea."  These  facts  are  extremely  important.  They  lead  to  a  cor- 
rect estimate  of  the  infection  experiments  repeatedly  practiced  of  late  on 
human  beings,  and,  on  the  other  hand,  they  have  a  great  practical  significance 
in  regard  to  the  danger  of  transmitting  cholera. 

Most  cholera  epidemics  happen  in  the  summer  months.  Liability  to  the 
disease  is  very  widespread,  although  some  remarkable  exceptions  are  seen.  Sex 
is  unimportant.  Age  has  more  influence.  The  disease  occurs  in  sucklings,  but, 
as  a  rule,  is  more  rare  among  children  than  among  adults.  Elderly  people  are 
very  apt  to  take  the  disease,  while  of  typhoid  fever  the  opposite  is  true.  Most 
authors  lay  great  stress  upon  predisposing  causes.  Among  these,  taking  cold 
is  not  so  important  as  are  errors  in  diet  and  mild  attacks  of  gastro-intestinal 
catarrh,  which  are  shown  by  numerous  observations  to  predispose  strongly  to 
the  disease,  because  the  acidity  of  the  gastric  contents  is  thus  diminished,  and 
the  retention  of  comma  bacilli  in  the  intestine  is  thus  facilitated.  The  stage 
of  incubation  seldom  lasts  over  one  to  three  da}rs. 

Clinical  History  and  Symptoms. — In  cholera,  as  in  most  acute  infectious 
diseases,  the  intensity  of  the  illness  varies  between  the  extremes  of  mildness 
and  severity,  so  that  usually  a  correct  interpretation  of  the  mildest  cases  is 
rendered  possible  only  by  the  knowledge  that  an  epidemic  exists  and  by  the 
discovery  of  comma  bacilli.  These  insignificant  cases  are  called  simple  chole- 
raic diarrhea.  The  symptoms  are  those  of  a  violent  acute  intestinal  catarrh; 
the  dejections  are  watery,  rather  large,  painless,  and  number  about  three  to 
eight  in  twenty-four  hours.  There  is  considerable  malaise,  complete  anorexia, 
and  thirst,  and  there  may  already  be  indications  of  severer  choleraic  symptoms 
— vomiting,  slight  pains  in  the  calves  of  the  legs,  and  diminished  secretion  of 
urine.  Many  cases  recover  after  a  few  days  or  a  week,  but  in  others  the  first 
mild  diarrhea  is  succeeded,  at  the  end  of  one  to  three  days,  or  rarely  latex  still, 
by  a  severe  attack  of  cholera.  .  In  such  cases  we  speak  of  a  "  premonitory 
diarrhea  of  cholera." 

The  mild  form  is  succeeded  in  a  gradual  transition  by  the  cases  designated 
as  "cholerine."  Cholerine  exhibits  the  symptoms  of  a  violent,  rather  sudden 
cholera  morbus.  It  often  begins  at  night.  To  the  diarrhea,  which  now  and 
then  displays  even  at  this  time  the  characteristics  of  pronounced  cholera,  vom- 
iting is  soon  added.     The  accompanying  constitutional  symptoms  are  rather 


102  ACUTE   GENERAL   INFECTIOUS   DISEASES 

severe.  There  is  great  languor  and  depression.  The  voice  grows  weak,  the 
extremities  are  cool,  the  pulse  is  small  and  accelerated,  painful  cramps  occur 
in  the  calves  of  the  legs,  the  urine  grows  scanty  and  perhaps  albuminous.  The 
whole  attack  lasts  about  a  week  or  two,  before  recovery  is  complete.  The  course 
of  the  disease  is  not  infrequently  varied  by  repeated  improvements  and  relapses. 

From  these  cases  of  medium  severity  there  is  again  a  continuous  line  of 
transition  to  the  pronounced  severe  form  of  cholera.  Statistics  as  to  the  fre- 
quency of  the  separate  forms  cannot  be  given,  since  many  of  the  milder  cases 
escape  observation. 

The  true  attack  of  cholera  may  begin  suddenly  with  the  severest  s}anptoms. 
As  a  rule,  however,  it  is  preceded,  as  already  stated,  by  a  first  stage  of  brief 
premonitory  diarrhea.  This,  after  one  to  three  days,  is  replaced  with  equal 
suddenness  by  the  severe  symptoms  of  the  second  or  "  algid  stage,"  or  "  cholera 
asphyxia."  Its  first  symptoms  are  the  abrupt  appearance  of  great  bodily  weak- 
ness, chilliness,  and  vertigo.  The  characteristic  gastro-intestinal  symptoms 
soon  declare  themselves. 

The  diarrhea  grows  very  violent.  At  short  intervals  there  are  copious 
]Dainless  dejections,  which  at  first  retain  somewhat  of  a  feculent  character,  but 
very  soon  present  a  characteristic  resemblance  to  rice  water,  gruel,  or  whey. 
A  single  stool  will  measure  a  little  less  than  half  a  pint  (gm.  200).  The 
stools  have  no  color  and  almost  no  odor.  They  are  watery,  and  usually  deposit 
a  finely  granular,  grayish- white  sediment  upon  standing.  Their  reaction  is 
neutral  or  alkaline.  Only  one  or  two  per  cent  is  solid  matter,  with  a  little 
albumen  and  a  relatively  large  amount  of  sodium  chlorid.  In  many  severe 
cases  the  dejections  contain  more  or  less  blood.  The  microscope  reveals  epi- 
thelium, triple  phosphate,  and  numerous  microorganisms.  Of  these  last,  a 
part  are  the  comma  bacilli,  and  a  part  are  bacteria  of  putrefaction,  etc. 

These  excessive  evacuations  are  but  very  rarely  absent.  They  are  more  apt 
to  fail  if  death  occurs  at  the  end  of  a  few  hours — cholera  sicca. 

[In  cholera  sicca  the  intestines  after  death  contain  the  characteristic  rice- 
water  material  which,  perhaps  owing  to  paralysis  of  the  muscular  coat,  was 
not  expelled  during  life.] 

The  appearance  of  the  diarrhea  is  soon  followed  by  frequent  though  rarely 
distressing  vomiting.  The  vomitus  consists  in  part  of  ingested  liquids  and 
in  part  of  an  actual  transudation  through  the  mucous  membrane  of  the  stom- 
ach and  intestine.     Hiccoughs  may  accompany  and  follow  the  emesis. 

In  addition  to  these  prominent  digestive  symptoms  of  vomiting  and  pro- 
fuse diarrhea  there  are  complete  anorexia  and  excessive  thirst.  The  tongue 
has  a  thick,  dry  coat.  The  abdomen  is  usually  flat  and  soft,  or  it  may  be  con- 
cave and  hard.  Sometimes  we  may  feel  fluctuation  in  the  intestines,  due  to 
their  being  filled  with  fluid.  There  is  not  much  real  abdominal  pain;  what 
there  is,  is  described  as  a  "  feeling  of  heat  and  pressure  "  around  the  umbilicus. 

At  the  same  time  very  severe  symptoms  develop  in  other  organs.  The  cir- 
culatory system  is  chiefly  affected. 

The  action  of  the  heart  may  be  excited  at  the  beginning  of  the  attack. 
The  patient  complains  of  palpitation  and  great  precordial  anxiety.  After  a 
brief  time,  however,  cardiac  weakness  appears,  and  continually  increases.  The 
action  of  the  heart  becomes  very  weak,  and  the  heart  sounds  feebler  and  feebler. 
The  pulse  at  the  wrist  grows  very  small,  and  is  usually  somewhat  accelerated, 


CHOLERA  103 

the  artery  narrow  and  contracted.  In  a  severe  case  the  pulse  vanishee  com- 
pletely after  a  few  hours. 

This  collapse  of  circulation  makes  itself  quickly  evident  in  the  appearance 
of  the  patient.  The  face  and  extremities  grow  cool,  ami  then  ice-cold;  the 
complexion  becomes  partly  livid  ami  pailly  a  bluish  gray;  the  lips  are  almosl 
black.  The  surface  temperature  may  Tall  below  \)~>"  F.  ('.','{'  ('.),  while  in  the 
rectum  febrile  temperatures  may  often  be  observed,  reaching  102°  V.  (39°  C.) 
and  higher.  The  eye  and  cheek  grow  very  hollow,  the  skin  becomes  wrinkled, 
and  loses  all  its  elasticity.  The  voice  grows  hoarse  and  feeble  (voice  of  chol- 
era). Eespiration  is  laborious  and  superficial.  The  mind  may  remain  un- 
clouded to  the  end,  but  usually  there  is  great  apathy,  and  all  acuteness  of 
perception  is  destroyed.  Only  a  few  patients  are  restless  and  excited.  Reflex 
action  is  much  impaired. 

One  characteristic  symptom  is  the  cramps  in  the  muscles.  These  are  usu- 
ally very  painful,  and  consist  in  tonic  contractions  of  the  muscles,  particularly 
those  of  the  calf  of  the  leg,  but  also  those  of  the  toes,  thighs,  arms,  and  hands. 
The  cramps  occur  spontaneously  or  upon  the  least  provocation,  last  a  few 
minutes,  and  recur  at  short  intervals.  They  are  to  be  regarded  as  a  direct 
effect  of  poison,  and  occur,  too,  in  other  severe  acute  enteric  diseases,  especially 
cholera  morbus. 

In  a  well-developed  attack  of  cholera  there  is  almost  invariably  oliguria  or 
anuria.  The  urine,  if  any  be  secreted,  is  concentrated,  with  abundant  sedi- 
ment, and  it  very  often  contains  albumen.  In  many  cases  not  one  drop  of 
urine  reaches  the  bladder  for  days,  and  this  condition  persists  till  death  or 
recovery. 

The  symptoms  thus  far  depicted,  if  taken  as  a  whole,  represent  the  algid 
stage,  which  seldom  lasts  more  than  one  or  two  days.  In  many  cases  death 
occurs  during  this  period.  It  is  ushered  in  by  the  tokens  of  extreme  general 
prostration,  and  may  take  place  after  a  few  hours,  or  more  frequently  in  the 
second  half  of  the  first  day.  But  in  other  cases  the  "stage  of  reaction"  suc- 
ceeds. This  may  be  a  true  compensator}^  period,  leading  directly  to  conva- 
lescence. The  evacuations  become  less  frequent  and  more  feculent,  and  the 
vomiting  ceases.  The  pulse  becomes  stronger,  the  cyanosis  and  coolness  of 
the  extremities  diminish,  and  an  abundant  perspiration  is  not  infrequent. 
After  a  few  days  urine  is  again  excreted.  This  is  almost  invariably  quite 
albuminous,  and  usually  contains  casts  and  red  blood  globules.  If  convales- 
cence be  uninterrupted,  however,  the  urine  very  soon  becomes  perfectly  nor- 
mal, and  after  a  week  or  two  recovery  is  to  be  regarded  as  complete. 

Departures  from  this  favorable  course  of  the  stage  of  reaction  are  frequent. 
Recovery  may  be  interrupted  by  repeated  relapses  into  the  previous  condition, 
sometimes  with  a  fatal  result;  instead  of  convalescence,  there  is  developed  a 
severe  third  stage,  usually  with  fever.  This  stage  ordinarily  bears  the  generic 
name  of  cholera  typhoid,  although  it  is  subject  to  manifold  variations  in  its 
clinical  symptoms  as  well  as  its  exciting  causes. 

Cholera  typhoid  may  present  an  actually  typhoidal  general  condition  with 
severe  fever.  There  is  a  considerable  elevation  of  temperature,  headache,  and 
dullness.  The  pulse  is  full  and  rapid,  the  face  flushed.  The  skin,  particularly 
that  of  the  extremities,  sometimes  presents  the  so-called  choleraic  eruption,  in 
the  form  of  an  erythema,  roseola,  urticaria,  or  the  like.    This  variety  of  chol- 


104  ACUTE   GENERAL   INFECTIOUS   DISEASES 

era  typhoid  ends  after  a  few  days  in  recovery,  or  else  passes  into  one  of  the 
following  conditions : 

A  second  form  of  cholera  typhoid  is  distinguished  by  the  development  of 
the  most  diverse  local  inflammations.  Thus,  there  may  be  a  severe  dysenteric 
or  diphtheritic  inflammation  of  the  small  and  large  intestine,  attended  by 
offensive  purulent  and  bloody  stools.  Pneumonia  is  also  possible,  as  well  as 
purulent  bronchitis,  diphtheritic  inflammation  of  the  larynx,  pharynx,  bladder, 
and  female  genitals,  parotitis,  and  sometimes  erysipelas  and  pyaemia.  And 
when  we  consider  that,  besides  all  these  conditions,  the  usual  intestinal  symp- 
toms, or  those  of  choleraic  nephritis,  may  exist  also,  it  is  evident  how  varied  the 
clinical  picture  may  be.  The  development  of  these  local  affections  frequently 
lays  the  foundation  for  numerous  sequelae. 

Choleraic  nephritis  gives  rise  to  the  third  or  uraemic  variety  of  cholera 
typhoid.  The  secretion  of  urine  is  almost  suspended.  The  region  of  the  kid- 
neys is  sometimes  sensitive  on  pressure.  The  little  urine  that  is  still  passed 
contains  numerous  casts,  albumen,  and  frequently  renal  epithelium  and  white 
and  red  blood  globules.  Somewhere  toward  the  end  of  the  first  week,  or  pos- 
sibly earlier,  there  are  grave  nervous  symptoms,  to  be  regarded  as  uraemic  :  first 
there  is  headache  and  vomiting,  then  sopor  and  coma,  or  delirium  and  con- 
vulsions.   Most  of  these  cases  are  fatal. 

Pathology  and  Pathogenesis. — We  are  now  acquainted  with  the  manifold 
symptoms  and  varieties  of  the  disease.  If  we  seek  for  the  pathological  changes 
which  control  the  process,  and  endeavor  to  find  some  correspondence  between 
them  and  the  symptoms,  we  shall  be  disappointed.  At  least,  in  its  early  stages, 
cholera  is  merely  a  severe  local  disease  of  the  intestine.  We  find  the  serous 
layer  of  the  coils  of  the  small  intestine  rose-red  from  congestion.  The  mucous 
membrane  is  in  a  state  of  catarrhal  inflammation :  it  is  swollen,  reddened,  and 
at  first  covered  with  a  layer  of  tough,  transparent  mucus;  but  very  soon  an 
abundant  transudation  flows  into  the  canal,  so  that  the  coils  of  the  small  in- 
testines are  filled  with  a  large  amount  of  clear  fluid,  looking  like  rice  water 
or  gruel,  and  so  devoid  of  bile  as  to  indicate  the  suspension  of  its  secretion. 
The  signs  of  inflammation  of  the  mucous  membrane  now  grow  more  pro- 
nounced. The  solitary  follicles  and  Peyer's  patches  become  swollen,  with 
edges  of  a  vivid  red,  and  frequently  there  are  many  small  ecchymoses  in  the 
mucous  membrane.  The  extensive  desquamation  of  the  epithelial  lining  of 
the  intestine  has  also  been  regarded  as  important,  because  it  was  considered 
as  in  part  the  cause  of  the  copious  transudation.  Still  it  may  be  questioned 
whether  the  desquamation  is  not,  at  least  to  some  extent,  a  post-mortem 
change.  In  yet  later  stages  of  the  disease  the  intestinal  trouble  very  frequently 
assumes  a  croupous-diphtheritic  character.  The  surface  is  necrosed  and  ulcer- 
ated in  many  places,  and  the  contents  of  the  intestine  are  no  longer  colorless, 
but  sanious  and  bloody,  with  a  foul  odor. 

Otherwise  most  of  the  post-mortem  lesions  correspond  to  what  was  obvious 
at  the  bedside.  The  muscles  exhibit  an  early  and  persistent  rigor  mortis,  and 
frequently  contract  in  such  a  way  as  to  throw  the  corpse  into  some  unusual 
posture.  All  the  internal  organs  are  remarkably  dry,  pale,  and  anaemic.  The 
left  ventricle  is  contracted.  The  blood  lies  mostly  in  the  large  veins,  the  right 
side  of  the  heart,  and  the  cerebral  sinuses.  It  is  thickened,  is  but  little  clotted, 
and  is  said  to  resemble  the  juice  of  bilberries  or  huckleberries.    The  spleen  is 


CHOLERA  105 

not  enlarged — an  exception   to  Ehe  rale  in  infectious  diseases.     The  kid] 
present  marked  passive  congestion,  mosl  pronounced  in  the  cortex.    The  micro 
scope  reveals  a  greater  or  less  degree  of  parenchymatous  nephritis,  with  greal 
destruction  oi'  the  epithelium.    If  death  takes  place  at  a  rather  advanced  3t: 
of  the  disease,  the  tissues  have  lost  their  characteristic  dryness,  and  the  m 
diverse  local  lesions,  including  nephritis,  may  be  found   to  have  occasioned 
death. 

If  we  search  for  the  connection  between  the  pathological  changes  just  de- 
scribed and  the  cause  of  the  disease,  or  again  between  tbese  lesions  and  the 
clinical  symptoms,  the  first  point  to  guide  us  is  that  the  comma  bacilli  are 
found  only  in  the  lumen  of  the  intestine,  and  never  in  the  blood  or  in  other 
parts  of  the  body.  The  intestinal  symptoms  are  satisfactorily  explained  by  this 
abnormal  state  of  the  intestine,  but  for  all  the  other  grave  symptoms  we  have 
to  seek  some  special  cause.  The  desiccation  which  the  body  undergoes  as  a 
result  of  the  excessive  liquid  dejections  cannot  fail  to  affect  the  tissues,  but 
cannot  fully  explain  the  symptoms,  for  the  circulator}'  disturbances  and  the 
cardiac  failure  at  least  may  develop  before  large  evacuations  have  occurred. 
It  has  also  been  settled  beyond  question  by  means  of  the  newer  investigations 
that  precisely  the  worst  symptoms  of  cholera — especially  the  cardiac  weakness 
with  its  resulting  algidity  as  well  as  the  muscular  cramps,  the  subnormal  tem- 
perature, and  probably  also  the  nephritis — are  occasioned  by  the  toxic  pro- 
teins (endotoxins)  in  the  bacteria  or  by  the  chemical  results  of  tissue  meta- 
morphosis in  the  comma  bacilli.  It  is  an  interesting  circumstance  that  the 
amount  and  virulence  of  the  toxins  formed  by  the  comma  bacilli  seem  to  de- 
pend on  the  physical  characteristics  of  the  nutrient  material  on  which  the 
culture  grows. 

As  to  the  complications  which  occur  in  the  later  stages  of  the  disease  and 
which  are  embraced  under  the  generic  name  of  cholera  typhoid,  we  regard  them 
as  mainly  secondary.  The  choleraic  process  itself  does  not  cause  them,  but  is 
merely  the  occasion  for  their  appearance.  The  examination  of  the  intestines 
in  such  cases  shows  that  numerous  other  varieties  of  bacteria  follow  closely 
upon  the  comma  bacillus,  gaining  entrance  to  the  s}rstem  by  treading  in  its 
footsteps.  Cholera  nephritis  is  probably  due  to  various  causes.  Some  forms 
of  nephritis  seem  to  be  caused  by  specific  cholera  toxins  (in  analogy  with 
scarlatinal  nephritis),  while  others  are  probably  of  a  secondary  septic  nature. 

Diagnosis. — A  positive  diagnosis  of  cholera  can  be  made  only  by  finding  the 
comma  bacilli  in  the  stools.  When  an  epidemic  prevails  it  is  often  neither 
necessary  nor  possible  to  make  the  search  in  each  individual  case.  Sporadic 
cases  or  the  first  cases  of  a  beginning  epidemic  can  and  must  be  diagnosticated 
only  in  this  way,  which  gives  absolute  certainty.  For  this  alone  shows  the 
measures  necessary  for  the  prevention  of  the  spread  of  the  disease.  We  cannot 
give  here  a  detailed  account  of  the  bacteriological  diagnosis,  but  we  may  state 
briefly  that,  when  cholera  exists,  the  simple  microscopical  examination  of  a 
smear  preparation  sometimes  makes  the  diagnosis  extremely  probable. 

The  examination  of  the  cultures,  agglutination,  and  Pfeiffer's  test  (vide 
supra)  must  also  be  considered.  The  comma  bacilli  are  also  agglutinated  by 
the  blood  serum  of  persons  who  have  had  cholera. 

All  those  affections  whose  symptoms  are  like  those  of  cholera  may  be  con- 
founded with  true  cholera,  especially  cholera  morbus   (vide  infra)  ;  and  also 


106  ACUTE  GENERAL  INFECTIOUS   DISEASES 

certain  cases  of  poisoning,  especially  acute  arsenical  poisoning,  may  give  rise 
to  symptoms  wonderfully  like  cholera, 

Prognosis. — The  prognosis  should  always  be  guarded  at  the  beginning,  even 
if  the  symptoms  be  mild,  for,  as  already  mentioned,  a  simple  diarrhea  may 
prove  to  be  "  premonitory  "  of  a  severe  attack  of  cholera.  During  the  real  at- 
tack the  prognosis  grows  graver  in  proportion  as  the  case  presents  the  character- 
istics of  asphyxia  and  cyanosis.  The  mortality  in  many  epidemics  is  frightful. 
All  the  inhabitants  of  a  house  or  street  may  in  a  brief  period  be  swept  away. 
Accurate  statistics  are  difficult  to  give.  If  we  count  the  typical  cases  alone, 
the  mortality  is  not  infrequently  fifty  to  seventy  per  cent.  In  about  two  thirds 
of  the  fatal  cases  death  occurs  during  the  first  days  of  the  stage  of  asphyxia, 
and  in  about  one  third  during  the  second  period,  known  as  "  cholera  typhoid." 
The  influence  of  the  diet  and  the  hygienic  surroundings  of  the  patient  before 
his  illness  is  important.  A  greater  proportion  of  children  and  old  people 
perish  than  of  the  middle-aged. 

Prophylaxis  and  Treatment. — The  measures  to  be  taken  to  prevent  the 
spread  of  the  disease,  when  it  has  once  started  in  a  place,  can  be  only  briefly 
discussed  here.  The  chief  things  are  the  quickest  isolation  possible  of  the  first 
cases  that  occur,  the  disinfection  of  the  stools  and  all  linen,  objects,  etc.,  soiled 
by  the  stools,  and  finally  the  determination  of  the  source  of  infection  (drinking 
water,  etc.),  in  order  to  prevent  further  infection.  The  evacuations  (stools 
and  vomitus)  can  be  best  disinfected  with  a  five-per-cent  solution  of  carbolic 
acid  or  with  milk  of  lime,  chloric!  of  lime,  etc. ;  the  linen  and  other  objects 
should  be  disinfected  in  a  special  disinfecting  apparatus.  It  is  very  important 
to  keep  a  strict  oversight  of  the  drinking  water,  milk,  and  all  articles  of  food 
eaten  in  an  uncooked  condition. 

In  regard  to  individual  prophylaxis,  we  must  remember  especially  that  any 
slight  gastric  or  intestinal  catarrh  increases  the  liability  to  the  disease.  Hence, 
at  the  time  of  a  cholera  epidemic,  careful  dietetic  restrictions  are  imperatively 
necessary  and  every  disturbance  of  the  stomach  or  the  intestines,  even  the 
slightest,  needs  the  promptest  and  most  careful  treatment.  It  is  best  wholly 
to  avoid  the  use  of  water  that  has  not  been  boiled,  raw  vegetables,  etc. 

It  has  been  proved  possible  to  attain  protective  inoculation  against  cholera 
for  one  to  one  and  a  half  years  by  injecting  attenuated  cholera  bacilli  (Haff- 
kine)  or  by  inoculation  with  small  quantities  of  cholera-agar  cultures  pre- 
viously killed  by  heating  or  by  chloroform  vapors  (Pfeiffer  and  Kolle).  But 
to  what  extent  protective  inoculation  will  assume  practical  importance  cannot 
yet  be  told. 

In  the  treatment  of  the  cholera  attack  itself  many  physicians  even  now  use 
opium  (laudanum  or  pure  opium  in  powder,  gr.  ss.-j,  gm.  0.03  to  0.05),  while 
others,  especially  at  the  beginning  of  the  disease,  prefer  large  doses  of  calomel 
(gr.  v-x,  gm.  0.3  to  0.5,  several  times),  and  during  the  subsequent  course  they 
give  continued  small  doses  of  calomel  (gr.  ss.-j,  gm.  0.03  to  0.05,  every  two 
hours).  In  the  algid  stage  warmth  is  especially  advisable.  Hot  baths,  hot 
packs,  sweat-boxes  with  dry  or  moist  hot  air,  embrocations  of  hot  oil,  an  abun- 
dant supply  of  hot  drinks  (coffee,  tea,  mulled  wine,  broths)  are  praised  by  all 
physicians,  and  they  must  certainly  be  used.  The  remaining  treatment  is 
symptomatic;  morphin  or  ice  for  the  vomiting  and  embrocations  of  chloro- 
form oil  or  subcutaneous  injections  of  morphin  for  the  painful  cramps  in  the 


MALARIAL   DISEASES  107 

calves.    The  weaker  the  heart  becomes,  the  more  energetically  must  we  . 
stimulants  (injections  of  camphor,  champagne,  caffein,  etc.). 

Among  the  newer  methods  of  treatment  tried  during  the  last  epidemic  we 
may  mention  subcutaneous  infusions  of  warm  (40°  C.)  0.6-per-cenl  sail  solu- 
tion m  the  infraclavicular  region  or  under  the  skin  of  the  upper  thigh.  Half 
to  one  liter  (quart)  of  salt  solution  can  be  infused  several  times  daily.  In- 
travenous injections  have  given  still  better  results.  Cantani  strongly  recom- 
mends intestinal  injections  (" enter ocly sis ")  with  warm  tannin  solutions  at  a 
temperature  of  100°  to  104°  F.  (38°  to  40°  C).  The  fluid  contains  5  to  10 
parts  of  tannic  acid,  50  parts  of  gum  arabic,  and  2  or  3  parts  of  Laudanum  to 
2,000  parts  of  water.  As  an  internal  remedy  lactic  acid  has  been  especially 
recommended  (acid,  lact.,  fyss.;  aq.  destil.,  §vij;  syr.  simplicis,  f,iijs.-. ;  1  or  2 
tablespoonfuls  every  hour  or  more),  also  large  doses  of  talcum  or  bolus  alba. 
All  these  methods  are  believed  to  have  shown  some  favorable  results,  but  none 
of  them  has  been  able  to  attain  general  recognition  and  use. 

[The  vital  importance  of  the  serious  treatment  of  a  beginning  diarrhea  dur- 
ing a  cholera  epidemic  cannot  be  too  strongly  insisted  on.  Rest,  simple  diet, 
and  a  little  medication  will,  in  the  vast  majority  of  instances,  entirely  prevent 
grave  consequences.  The  apparently  trifling  character  of  the  symptoms  is  apt 
to  lead  people  into  a  false  security.  Those  who  can  leave  an  infected  district 
should  do  so  without  delay. 

With  reference  to  the  prevention  of  an  epidemic,  a  pure  water  supply  and 
strict  cleanliness  in  its  broad  sense  possess  far  more  virtue  than  cordons  of 
troops  or  measures  of  quarantine.  It  is  more  practicable  to  destroy  the  soil 
than  to  keep  out  the  seed  in  these  days  of  constant  and  rapid  international 
communication.  The  systematic  disinfection  of  all  cholera  discharges  or  arti- 
cles soiled  by  them  should  be  a  matter  of  course.] 

Great  caution  must  be  exercised  about  the  diet,  not  merely  during  the  at- 
tack itself,  but  for  a  considerable  time  afterwards.  At  first  we  can  allow  only 
thin  porridge,  milk,  broths,  and  toast  or  rusks.  It  is  advisable  to  administer 
dilute  hydrochloric  acid  with  the  food. 

The  treatment  of  cholera  typhoid  varies  greatly,  of  course,  according  to 
the  kind  of  attack.  The  separate  complications  should  receive  their  customary 
treatment. 


CHAPTER    XIV 

MALARIAL    DISEASES 

(Intermittent  Fever.     Fever  and  Ague.     Swamp  Fever) 

iEtiology  and  Pathological  Anatomy. — Malarial  poisoning  is  the  best  exam- 
ple of  what  was  formerly  called  a  purely  "  miasmatic  "  affection.  The  disease 
producers  are  without  doubt  localized  in  certain  places,  in  which  every  human 
being  is  liable  to  become  its  victim;  but  if  an  infected  person  comes  to  a  place 
free  from  malaria  and  not  naturally  favorable  to  its  development,  there  is  no 
danger  that  he  will  cause  the  disease  in  others.  The  disease  is  never  caught 
through  contact  with  the  patient.     It  is  not  at  all  contagious;  the  malarial 


108  ACUTE   GENERAL  INFECTIOUS   DISEASES 

poison,  after  it  has  once  penetrated  into  the  body,  has  practically  no  oppor- 
tunity to  escape  again  in  an  efficient  form  from  the  diseased  system  into  the 
outer  world;  but  the  blood  of  a  patient  injected  into  a  healthy  person  may 
transfer  the  disease  (Gerhardt  and  others). 

If  we  except  the  polar  zones,  there  are  few  regions  where  malaria  is  not 
endemic  in  certain  parts,  at  least  from  time  to  time,  if  not  constantly.  There 
is,  however,  great  variation  in  the  virulence  as  well  as  in  the  number  of  cases. 
Moreover,  the  disease  is  in  many  places  becoming  less  and  less  frequent  because 
of  the  general  improvement  in  the  sanitary  and  social  conditions.  While  the 
common  forms  of  intermittent  fever  are  very  frequent  in  Germany,  in  numer- 
-ous  places,  especially  on  the  shores  of  the  North  and  Baltic  Seas,  and  also  in 
the  alluvial  lands  of  the  Vistula,  Oder,  Elbe,  etc.,  yet  the  grave  forms  of  the 
disease  are  very  rare.  Other  lands  are  notorious  for  the  severe  malarial  dis- 
eases— e.  g.,  Hungary,  the  lands  lying  on  the  lower  Danube,  the  Eoman  Cam- 
pagna,  the  Pontine  marshes,  Sicily,  and  numerous  districts  in  other  parts  of 
the  world,  chiefly  tropical. 

All  these  long-known  facts,  proved  by  experience,  have  been  explained  by 
the  discovery  of  the  specific  producer  of  malaria  and  the  manner  in  which  it  is 
transmitted  to  man. 

The  malaria  producer  was  first  described  by  Laveran  in  1881,  and  soon 
after  by  Marchiafava  and  Celli.  Since  then  many  other  observers,  especially 
in  Italy,  have  investigated  the  subject  and  have  given  us  very  interesting  in- 
formation about  these  peculiar  parasites.  The  real  process  of  malarial  infec- 
tion through  mosquitoes  has,  however,  only  become  known  to  us  by  Eoss's 
investigations  in  India,  incited  by  Manson,  and  by  the  later  work  of  Grassi 
in  Italy.  In  London,  where  malaria  never  occurs,  Manson  had  healthy  per- 
sons bitten  by  anopheles  previously  nourished  with  the  blood  of  malarial 
patients  in  Rome,  and  the  subjects  fell  sick  of  malaria. 

All  malarial  diseases  are  due  to  the  invasion  of  the  red  blood  corpuscles 
by  a  special  kind  of  protozoa,  the  so-called  malarial  plasmodium.  The  malaria 
producers  are  classed  among  the  sporozoa  group — i.  e.,  among  the  so-called 
hemosporiclia,  which  are  present  in  the  blood  of  numerous  animals  (frogs, 
reptiles,  birds,  mammals).  In  human  malaria,  several  related  but  not  iden- 
tical forms  must  be  considered.  We  differentiate  the  parasites  of  the  tertian 
(and  quotidian,  vide  infra),  those  of  the  quartan  and  those  of  the  severe,  per- 
nicious forms  (vide  table) . 

The  incubation  period  of  the  plasmodium  of  the  tertian  fever  is  forty- 
eight  hours.  By  staining  a  smear  of  the  patient's  blood  with  methylene  blue 
(and  numerous  other  stains  which  need  not  be  set  forth  here),  small  blue  rings 
can  be  found  in  and  on  the  red  corpuscles;  the  rings  have  a  thinner  and  a 
crescentic  thicker  half.  In  the  center  of  the  thinner  half  there  is  a  small 
nucleus.  These  bodies,  resembling  in  shape  a  signet  ring,  are  called  "  small 
tertian  rings."  After  about  twenty-four  hours  the  attacked  blood  corpuscles 
have  become  pale,  materially  larger,  irregularly  formed.  The  parasites  in  them 
have  grown  considerably,  but  still  show  a  somewhat  irregular  ring  form 
("large  tertian  rings").  They  contain  abundant  pigment  distributed  in 
very  fine  granules.  Some  parasites  have  wholly  lost  their  ring-like  shape  and 
jH-esent  the  most  varied  amoeboid  forms.  Finally,  all  parasites  grow  to  larger- 
sized  clumps  which  occupy  almost  the  entire  corpuscle.    The  pigment  in  them 


A 


5  5 


PLATE    I 


1 


B 


fto 


^^w 
*# 


■-:  / 


C 


A.— Malaria.  Large  Tertian  Parasite,  a-d,  Intracorpuscular  developmental  forms; 
e,  Plasmodium  undergoing  segmentation;  /,  macrogamet;  g,  miorogametocyte.  (/  and 
g,  sexual  types.) 

B—  Malaria.  Quartan  Parasite.  (Somewhat  schematic.)  a-e,  Intraglobular  devel- 
opmental forms;  /,  free  spores;  g,  macrogamet;  h,  miorogametocyte.     (g  and  h,  sexual 

types.) 

C— Malaria.  Severe  Tropical  Form,  a,  small;  6,  large  tropic  ring;  c  and  d,  intra- 
globular crescentic  forms;  e,  free  crescentic  form;  /,  flagellated  form.  (Microga- 
metocyte.) 


MALARIAL   DISEASES  109 

collects  more  and  more  to  single  clumps  and  rows,  until  ii  finally  agglutina 
to  one  01  two  clumps  in  the  center  of  the  parasites.  Now  numerous  individual 
stripes  appear  in  the  body  of  the  parasite  bo  thai  ii  resembles  a  raspberry. 
The  last  capsule  of  the  red  corpuscle  bursts,  and  fifteen  to  twenty-five  small 
spores  (gymnospores),  created  by  asexual  division,  swarm  into  the  Mood.  The 
spores  penetrate  into  new  red  corpuscles,  and  a  new  attack  of  fever  ens 

But  besides  this  asexual  spore  formation,  peculiar  processes,  preparatory 
to  the  other  form  of  propagation — the  sexual  form — can  be  seen  in  some  of 
the  full-grown  plasmodia  of  the  fresh  blood  preparation.  Some  plasmodia  de- 
velop to  the  so-called  gametae — i.  e.,  to  small  male  gametae  with  hyaline  plasma, 
from  which  grow  out  four  to  eight  long,  thin,  fiagella  (spermatozoa),  and  to 
larger,  fine-graniiled  female  gametae.  The  fertilization  of  flu-  female  maero- 
gametae  occurs  partly  in  the  blood,  but  still  more  in  the  stomach  of  the  female 
mosquito  (anopheles).  The  further  development  of  the  female  gametas,  how- 
ever, only  occurs  in  the  body  of  the  mosquito.  From  the  fertilized  macro- 
gametae  there  form  small,  crescentically  curved  worms  (oocinetae),  which  per- 
forate into  the  stomach  walls  of  the  insect.  After  about  two  or  three  days 
they  grow  up  to  so-called  oocysts,  which  after  a  further  two  to  three  days 
show  in  their  interior  numerous  small  globes  (daughter  cysts,  sporoblasts). 
Finally,  the  oocyst  is  filled  with  innumerable  small  crescentic  germs,  which  in 
their  turn  have  been  generated  in  the  sporoblasts.  Xow  the  cysts  burst,  the 
crescentic  germs  get  into  the  peritoneal  cavity,  and  thence  by  way  of  the 
lymphatic  stream  into  the  salivary  glands  of  the  mosquitoes,  where  they  are 
demonstrable  in  enormous  numbers  about  eight  to  ten  days  after  the  insects 
have  sucked  the  blood.  By  the  sting  of  such  insects  crescentic  germs  are 
transferred  into  the  blood  of  the  bitten  person.  From  them  there  develop,  in 
a  manner  not  yet  fully  known,  the  malaria  plasmodia  which  cause  the  febrile 
attacks. 

The  parasite  of  quartan  fever  shows  at  first  quite  the  same  form  as  the 
small  tertian  rings  (vide  supra).  But  after  twenty-four  hours  the  ring  trans- 
forms itself  into  a  pigmented  band,  which  goes  diagonally  across  the  blood 
corpuscles  and  materially  expands  in  the  next  twenty-four  hours.  The  at- 
tacked blood  corpuscles  otherwise  retain,  their  usual  size  and  coloration. 
Finally,  the  parasite  entirely  occupies  the  blood  corpuscle  and  breaks  up.  The 
entire  development  takes  seventy-two  hours.  With  it  there  occur  gametae  for- 
mation and  sexual  propagation  in  the  mosquito's  stomach,  entirely  analogous 
to  what  has  just  been  described  for  the  tertian  parasite. 

The  parasite  of  tropical  fever  forms  small  rings  which  enlarge  in  the  course 
of  the  fever  ("  small  "  and  "  large  tropic  rings  ") .  The  blood  corpuscles  them- 
selves do  not  become  larger  and  paler.  The  gametae  of  the  tropic  parasites 
appear  in  the  form  of  small  moon  crescents.  We  cannot  here  discuss  the 
numerous  interesting  details. 

By  the  discovery  of  the  important  role  which  the  mosquito  plays  in  the 
spread  of  malaria,  a  mass  of  epidemiologic  facts  regarding  the  occurrence  of 
the  disease  have  at  once  been  cleared  up.  We  know  that  only  the  anopheles  can 
transmit  the  disease,  not  the  culex  varieties.  It  is  further  noteworthy  that 
only  the  female  anopheles  subsist  on  blood,  and  therefore  can  transmit  the 
malaria.  Only  where  temperature  and  moisture  conditions  satisfy  the  life 
needs  of  the  anopheles  can  malaria  develop.     Where  levees  are  drained  and 


110  ACUTE   GENERAL   INFECTIOUS   DISEASES 

the  mosquitoes  disappear,  there  malaria  ceases.  Only  where  mosquitoes  can 
be  the  agents  of  transmission  is  the  importation  of  the  disease  by  a  malaria 
patient  into  a  malaria-free  region  possible.  As  mosquitoes  exist  only  in  the 
warm  season,  malaria  is  chiefly  a  summer  disease.  It  has  long  been  known 
that  in  malarial  regions  it  is  especially  dangerous  to  spend  the  night  in  the 
open  air  or  to  sleep  with  open  windows.  This  is  at  once  explained  by  the  fact 
that  mosquitoes  bite  only  at  night.  The  mosquitoes  do  not  fly  very  high  above 
ground;  this  agrees  with  the  fact  long  taught  by  experience  that  it  is  par- 
ticularly dangerous  to  sleep  on  the  ground,  and  much  less  so  in  elevated  places. 
Everything  which  protects  from  the  mosquito — nets,  fires,  etc. — also  protects 
from  malaria.  When,  through  a  universal,  thorough  treatment  with  quinin 
(vide  infra),  the  plasmodia  in  the  blood  of  the  human  beings  in  a  district  are 
destroyed,  the  sickness  is  more  and  more  restricted,  despite  the  most  numerous 
anopheles. 

To  all  appearances  the  malarial  plasmodium  and  its  various  stages  of  de- 
velopment cannot  long  maintain  a  separate  existence  outside  the  human  body 
and  the  mosquito's  body.  This  fact  affords  the  best  security  that  gradually 
it  will  be  possible  to  exterminate  malaria.  The  period  of  incubation,  from 
the  time  of  the  infection  by  the  anopheles'  bite  till  the  first  attack  of  fever, 
lasts  at  least  five  to  six  days,  but  may  take  as  long  as  twenty-one  days.  Suscep- 
tibility to  the  disease  is  very  general.  No  race,  no  age,  no  sex  is  immune  from 
malaria. 

The  investigations  with  regard  to  the  plasmodium  of  malaria  have  also 
explained  the  long-recognized  fact  that  in  chronic  malaria  large  amounts  of 
pigment  collect  in  the  internal  viscera.  The  pigment  is  a  metabolic  product 
of  the  parasites  and  arises  from  the  hemoglobin  of  the  attacked  red  blood 
corpuscles.  The  liberated  pigment  is  taken  up  by  the  leucocytes  and  depos- 
ited in  the  inner  organs.  These  deposits  are  most  abundant  in  the  spleen, 
which  in  the  chronic  varieties  of  the  disease  develops  into  a  firm,  hard  tumor ; 
but  they  are  also  found  in  the  bone  marrow,  liver,  brain,  and  kidneys,  leading 
finally  in  the  liver  and  the  kidneys,  in  frequent  instances,  to  processes  of 
chronic  degeneration  and  inflammation.  It  is  especially  noteworthy  that  in 
those  patients  who  present  the  most  marked  cerebral  disturbances  (perni- 
cious comatose  fever,  vide  infra),  the  cerebral  capillaries  are  found  to  be  com- 
pletely occluded  with  pigmented  plasmodia. 

[Periodical  fever  is  very  widely  distributed  in  the  United  States,  and  in 
the  southern  portions  occurs  in  severe,  though  not  in  the  severest,  forms.  Some 
regions  which  were  formerly  free  from  it  are  no  longer  so,  and,  vice  versa, 
some  regions  which  were  greatly  subject  to  it  are  now  exempt. 

The  hopes  which  have  been  entertained  in  some  quarters  that  malarial 
regions  might  be  rendered  healthy  by  large  plantations  of  the  Australian  euca- 
lyptus globulus,  a  rapidly  growing  tree  which  absorbs  immense  quantities  of 
water,  do  not  seem  likely  to  be  realized  in  the  light  of  French  experience  in 
Africa,  and  in  that  of  the  Trappist  monks  in  Italy. 

The  following  details  may  be  of  use  to  those  who  are  not  familiar  with 
the  method  of  blood  examination :  The  finger  tips  should  first  be  scrubbed 
with  a  nailbrush,  and  soap  and  water,  and  then  washed  in  alcohol  or  ether, 
to  obviate  the  danger  of  mistaking  minute  particles  of  dirt  for  the  pigment- 
granules  derived  from  the  destruction  of  red  blood  corpuscles.     A  portion  of 


MALARIAL   DISEASES  111 

a  drop  of  blood  is  then  to  be  received  on  a  scrupulously  clean  object-  or  cover- 
glass,  and  squeezed  out  between  the  two,  so  that  a  thin  layer  of  blood  with 

separation  of  the  individual  corpuscles  is  seemed.  The  amoeboid  form-  of 
the  plasmodium  retain  their  movements  for  a  number  of  minutes  in  a  warm 
room,  much  longer,  of  course,  with  a  warm  stage.  The  presence  of  pigment- 
granules  in  the  red.  corpuscles  may  be  the  readiest  indication  of  the  presence 
of  the  organism.  The  crescentic  forms  are  found  more  especially  in  chronic 
cases  which  have  been  under  treatment  by  quinin,  as  is  stated  by  Osier.  Many 
of  the  other  forms  can  be  found  in  the  blood  only  during  a  paroxysm. 

In  dried  and  stained  specimens  it  is  also  possible  to  detect  the  organisms, 
but  amoeboid  movement  is,  of  course,  lost.] 

We  shall  consider  below  chiefly  the  common  forms  of  intermittent,  such 
as  appear  in  Germany,  contenting  ourselves  with  a  very  brief  description  of  the 
severer  forms. 

Varieties  of  Malarial  Disease. — 1.  Intermittent  Fever. — This  is  the 
simplest  and  most  frequent  form,  and  has  for  its  especial  characteristic  the 
relative  brevity  of  the  febrile  attacks,  which  almost  always  exhibit  a  remark- 
ably uniform  type.  A  febrile  attack  of  this  kind  is  frequently  the  very  first 
symptom  of  the  disease.  In  other  cases  the  paroxysm  of  fever  is  preceded 
by  a  prodromal  stage  lasting  several  days,  during  which  the  patient  feels 
languid,  has  no  real  appetite,  complains  of  headache  and  pain  in  the  back  of 
the  neck  and  in  the  limbs,  and  often  even  thus  early  presents  a  slightly  yel- 
lowish complexion  and  an  enlarged  spleen. 

In  the  typical  attack  of  intermittent  fever  there  are  three  stages.  The 
attack  begins  with  a  chill.  There  is  pronounced  malaise,  attended  by  intense 
chilliness  and  more  or  less  shivering.  The  skin  is  cool  and  pale,  the  face  may 
be  somewhat  livid.  The  temperature  of  the  interior  of  the  body  is  elevated, 
and  rapidly  rises  higher.  In  by  far  the  greater  number  of  cases  the  attack 
occurs  in  the  morning,  or  at  least  before  noon,  and  but  seldom  later  in  the 
day.  This  cold  stage  varies  greatly  in  length,  usually  lasting  an  hour 
or  two. 

The  chilliness  is  followed  by  the  hot  stage.  The  skin  grows  burning  hot, 
the  face  flushes,  the  pulse,  which  was  before  small,  becomes  full,  and  the  action 
of  the  heart  is  excited.  At  first  the  temperature  continues  to  increase,  and 
reaches  in  this  stage  its  maximum  for  the  attack.  It  is  exceptional  for  it  to 
remain  under  104°  F.  (40°  C),  and  by  no  means  rare  for  it  to  touch  106°,  or 
even  107°  F.  (41°  to  41.5°  C).  This  stage  almost  always  lasts  longer  than  the 
preceding,  generally  about  three  to  five  hours.  The  temperature  may  begin  to 
fall  as  early  as  the  latter  part  of  the  hot  stage,  but  may  persist  till  the  begin- 
ning of  the  third  stage. 

In  this  sweating  stage  the  skin  grows  moist,  and  there  is  soon  a  profuse 
general  perspiration.  The  patient  begins  to  feel  much  better.  In  a  few  hours 
the  temperature  usually  becomes  normal,  and,  after  lasting  in  all  about  eight 
to  twelve  hours,  the  attack  is  over.  It  may  be  shorter  or  rarely  longer.  Usu- 
ally, however,  the  temperature  keeps  on  sinking  slowly,  so  as  to  be  still  subnor- 
mal even  on  the  next  morning,  perhaps  not  above  97°  F.  (36°  C). 

There  are  certain  peculiarities  in  the  temperature  curve  which  we  have 
ourselves  observed.  The  elevation  of  temperature  is  almost  invariably  more 
rapid  than  its  decline.    The  rise  is  most  abrupt  during  the  first  hours  of  the 


112 


ACUTE  GENERAL  INFECTIOUS  DISEASES 


cold  stage,  and  slower  during  the  first  portion  of  the  hot  stage.  The  ascent 
is  but  very  seldom  interrupted.  During  the  hot  stage,  when  the  fever  is 
highest,  in  the  neighborhood  of  106°  F.  (41°  C),  there  are  not  infrequently 
two  little  summits  to  the  fever  curve,  if  the  temperature  be  taken  at  short 
intervals.  But  the  temperature  may  for  hours  remain  the  same.  The  tem- 
perature generally  begins  to  fall  some  little  time  before  the  perspiration  is 
evident.  The  decline  is  slow.  It  may  be  perfectly  continuous,  or  it  may  be 
interrupted  by  fresh  elevations,  which  are  sometimes  slight  and  sometimes 
considerable.  In  many  cases  the  descent  is  by  steps,  the  temperature  remain- 
ing the  same  for  half  an  hour  or  an  hour,  and  then  abruptly  falling  a  couple 
of  degrees  and  remaining  for  a  time  at  this  new  level. 


41.0° 


40.0° 


39.0° 


38.0° 


37.0° 


36.0° 


41.0° 


40.0° 


39.0° 


38.0° 


37.0° 


36.0° 


Fig.  19. — Quotidian  intermittent  fever. 


Fig.  20. — Tertian  intermittent  fever. 


The  chief  characteristic  is  not,  however,  the  nature  of  the  single  attacks, 
but  the  peculiar  manner  of  their  repetition.  If  the  case  is  not  under  treat- 
ment, the  single  attacks  keep  recurring  for  a  long  time  every  second  day. 
This  type  of  tertian  intermittent  fever  (cf.  Figs.  19  and  20)  is  probably  the 
most  frequent.  Not  infrequently  daily  attacks  of  fever  occur  (quotidian  inter- 
mittent). But  this  quotidian  fever  is  nothing  more  than  a  double  infection 
with  tertian  parasites,  the  attacks  being  caused  by  two  different  generations. 
If  there  are  two  attacks  in  one  day,  a  rare  event  among  us,  we  have  a  double 
quotidian.  If  there  is  a  violent  attack  every  second  day,  and  on  the  inter- 
vening days  there  are  milder  attacks,  it  is  a  case  of  double  tertian.  Very 
often  the  attacks  do  not  recur  at  just  the  same  time  of  day,  but  a  few  hours 
earlier  each  time.  Less  frequently  they  are  later.  This  peculiarity  is  expressed 
by  the  term  "  anticipating "  or  "  retarding,"  as  the  case  may  be — e.  g.,  a 
retarding  tertian  ague.  In  cases  of  long  standing,  the  paroxysms  may  finally 
lose  all  regularity,  so  that  the  fever  is  described  as  "  erratic." 

All  these  irregularities  of  the  fever  are  certainly  related  to  variations  in 
the  development  of  the  parasites  and  their  several  generations.  The  typical 
intermittent  quartan  fever,  in  which  the  attacks  appear  only  after  seventy- 


MALARIAL   DISEASES  I  L3 

two  hours  each  time,  owe  their  occurrence  to  a  special  variety  of  the  parasites 
(the  quartan  parasites,  vide  supra). 

Next  to  the  febrile  attacks,  the  swelling  of  the  spleen  is  the  mosl  constant 
and  important  symptom.  It  is  usually  considerable  and  capable  of  demon- 
stration by  percussion  and  palpation.  At  first  the  tumor  increases  with  every 
fresh  attack,  and  diminishes  but  little  during  the  intervals.  After  the  patient 
is  freed  from  his  attacks  of  fever  the  spleen  may  continue  enlarged  for  some 
time.  It  is  tender  on  pressure.  [Certainly  in  many  cases  tenderness  is 
absent. — V.]  The  liver  may  likewise  be  swollen,  but  this  is  less  constant  and 
also  less  important. 

Certain  changes  in  the  skin  are  very  characteristic,  chief  among  which  is 
a  peculiar  yellowish-brown  discoloration.  This  is  due  to  an  abnormal  deposi- 
tion of  pigment  in  the  skin.  Herpes  on  the  lips  or  nose  is  seen  very  fre- 
quently during  the  attacks.  We  have  seen  one  case  of  herpes  on  the  eornea. 
Mention  has  also  been  made  of  urticaria,  purpura,  and  other  eruptions. 

Other  internal  organs  than  those  already  spoken  of  are  rarely  much  dis- 
turbed. One  symptom  should  be  mentioned,  which  we  have  ourselves  seen 
several  times,  viz.,  a  quite  marked  acute  dilatation  of  the  heart  during  the 
attack.  There  were  no  bad  results,  and  the  normal  condition  was  soon  rees- 
tablished. We  may  hear  during  the  attack  functional  cardiac  murmurs  of  a 
blowing  character.  Thoracic  examination,  particularly  if  made  during  the 
attack,  may  afford  signs  of  a  dry  bronchitis.  Sometimes  there  is  considerable 
diarrhea,  or  other  evidence  of  intestinal  derangement.  Catarrhal  jaundice  is 
confined  to  the  severer  cases.  Sometimes  the  urine  has  a  moderate  amount  of 
albumen.  Genuine  nephritis  is  met  with  only  in  the  graver  varieties  of  the 
disease.  The  increased  excretion  of  urea  on  the  days  of  the  fever  results,  as 
in  any  fever,  from  the  increased  destruction  of  albumen.  Severe  pain  in  the 
cervical  and  upper  dorsal  vertebrae  is  regarded  as  characteristic  of  intermittent. 

Besides  the  typical  attacks,  rudimentary  and  modified  ones  are  not  rare, 
in  which  the  separate  stages  are  ill  defined,  or  in  part  wanting.  We  are  most 
apt  to  see  this  in  cases  which  have  been  already  treated  with  quinin.  Chil- 
dren do  not  have  a  true  rigor.  They  merely  become  pale  or  livid.  They  may 
present  marked  nervous  symptoms. 

2.  Pernicious  Intermittent  Fever. — The  malarial  fever  caused  by  tropic 
parasites,  briefly  described  above,  also  runs  its  course  in  single  attacks,  but 
these  often  last  for  a  long  time  and  occasionally  occur  in  such  rapid  succes- 
sion that  an  almost  continual  fever  results.  The  single  stages  of  the  febrile 
attack  are  not  so  sharply  defined  as  in  the  ordinary  intermittent  form.  The 
splenic  swelling  develops  only  in  the  later  course  of  the  disease,  while  from 
the  beginning  a  severe  anaemia  is  prominent.  The  severer  forms  of  pernicious 
fever  appear  especially  through  relapses  or  with  renewed  infections.  Pro- 
nounced nervous  symptoms  are  most  frequent.  There  may  be  unconsciousness, 
coma,  delirium,  or  epileptiform  or  tetanic  convulsions.  None  of  these  symp- 
toms persists  longer,  as  a  rule,  than  does  the  common  sort  of  an  attack,  and  in 
a  favorable  case  they  vanish  completely  when  the  sweating,  which  is  usually 
profuse,  begins.  The  great  danger  comes  from  the  recurrence  of  the  attacks. 
A  second  form  of  pernicious  intermittent  fever  causes  violent  gastro-intestinal 
symptoms,  which  may  almost  exactly  imitate  the  algid  stage  of  cholera,  with 
vomiting,  diarrhea,  and  collapse;  or  there  may  be  severe  cardialgia,  dysentery, 


114  ACUTE   GENERAL   INFECTIOUS   DISEASES 

and  the  like.  In  the  so-called  pernicious  intermittent  with  jaundice,  intense 
jaundice  appears  during  the  attack,  with  vomiting  and  diarrhea,  and  some- 
times the  gravest  nervous  symptoms.  Eelated  thereto  is  the  pernicious  biliary 
hemoglobinuric  fever,  a  severe  form  of  malaria  especially  prevalent  in  West 
and  East  Africa,  characterized  by  icterus,  severe  gastric  symptoms,  and 
marked  hemoglobinuria ;  hence  the  name  "  black-water  fever."  As  Koch  has 
shown,  similar  phenomena  can  be  caused  in  predisposed  persons  by  large  doses 
of  quinin. 

[The  pernicious  form  occurs  in  isolated  cases  wherever  the  ordinary 
variety  of  the  disease  prevails,  but  is  much  more  common  in  the  Southern 
and  Western  States,  and  there  varies  in  frequency  in  different  years.  Period- 
icity in  the  attack  is  not  always  observed.  The  pernicious  character  is  not 
always  manifested  in  the  first  attack,  one  or  more  mild  paroxysms  being  often 
precedent.  In  this  country  the  algid  form  of  pernicious  periodic  fever  is  often 
called  "  congestive  chills,"  and  this  form  is  more  common  than  the  comatose 
or  another  form  mentioned  by  the  author — the  hemorrhagic.  In  the  latter 
the  blood  escapes  from  the  kidneys,  and  less  constantly  from  the  mucous 
membrane.  During  the  civil  war  the  mortality  among  the  white  soldiers  of 
the  United  States  army  from  pernicious  malarial  fever  was  23.91  per  cent.] 

3.  Chronic  Malarial  Cachexia. — In  the  true  malarial  regions  indi- 
viduals who  have  frequently  suffered  from  pronounced  intermittent  and  remit- 
tent malarial  fever  may  also  acquire  a  chronic  diseased  condition,  appearing 
sometimes  under  most  diverse  forms  and  being  due  to  the  chronic  malarial  in- 
fection. These  patients  usually  show  marked  anasmia  and  a  decided  yellowish 
malarial  complexion.  Occasionally  real  febrile  attacks  do  not  occur  at  all, 
but  there  exist  only  symptoms  of  general  debility,  anorexia,  nausea,  tendency 
to  diarrhea,  or,  more  rarely,  constipation,  a  feeling  of  fullness  in  the  head, 
insomnia,  frequent  perspiration,  muscle  and  joint  pains,  dyspnoea,  palpitation, 
etc.  In  other  cases  these  symptoms  are  aggravated.  Severe  nervous  phe- 
nomena, as  trembling,  paralyses,  psychic  disturbances,  intestinal  symptoms,  or 
icterus  may  occur.  Dropsical  conditions  develop,  and  epistaxis,  ecchymoses, 
and  scorbutic  symptoms  have  been  observed.  Examination  of  the  inner  organs 
often  shows  large,  firm,  splenic  tumor  and  hepatic  enlargement.  Ascites  oc- 
curs but  rarely.  In  some  cases  irregular  febrile  conditions  still  occur  (chronic 
malarial  fever),  but  in  their  blood  plasmodia  are  demonstrable  only  with 
difficulty  and  in  small  numbers.  Finally,  secondary  diseases  are  possible — e.  g., 
tuberculosis,  amyloid,  or  dysentery — and  these  may  prove  the  immediate  cause 
of  death.  The  milder  forms  may  be  cured,  but  seldom  unless  the  patient 
abandons  forever  the  malarial  district. 

4.  Masked  Intermittent. — This  is  the  designation  of  cases  in  which,  al- 
though there  is  no  fever,  certain  other  disturbances  arise  in  regular  intermit- 
tent attacks.  Chief  among  these  is  neuralgia.  Its  favorite  seat  is  the  supra- 
orbital branch  of  the  trigeminus.  It  may  occur  in  the  other  branches  of  the 
same  nerve,  or  in  the  sciatic,  the  anterior  crural,  the  nerves  of  the  brachial 
plexus,  and  elsewhere.  Cardialgia  and  enteralgia  may  occur  in  the  same  way. 
These  attacks  last  from  thirty  minutes  to  several  hours,  and  are  frequently 
associated  with  all  sorts  of  constitutional  symptoms,  but,  as  we  have  said,  are 
afebrile.  There  may  be  a  splenic  tumor,  which  aids  diagnosis;  but  this  sign 
may  be  wanting. 


MALARIAL   DISEASES  115 

Numerous  other  Intermittenl   disorders   besides   neuralgia  have  been   de 
scribed  as  masked  intermittent.     The  list  includes  gastric  and  intestinal 
turbances,  cramps,  bleeding,  etc.     We  musl  add,  however,  thai  those  who  have 
described  diseases  of  this  sort,  some  of  which  seem  3trange  enough,  have  no! 
always  been  us  critical  as  they  ought,  and  thai  the  connection  between  many 
cases  of  "masked  intermittent  "  and  true  malaria  is  more  than  doubtful,  par- 
ticularly as  Hie  demonstration  of  the  plasmodium  in  the  blood  in  cases  of 
called  "masked  malaria  "  is  almosl   never  possible. 

[5.  Typho-Malabial  Fever. — This  is  a  term  which  was  formerly  in  use, 
but  it  is  not  a  distinct  disease.  It  expresses  a  combination  in  the  same  indi- 
vidual at  the  same  time  of  the  effects  of  the  special  poison  causative  of  each 
affection.  Typhoid  being  a  continued  fever,  its  complication  with  malaria 
results  in  a  pyrexia  of  a  remittent  type.  The  combination  of  the  two  occurs 
in  malarial  regions,  especially  in  the  Southern  State-,  and  may  be  seen  in 
nonmalarial  regions  in  the  persons  of  those  in  whom  malaria,  contracted  else- 
where, is  in  a  more  or  less  active  state. 

The  characteristic  symptoms  of  Hie  two  diseases  arc  intermingled,  those  of 
typhoid,  the  graver  disease,  usually  predominating.  The  history  of  the  case 
and  careful  observation  of  the  symptoms  will  generally  clear  up  any  douhts 
felt  as  to  the  diagnosis  in  the  early  stages.  It  would  naturally  he  supposed 
that  the  combined  affections  must  produce  an  illness  more  severe  in  character 
and  more  unfavorable  as  regards  prognosis  than  belongs  to  simple  typhoid. 
Such  does  not,  however,  seem  to  be  the  case.  Woodward's  statistic-  .-how  that 
the  mortality  of  uncomplicated  typhoid  was  far  greater  among  the  white  and 
colored  troops  alike  during  our  late  Civil  War  than  was  the  mortality  of  typho- 
malarial  fever. 

The  treatment  as  regards  the  typhoid  fever  differs  in  no  way  from 
that  suitable  for  cases  of  the  ordinary  affection;  the  periodic  element 
demands  the  management  appropriate  to  simple  intermittent  or  remittent 
fever.] 

Diagnosis. — It  is  often  very  difficult  to  diagnosticate  a  case  of  intermittent 
fever  at  the  first  visit,  particularly  in  a  place  where  malarial  poisoning  is  in- 
frequent. The  history  of  the  case  is  not  always  enough  to  put  one  on  the 
right  track ;  and  a  single  examination  of  the  patient  may  prove  equally  nega- 
tive in  its  practical  results,  whether  it  is  made  during  the  febrile  stage  or  in 
the  interval.  Continued  observation,  however,  will  almost  always  disclose  the 
regularity  of  the  febrile  attacks,  the  splenic  tumor,  the  characteristic  com- 
plexion, and  the  herpes;  and  our  diagnosis  becomes  evident.  Still,  it  is  not 
very  exceptional  for  an  intermitting  fever  to  be  taken  at  first  for  an  intermit- 
tent malarial  one,  while  eventually  some  quite  different  disease  is  found  to 
produce  the  symptom.  Pyaemia  may  give  rise  to  mistakes  of  this  kind;  also 
purulent  phlebitis,  acute  ulcerative  endocarditis,  and  even  tuberculosis.  We 
should  be  very  cautious  in  making  a  hasty  diagnosis  of  "  irregular  intermittent 
fever."  Our  own  experience  has  taught  us  that  almost  invariably  the  case 
turns  out  to  be  something  else.  Where  there  is  doubt  we  may,  in  addition 
to  a  careful  consideration  of  all  the  symptoms  and  a  thorough  physical  ex- 
amination, be  aided  by  the  therapeutic  action  of  quinin  (vide  infra).  If  a 
high  fever  of  intermitting  type  is  affected  by  large  doses  of  quinin  but  tem- 
porarily if  at  all,  then  a  diagnosis  of  malarial  intermittent  fever  is  rendered 


116  ACUTE  GENERAL  INFECTIOUS  DISEASES 

doubtful.  An  absolutely  certain  diagnosis  can  be  made  only  by  finding  the 
plasmodia  in  the  blood  under  the  microscope. 

After  due  practice  and  by  the  use  of  lenses  of  sufficient  magnifying  power, 
the  parasites  may  frequently  be  recognized  in  the  unstained  blood.  The 
preparation  should  be  thin.  Staining  with  methylene  blue  and  eosin  brings 
out  the  structure  more  clearly.  We  have  already  said  that  the  greatest  skep- 
ticism is  requisite  in  the  diagnosis  of  "  masked  intermittent." 

Treatment. — Malarial  poisoning  is  one  of  the  few  diseases  upon  which  we 
can  make  a  direct  attack  with  assured  success.  In  quinin  we  possess  a  remedy 
which  probably  acts  upon  the  very  cause  of  the  disease,  and  its  therapeutic 
efficacy  is  undisputed.  Quinin  is  therefore  the  sovereign  remedy  in  all  forms 
of  malarial  poisoning,  and  is  often  the  only  drug  employed.  In  the  mild  cases, 
which  are  the  only  kind  that  occur  in  Germany,  we  do  not  usually  give  the 
remedy  upon  the  instant  that  the  patient  comes  under  treatment.  It  is  best 
to  wait  for  one  or  two  attacks,  partly  to  make  sure  of  our  diagnosis,  and  partly 
to  learn  what  the  type  of  the  fever  is,  whether  quotidian,  tertian,  anticipating, 
or  recurring  at  the  same  hour;  and  in  most  cases  this  delay  works  no  harm 
to  the  patient.  During  the  attack  itself  there  is  seldom  any  use  in  special 
treatment.  Of  course,  the  patient  must  stay  in  bed  and  be  kept  warm  during 
the  cold  stage,  and  have  lighter  coverings  during  the  hot  stage.  During  the 
afebrile  interval  the  patient  may  be  up  if  he  feels  strong  enough  and  is 
careful.  Quinin  (hydrochlorate  or  sulphate)  is  given  about  five  or  six  hours 
before  the  next  attack  is  due.  It  is  best  to  administer  one  large  dose  of  20 
to  30  gr.  (gm.  1.5  to  2),  either  in  solution  or  in  capsules  of  7  gr.  (gm.  0.5) 
each.  If  the  quinin  be  given  in  powder  or  capsules,  it  is  a  good  way  to  follow 
it  with  a  few  drops  of  muriatic  acid,  to  promote  its  solution  in  the  stomach. 
Often  one  large  dose  prevents  the  next  attack.  In  other  cases  it  does  occur, 
but  with  less  subjective  disturbance,  no  chill,  and  more  moderate  fever.  We 
must  then  give  another  large  dose  before  the  second  attack  is  expected.  If 
the  attack  does  not  take  place,  then  we  may  give  for  several  days  quinin  to 
the  amount  of  8  gr.  (gm.  0.5)  per  diem.  After  all,  relapses  are  possible,  even 
at  the  end  of  several  weeks ;  but  they  yield  readily  to  quinin. 

The  substitutes  for  quinin  proposed  in  various  quarters — conchinin,  cin- 
chonidin,  euquinin,  etc. — have  proved  to  be  less  effective. 

In  the  treatment  of  pernicious  intermittent  fever,  of  the  masked  forms,  of 
the  remittent  and  continued  fevers,  the  chief  remedy  is  likewise  quinin,  given 
in  sufficient  doses.  Baccelli  has  shown  that  sometimes  in  pernicious  fever  the 
direct  injection  of  quinin  into  a  vein  may  save  life.  Much  less  reliable  is 
methylene  blue,  four  to  six  times  daily,  gm.  0.1  (gr.  jss.),  in  gelatin  capsules. 
In  all  cases  of  considerable  duration  it  is  also  of  the  greatest  importance  to 
remove  the  patient  from  the  malarial  region,  if  it  can  possibly  be  done.  This 
often  proves  to  be  the  only  way  to  avoid  relapses  and  attain  a  perfect 
cure. 

In  cases  of  longer  standing,  quinin  sometimes  loses  its  power.  Then  we 
resort  to  arsenic.  It  is  frequently  employed  in  malarial  cachexia  and  in 
intermittent  neuralgia,  either  alone  or  combined  with  iron.  We  give  gtt.  v 
to  viij  of  Fowler's  solution  two  or  three  times  a  day  in  water.  It  is  still 
better  to  give  pills  of  arsenious  acid  containing  -^  to  ^V  gr.  (gm.  0.002  to 
0.003)    and  gradually  increasing  to  a  daily  dose  of  £  to  i  gr.    (gm.  0.01 


MALARIAL    DISEASES  117 

to  0.012).    That  careful  symptomatic  and  dietetic  treatment  is  also  essential 

is  a  matter  of  course. 

■  [There  is  nothing  to  be  gained  by  allowing  a  patient  to  have  an  unneces- 
sary chill.  If  there  is  a  reasonable  probability  that  bis  paroxysms  are  due  to 
malaria,  a  prompt  efforl  should  be  made  to  cut  them  short.  Four  bom 
the  shortest  time  that  it  is  safe  to  allow  for  quinin  by  the  stomach  with 
probability  that  tbe  expected  chill  will  be  prevented.  The  drug  acts  much 
more  promptly  when  given  hypodermic-ally.  The  hydrobromate  is  preferred 
by  some  to  the  sulphate  for  subcutaneous  use  on  account  of  the  necessity  of 
using  acid  to  dissolve  the  latter,  and  the  consequenl  risk  of  abscess.  Such  a 
risk  should  have  no  weight  if  the  physician  has  any  suspicion  that  he  has  to 
deal  with  the  pernicious  form  of  the  disease.  If  the  stomach  is  irritable, 
the  remedy  can  be  given  by  enema.  Quinin  can  also  be  given  by  supposi- 
tory, though  it  may  thus  produce  some  irritability  of  the  rectum;  but  the 
impossibility  of  disguising  the  bitter  taste  of  the  remedy  or  of  making  chil- 
dren swallow  capsules  renders  this  a  valuable  means  of  treatment  sometimes 
in  infants  and  young  children. 

Warburg's  tincture  is  an  antiperiodic  which  does  good  service  in  cases 
which  do  not  yield  to  the  ordinary  methods  of  treatment. 

The  hypodermic  injection  of  pilocarpin  is  reported  to  abort  an  impending 
chill. 

Some  prefer  divided  and  smaller  to  the  single  and  large  dose  of  quinin  or 
one  of  its  substitutes,  a  difference  of  view  which  is  of  minor  importance. 

In  the  remittent  forms  boldness  in  the  use  of  quinin  is  required.  Cinchon- 
ism  should  be  induced  as  promptly  as  may  be,  and  maintained  to  a  mild  degree 
for  several  days;  the  quantity  of  the  drug  can  then  be  gradually  diminished. 

The  treatment  of  the  pernicious  forms  of  periodic  fever  presents  itself 
under  three  main  heads : 

1.  The  prevention  of  pernicious  paroxysms. 

2.  The  treatment  of  the  paroxysms  when  present. 

3.  The  prevention  of  a  recurrence. 

1.  We  have  seen  that  very  frequently  the  pernicious  character  is  manifested 
after  the  occurrence  of  one  or  more  mild  attacks ;  consequently,  in  localities  and 
seasons  marked  by  the  occurrence  of  grave  cases  it  is  an  imperative  duty  to 
treat  every  mild  case  promptly  and  energetically,  a  course  which  unquestion- 
ably saves  many  a  life. 

2.  The  management  of  the  paroxysm  differs  according  to  the  form  which  it 
assumes;  in  other  words,  is  largely  symptomatic.  Bemiss  (Pepper's  "  System 
of  Medicine")  says:  "The  cure  of  a  congestive  chill  is  one  of  the  most  dif- 
ficult problems  the  physician  can  possibly  encounter."  Heat  externally,  opium 
and  chloroform  by  the  mouth,  and  morphin  and  atropin  subcutaneously,  nutri- 
tion b}r  the  stomach  or  rectum,  according  to  circumstances,  and  alcoholics  if 
the  action  of  the  heart  is  feeble,  are  the  measures  of  widest  application. 

Whatever  the  type  of  the  attack,  a  weak  heart  calls  for  alcoholic  stimula- 
tion.    Cinchonism  is  always  to  be  induced  as  rapidly  as  possible. 

In  the  comatose  form  it  is  to  be  remembered  that  the  cerebral  and  other 
nervous  symptoms  are  not  due  to  congestion,  but  probably  to  a  combination 
of  the  malarial  and  secondary  blood  poisons.  To  quote  Bemiss  again :  "  Efforts 
to  nourish  the  patient  must  never  be  relaxed.     One  must  see  many  of  these 


118  ACUTE   GENERAL  INFECTIOUS   DISEASES 

cases  before  he  can  realize  how  often  they  recover  from  conditions  apparently 
hopeless  when  promptly  treated  and  properly  nourished." 

The  hemorrhagic  form,  like  the  others,  demands  cinchonism  and  careful 
nutrition,  but  also  hemostatics.  Purgative  doses  of  calomel  are  indicated  in 
some  cases  of  each  form,  but  should  not  be  given  in  a  routine  manner. 

3.  Prompt  cinchonism  is  the  chief  means  of  attaining  the  third  aim  of 
treatment.  Eemoval  to  a  healthy  locality  should  be  secured  if  possible,  and 
the  general  condition  of  the  patient  requires  careful  attention. 

It  remains  to  add  that  those  going  to  a  malarial  region  can  often  avoid 
contracting  the  disease  by  taking  advice  of  a  local  physician  as  to  hygienic 
precautions,  and  by  moderate  divided  doses  of  quinin.] 


CHAPTEE    XV 
DENGUE 

[This  affection  has  never  appeared  in  Germany,  and  hence,  doubtless,  was 
omitted  by  the  author.  The  name  "  dengue  "  is  supposed  to  be  a  Spanish 
corruption  of  dandy,  the  term  dandy  fever  having  been  applied  to  the  disease 
by  the  "West  India  negroes  on  account  of  the  stiff  carriage  of  those  affected  by 
it.    Another  name  is  "  break-bone  fever." 

The  disease  generally  appears  in  epidemics,  and  is  almost  exclusively  con- 
fined to  tropical  and  semitropical  countries.  In  1780  an  epidemic  supposed 
to  be  dengue  prevailed  in  Philadelphia,  and  outbreaks  have  occurred  repeatedly 
in  the  Southern  States  in  the  last  hundred  years.  In  1880  Charleston,  Savan- 
nah, New  Orleans,  and  other  Southern  cities  were  visited  by  it.  It  is  prevalent 
in  Texas,  and  has  recently  occurred  in  the  Philippines. 

iEtiology. — As  to  the  causation  but  little  is  known.  Those  who  have  had 
opportunities  of  studying  the  disease  consider  it  both  contagious  and  infec- 
tious, and  the  inference  that  it  depends  on  a  specific  germ  is  readily  suggested. 
It  seems  to  prefer  low  lands  along  the  seashore,  and  to  be  influenced  by  mete- 
orological conditions  in  that  it  generally  prevails  during  the  summer  and  dis- 
appears as  cold  weather  comes  on.  Neither  age,  sex,  nor  condition  affords  any 
protection  from  the  disease ;  it  was  thought  by  Dickson  that  one  attack  gen- 
erally confers  immunity  for  life. 

Pathology. — The  disease  is  so  rarely  fatal  that  few  opportunities  have  been 
afforded  for  its  post-mortem  study.  So  far  as  is  known,  it  has  no  peculiar 
lesions.  The  prominence  and  the  character  of  the  muscle  and  joint  pains 
have  led  some  observers  to  think  the  affection  related  in  some  way  to  rheu- 
matism. 

Symptoms  and  Course. — The  onset  is  usually  sudden,  but  a  pronounced 
chill  is  said  never  to  occur.  Prodromata  similar  to  those  of  other  infectious 
diseases  are  sometimes  observed,  but  the  first  symptom  is  very  often  pain  and 
stiffness  in  the  muscles  and  joints,  with  frequent  swelling  of  the  latter.  The 
large  and  small  joints  are  equally  affected,  and  the  pain  is  increased  by  motion. 
With  the  pain  there  is  a  rise  in  temperature  and  in  the  frequency  of  the  pulse. 
The  pain  is  apt  to  increase  during  the  first  two  or  three  days  and  disappear 


YKLI.OW     I  I.U.I:  Hg 

on  the  fifth,  but  irregular  remissions  are  liable  to  occur.  As  the  thermometer 
falls  the  pain  and  other  symptoms  diminish,  bui  reappear  in  full  force  with 
any  subsequent  rise.  During  the  later  days  of  the  disease  a  -l:in  eruption 
appears  on  the  upper  pari  of  the  body,  and  in  severe  cases  becomes  general  in 
about  two  days.  Tin's  eruption  is  very  variable  in  character;  ii  may  appear 
simply  as  an  erythema,  or  simulate  the  eruptions  of  scarlel  fever,  rubeola, 
lichen,  or  urticaria;  it  is  apt  to  be  associated  with  well-marked  heat  and  itch- 
ing of  the  skin.  Jn  mild  cases  tin;  eruption  i-  evanescent  or  absent.  Swelling 
of  the  lymphatic  glands  is  not  uncommon;  in  severe  cases  the  mucous  mem- 
brane of  the  mouth  and  nose  is  reddened,  and  hemorrhage  from  the  outlets  of 
the  body  lias  been  observed.  Pregnant  women  are  apt  to  miscarry.  Delirium  is 
rare  in  adults,  hut  common  in  children;  the  face  is  generally  Hushed,  and  the 
eyes  are  injected;  the  tongue  becomes  increasingly  coated  as  the  disease  pro- 
gresses, the  appetite  is  lost,  nausea  is  not  uncommon,  vomiting  i-  rare.  The 
bowels  and  the  kidneys  present  no  constant  or  distinctive  symptoms. 

In  mild  cases  recovery  is  sometimes  rapid;  sometimes,  and  especially  after 
severe  cases,  convalescence  is  very  tedious,  the  muscular  and  articular  pain  and 
stiffness  passing  off  gradually,  and  the  glandular  swelling  lasting  for  weeks. 
Copious  skin  eruptions  are  followed  by  desquamation. 

Diagnosis  and  Prognosis. — As  to  diagnosis  there  can  seldom  be  any  dif- 
ficulty during  the  prevalence  of  an  epidemic.  The  first' cases  are  the  only  ones 
which  are  liable  to  he  mistaken,  and  even  their  nature  cannot  remain  long  in 
doubt.     The  prognosis  is  uniformly  good. 

Treatment. — We  are  acquainted  with  no  agent  capable  of  aborting  or  cut- 
ting short  the  disease;  nor  is  there  any  known  measure  of  prophylaxis  except 
for  an  individual  to  keep  away  from  those  places  in  which  the  affection  is 
known  to  prevail. 

The  treatment  of  the  attack  is  simply  symptomatic;  notahle  pain  calls  for 
opium  in  some  form:  Quinin  has  not  seemed  to  be  of  service.  Debility  follow- 
ing the  attack  demands  suitable  alimentation  and  tonics.] 


CHAPTEE    XVI 

YELLOW    FEVER 

[This  disease  is  not  a  visitant  of  Germany,  but  its  consideration  cannot 
be  omitted  from  a  text-book  on  the  practice  of  medicine  for  use  in  America. 
In  the  following  description  the  aim  will  be  to  bring  out  the  more  important 
features  of  the  disease,  while  for  fuller  details  the  reader  is  referred  to  larger 
works  and  monographs. 

iEtiology. — Yellow  fever  is  an  acute  infectious  disease,  confined  within 
certain  geographical  limits,  and  occurring  chiefly  in  epidemics  of  greater  or 
less  extent.  In  certain  localities,  notably  Havana,  Eio  de  Janeiro,  Vera  Cruz, 
and  other  Spanish-American  ports,  it  has  until  recently  been  endemic.  The 
influence  of  temperature  is  well  established;  the  disease  prevails,  namely, 
during  the  summer  or  the  warm  season,  and  is  abruptly  arrested  by  one  or 


120  ACUTE   GENERAL   INFECTIOUS   DISEASES 

two  decided  frosts;  dampness  is  favorable  to  it.  That  it  depends  ultimately 
on  a  special  cause  and  does  not  originate  de  novo  are  undisputed  facts.  The 
specific  organism  seems  to  be  of  ultramicroscopic  minuteness,  but  separable, 
however,  from  the  blood-serum  by  filtration.  Infection  appears  to  be  more 
active  at  night  than  during  the  day,  prefers  low-lying  districts,  and  in  them 
hugs  the  ground  to  a  certain  extent.  It  is  limited  to  the  sea  coast  and  to 
altitudes  of  less  than  1,000  feet.  Bad  sanitary  conditions  are  most  important 
accessory  causes  of  the  disease.  It  is  a  remarkable  fact  that  in  large  cities 
the  infection  may  be  of  great  virulence,  but  confined  to  a  limited  district  or 
districts,  by  carefully  shunning  which  unprotected  persons  are  comparatively 
safe.  An  infected  area  is  apt  to  extend  itself,  but  the  progress  is  slow,  and 
is  interrupted  by  streams  of  water,  high  walls,  or  simply  streets. 

In  1881,  Finlay,  of  Havana,  suggested  that  yellow  fever  might  be  trans- 
mitted by  mosquitoes.  In  1900  the  Yellow  Fever  Commission  of  the  United 
States  Army,  composed  of  Drs.  Eeed,  Carroll,  Lazear,  and  Agramonte,  demon- 
strated that  a  certain  mosquito,  Stegomyia  fasciata,  conveys  the  disease  from 
one  human  being  to  another.  An  interval  of  at  least  twelve  days  seems  to 
be  necessary  for  the  infected  mosquito  to  become  virulent.  It  was  also 
demonstrated  that  articles  of  clothing  and  bed  linen  soiled  by  the  sick  have 
no  power  to  spread  the  disease.  These  facts  have  been  amply  confirmed  by 
the  success  obtained  in  Havana  and  Panama  in  suppressing  yellow  fever  by 
exterminating  the  mosquito. 

As  a  rule,  one  attack  of  the  disease  renders  the  system  of  that  person 
insusceptible  forever  after;  the  natives  of  a  yellow-fever  district  are  far  less 
liable  to  contract  the  disease  than  are  those  who  move  into  the  district  from 
elsewhere,  probably  because  they  have  had  the  disease  in  a  mild  form  in 
childhood.  The  negro  race  is  susceptible  to  the  disease,  though  in  a  less 
degree  than  the  whites,  and  in  the  colored  the  affection  is  far  less  fatal. 
Neither  age  nor  sex  has  any  special  bearing  on  susceptibility.  The  stage  of 
incubation  is  usually  three  or  four  days.  Inoculation  experiments  showed 
an  incubation  period  varying  from  forty-one  hours  to  five  days  seventeen 
hours. 

Pathological  Anatomy. — The  disease  involves  no  constant  and  peculiar 
lesions.  In  rapidly  fatal  cases,  congestion  and  often  hemorrhage  are  found, 
especially  in  the  nervous  system,  liver,  kidneys,  and  digestive  tract.  In  fatal 
cases  of  longer  duration  more  or  less  parenchymatous  degeneration  is  found. 
A  fatty  degeneration  of  the  liver  is  quite  common,  and  imparts  a  yellow  color- 
ation to  the  organ,  giving  rise  to  the  terms  cafe,  au  lait,  or  boxwood  liver. 
Jaundice  of  the  skin  and  tissues  generally  is  also  observable  after  death,  and 
depends  upon  causes  in  no  way  connected  with  mechanical  obstruction  to  the 
flow  of  bile  into  the  intestine  during  life.  Splenic  enlargement  is  conspicuous 
by  its  absence. 

Course  and  Symptoms. — The  onset  of  the  disease  is  generally  sudden,  but 
it  may  be  preceded  for  a  few  days  by  malaise  and  other  signs  of  general  con- 
stitutional disturbance;  the  initial  chill  is  seldom  severe,  reaction  following 
soon  and  the  thermometer  rising  to  102°  to  105°  F. ;  hyperpyrexia  is  rare. 
The  pulse  rate  does  not  increase  proportionately  with  the  fever.  The  face 
becomes  flushed  and  the  eyes  injected  and  watery;  a  slight  jaundice  at  this 
early  stage  is  very  characteristic;  headache  and  pain  in  the  back  are  early 


YELLOW   J  KYI  I;  121 

and  usually  very  prominent  symptoms.    The  bowels  are  confined;  the  tongue 
is  apt  to  be  clean   if  it   was  so  before  the  disease  came  on;  the  stomach 
usually  somewhat  irritable,  and  there  may  be  vomiting;  moderate  epigastric 

tenderness  is  co ion;  the  mind   remains  clear,  as  a    rule,  bul   delirium   is 

not  very  uncommon,  and  in  children  a  convulsion  may  usher  in  the  attack 
as  in  other  acute  infectious  diseases;  slighl  albuminuria  is  apt  to  occur  as 
early  as  the  second,  third,  or  fourth  day.  This  hoi  or  febrile  stage  may  Ias1 
from  twelve  hours  to  several  days.  The  pulse  generall)  declines  in  frequency 
before  the  disease  has  readied  its  maximum.  As  the  fever  disappears  the 
other  symptoms  vanish  also,  and  the  second,  or  "stage  of  calm,"  begins. 
From  this  point  recovery  may  he  rapid  and  uninterrupted,  the  whole  disease 
consisting  of  hut  a  single  febrile  paroxysm  of  greater  or  less  intensity  and 
of  short  duration. 

In  grave  cases,  and  gravity  is'  often  foreshadowed  in  the  first  stage  by 
marked  capillary  congestion  of  the  surface  of  the  body  irrespective  of  the  in- 
tensity of  the  other  symptoms,  and  after  a  stage  of  calm  lasting  for  some  hours, 
hut  rarely  exceeding  twenty-four,  more  distinctive  symptoms  appear.  The 
pulse  is  very  compressible,  the  surface  of  the  body  is  cool,  vomiting  occurs  or 
becomes  more  prominent,  and  hemorrhage  is  now  apt  to  take  place.  The 
escape  of  blood  into  the  stomach,  its  retention  and  the  changes  which  it  there 
undergoes,  and  its  subsequent  expulsion,  explain  the  dreaded  and  characteristic 
symptom  known  as  "black  vomit."  Tarry  stools  sometimes  are  observed. 
Hemorrhage  elsewhere  is  also  common,  occurring  from  the  gums,  the  nose, 
eyes,  uterus,  kidneys,  into  the  skin,  etc.  Albuminuria  with  casts  is  very  com- 
mon. Jaundice,  sometimes  of  a  lemon-yellow  hue,  comes  on,  and  is  rarely 
lacking  in  severe  cases.  From  this  symptom  the  name  of  the  disease  is 
derived. 

In  cases  marked  by  more  or  less  complete  suppression  of  urine,  coma  and 
convulsions,  probably  largely  ursemic,  come  on.  Some  severe  cases  are  of  the 
"  walking  "  type,  the  patients  going  about  while  the  malady  is  far  advanced, 
or  even  up  to  the  time  of  death.  As  a  rule,  however,  muscular  prostration  is 
marked. 

If  the  disease  does  not  prove  fatal  in  this  third  stage,  convalescence  comes 
on  more  or  less  gradually,  and  is  followed  by  complete  recovery;  relapses, 
however,  occasionally  occur. 

The  duration  of  the  affection  is  variable,  but,  on  the  whole,  short,  usually 
being  less  than  a  week. 

Diagnosis. — In  mild  cases  the  symptoms  are  not  distinctive,  and  the  diag- 
nosis at  the  commencement  of  an  epidemic  is  not  likely  to  be  reached  except 
by  an  experienced  observer,  and  even  by  him  more  or  less  conjecturally.  Dur- 
ing an  epidemic  the  severe  lumbar  pain,  the  headache,  the  suffusion  of  the  eyes, 
the  early  jaundice,  the  disproportionately  slow  pulse,  the  early  albuminuria, 
and  the  moderate  gastric  irritability  are  all-sufficient  for  diagnostic  purposes. 
Severer  cases  are  also  marked  by  capillary  congestion  of  the  surface  of  the 
body,  and  the  third  stage  with  the  black  vomit,  hemorrhage,  jaundice,  slow 
pulse,  scanty  urine,  and  prostration  is  characteristic.  Of  course,  all  the  above 
symptoms  are  not  present  in  every  case.  One  disease  which  might  give 
rise  to  confusion  is  remittent  fever  with  jaundice.  This  affection  has  a  dif- 
ferent temperature  curve,  is  not  confined  to  the  yellow-fever  zone,  has  specific 
9 


122  ACUTE   GENERAL   INFECTIOUS   DISEASES 

organisms  in  the  blood,  is  controlled  by  quinin,  and  is  not  accompanied  by 
black  vomit. 

Dengue  and  yellow  fever  have  points  of  resemblance.  In  yellow  fever, 
however,  the  pulse  is  slow  in  proportion  to  the  temperature.  In  both  dis- 
eases there  are  severe  pains,  but  in  yellow  fever  these  are  muscular,  while  in 
dengue  they  seem  to  involve  the  bones  and  joints,  and  the  joints  are  stiff 
and  sometimes  swollen.  Jaundice  is  much  more  common  in  dengue  than  in 
yellow  fever,  and  it  appears  earlier.  An  eruption  is  very  unusual  in  yellow 
fever  and  rather  common  in  dengue.  Vomiting  and  nephritis  are  the  rule 
in  yellow  fever  and  exceptional  in  dengue.  Hemorrhages  are  much  more 
frequent  and  severe  in  yellow  fever  than  in  dengue. 

Prognosis. — This  varies  in  any  given  locality  with  the  character  of  the 
prevalent  epidemic.  The  death  rate  is  sometimes  very  high,  sometimes  mod- 
erate; it  is  greater  in  hospital  than  in  private  practice. 

In  the  first  stage  of  the  disease  the  chief  element  in  the  formation  of  the 
prognosis  seems  to  be  the  presence  of  marked  and  general  capillary  congestion 
of  the  skin,  a  symptom  which  foretells  a  severe  attack.  The  absence  of  this 
symptom  is  rather  less  important  than  its  presence.  Cases  may  turn  out  to  be 
severe  in  which  it  is  lacking.  The  frequent  deceptiveness  of  the  stage  of  calm 
is  to  be  remembered. 

Yellowness,  black  vomit,  and  suppression  of  urine  are  symptoms  de- 
noting the  greatest  gravity,  but  do  not  justify  the  complete  abandonment 
of  hope. 

Treatment. — There  are  no  means  in  our  power  of  aborting  the  disease. 
Prevention  is  to  be  attained  by  banishing  the  mosquito  both  from  the  sick 
and  from  the  whole  region. 

The  earlier  proper  treatment  can  be  instituted  the  better.  Absolute  rest 
and  good  ventilation  are  the  first  requisites.  The  patient  should  not  be 
chilled.  Emetics  and  cathartics  are  not  indicated  by  the  disease  itself;  the 
condition  of  the  stomach  and  bowels  should  be  inquired  into,  and  indigestible 
food  or  an  accumulation  of  feces  should  be  removed  if  present.  A  hot  mustard 
foot  bath  early  in  the  attack  is  useful.  For  the  lumbar  pains,  phenacetin  or 
morphin  is  indicated.  Sinapisms,  or  other  similar  external  counterirritants, 
with  ice  internally,  and  hydrocyanic  acid,  cocain,  or  chloroform  are  serviceable 
against  gastric  irritability.  High  fever  is  to  be  combated  by  cold  spongings, 
the  wet  pack,  and  the  cold  bath.  For  hemorrhage,  styptic  remedies  may  be 
used,  though  it  is  doubtful  whether,  when  given  internally,  they  are  really 
of  much  benefit.  Of  course,  no  medication  is  to  be  resorted  to  which  is  likely 
to  heighten  a  tendency  to  emesis. 

Sternberg's  formula  for  internal  use  is  said  to  be  valuable  for  quieting 
the  stomach  and  promoting  diuresis.  It  is  as  follows:  Sod.  bicarb.,  gr.  cl; 
hydrarg.  chlorid.  corros.,  gr.  % ;  aquae  purse,  0  ij.  M.  S.  Three  tablespoon- 
fuls,  ice-cold,  hourly. 

Suppression  of  urine  is  to  be  met  by  dry  cups  to  the  loins,  diuretic  reme- 
dies internally  if  the  condition  of  the  stomach  allowSj  or  the  hot-air  bath.  The 
results  of  pilocarpin  are  disappointing  according  to  Bemiss,  who  states  that 
he  has  seen  good  effects  from  large  enemata  of  water,  preferably  cold,  if  there 
be  notable  fever  in  these  cases.  Prostration  is  an  indication  for  the  use  of 
alcoholic  stimulants,  among  which  iced  dry  champagne  ranks  high.    It  will  be 


PLAGUE  123 

seen  that  the  treatment  is  entifely  symptomatic.  The  disease  i-  self-limitedj 
has  a  short  course,  and  the  patient  will  recover  if  he  can  be  kepi  alive  until 
the  poison  is  exhausted.  During  the  attack  and  until  convalescence  Le  thor- 
oughly established  the  management  of  the  diel  is  all-important.  Small  quan- 
tities of  the  most  easily  assimilable  food  may  be  given  al  shorl  intervals  if  they 
are  tolerated  by  the  stomach;  if  not,  alimentation  must  be  by  the  rectum,  and 
the  lower  bowel  in  this  disease  is  generally  in  a  fair  condition  for  this  method 
of  nutrition.  The  subcutaneous  or  intravenous  use  of  normal  salt  solution 
may  be  serviceable. 

Courage  and  hopefulness  on  the  part  of  the  physician  may  do  much  good, 
and  the  services  of  a  skillful  and  experienced  nurse  are  of  the  utmost  impor- 
tance. 


CHAPTER    XVII 
PLAGUE i 

JEtiology. — The  accounts  which  we  have  of  the  prevalence  of  plague  date 
back  almost  as  far  as  the  earliest  authentic  records  of  history.  As  early  as  from 
the  third  and  sixth  century  a.d.  details  have  been  furnished  of  widespread  and 
devastating  epidemics.  The  terrible  ravages  of  the  plague — the  "  black  death  " 
— in  the  fourteenth  century  are  well  known.  Between  1346  and  1351  about 
twenty-five  millions  of  people  are  said  to  have  died  of  it  in  Europe,  and  about 
as  many  more  in  the  Orient.  Since  then  numerous  epidemics  have  recurred 
again  and  again.  In  the  last  decades  they  have  been  limited  chiefly  to  the 
Asiatic  and  African  domiciles  of  the  disease — above  all,  India,  China,  Persia, 
Egypt,  etc.  But  the  growing  intercommunication  of  nations  has  always  sup- 
plied opportunities  for  the  spread  of  the  disease,  and  within  recent  years 
not  only  America  and  Australia  but  also  Europe  has  been  threatened.  But, 
thanks  to  our  sanitary  institutions,  we  need  hardly  fear  it  will  ever  again 
reach  such  dimensions  in  civilized  countries  as  it  did  in  previous  centuries. 
The  early  and  correct  recognition  and  the  thorough  isolation  of  the  first  cases 
that  spring  up  in  a  locality  are  of  the  utmost  importance.  Now  that  Yersin 
and  Kitasato  have  identified  the  specific  cause  of  the  disease,  the  diagnosis  has 
become  simple  and  certain. 

The  plague  bacilli  (vide  Fig.  21  a  and  b)  are  short,  immotile  rods  readily 
stained  in  cover-glass  preparation  with  anilin  dyes,  particularly  with  methyl- 
ene blue.  The  ends  of  the  rods  take  up  the  color  much  more  strongly  than  do 
the  middle  portions  (so-called  "polar  coloration'").  The  growing  of  a  pure 
culture  of  the  bacilli  on  ordinary  nutrient  media,  too,  offers  no  special  difficul- 
ties. Permanent  forms  (spores)  are  not  known.  Warming  to  60°  C.  (122°  F.) 
kills  the  bacilli  in  a  short  time,  boiling  heat  almost  instantaneously.  Dried 
on  linen  or  the  like,  the  bacilli  may  retain  vitality  for  several  weeks  at  mod- 

1  As  I  have  had  no  personal  experience  with  plague,  the  following  presentation  is  based 
exclusively  upon  a  stud3?  of  recent  literature  on  this  important  disease.  I  must  mention,  first  of 
all,  the  monograph  of  H.  F.  Miiller  and  R.  Poch  in  Nothnagel's  "Specielle  Pathologie. "  A 
good  description  of  plague,  as  well  as  of  all  other  infectious  diseases  of  the  tropics,  is  given  in  the 
commendable  book  of  B.  Scheube,  "Die  Krankheiten  der  warmen  Lander."     Jena,  G.  Fischer. 


124  ACUTE   GENERAL   INFECTIOUS   DISEASES 

erate  temperature.  The  plague  bacilli  occur  in  all  specific  manifestations  of 
the  disease,  especially  in  the  tissues  and  tissue  juices  of  recent  plague  buboes,, 
carbuncles,  and  skin  vesicles.  But  in  the  pus  of  the  spontaneous  plague  boils 
they  are  absent  or  only  sparsely  -present.  The  plague  bacilli  are  extraordi- 
narily abundant  in  the  sputum  of  jDlague  pneumonia  or  in  the  terminal  pul- 
monary oedema,  as  also  in  every  drop  of  blood  of  severe,  advanced  cases. 


a  b 

Fig.  21. — Plague  bacilli,     a,  in  pus;    b,  in  sputum.      (From  Vierordt.) 

The  transmission  of  the  disease  proceeds  at  first  from  person  to  person. 
Chiefly  through  the  expectoration,  and  less  so  through  other  excretions,  the 
bacilli  reach  the  patient's  environment,  and  are  then  transmitted  directly  or 
through  the  mediation  of  fomites  to  another  individual,  by  locating  in  a  small 
skin  lesion  or  by  reaching  and  establishing  themselves  in  the  mucous  mem- 
branes of  the  buccal  and  pharyngeal  cavity,  the  nasal  cavity  or  the  bronchi. 
A  sudden  appearance  of  numerous  cases,  as  occurs  in  some  typhoid  and  cholera 
epidemics  from  infected  drinking  water,  is  not  observable  in  plague.  Usually 
plague  epidemics  spread  but  slowly,  but  ultimately  they  often  attain  remark- 
able dimensions.  After  the  apparent  cessation  of  the  epidemic,  there  occurs 
not  rarely  a  second  outbreak,  which  under  given  circumstances  may  even  be 
of  greater  violence. 

An  indubitably  prominent  role  in  the  dissemination  of  plague  is  played  by 
diseased  animals,  above  all  by  rats.  Like  other  rodents,  rats  are  very  suscep- 
tible to  plague.  The  disease  spreads  among  them  to  the  greatest  extent  by 
their  gnawing  on  dead  animals,  and  as  the  excretions  of  rats  contain  plague 
bacilli,  they  surety  contribute  much  to  the  spread  from  house  to  house.  It  has 
long  been  known  that  an  outbreak  of  plague  is  often  preceded  by  a  striking 
mortality  among  rats.  Insects  (fleas,  mosquitoes,  etc.)  may  also  contribute 
to  the  dissemination  of  the  disease.  [It  is  believed  that  fleas  from  infested 
rats,  while  biting  human  beings  discharge  excrement  containing  plague  bacilli 
which  are  inoculated  into  the  tiny  wound  by  scratching.  In  the  West  squirrels 
have  become  infested  with  the  plague.]  From  all  that  has  been  said,  it  follows 
that  the  more  unfavorable  the  hygienic  conditions,  the  more  poverty,  filth,  and 
want  exist  in  a  community,  the  more  easily  does  plague  gain  ground. 

Symptoms  and  Course. — In  developed  cases  plague  usually  begins  quite 
suddenly  with  chills,  high  fever,  and  severe  general  symptoms.  The  latter 
consist  in  an  unusually  severe  headache,  in  lumbar  pains,  and  a  feeling  of  very 


PLAGUE  125 

great  general  debility.  Very  soon  consciousness  is  clouded,  a  condition  of 
mental  stupor  similar  to  inebriety  supervenes,  associated  with  complete  apathy, 
or,  in  other  cases,  with  conditions  of  anxiety  and  excitement.  The  fever  is  high 
(40°  to  41°  C.  =  101°  to  105.8°  F.),  remitting  but  little;  the  pulse  is  accel- 
erated, at  first  full  and  dicrotic,  and  later  small  and  irregular.  The  face  is 
at  first  reddened  and  afterwards  pale,  the  eyes  sunken  and  fixed.  The  tongue 
is  dry,  and  often  looks  as  though  whitewashed  with  lime.  The  spleen  is  dis- 
tinctly swollen,  and  the  liver,  too,  is  enlarged.  The  urine  is  concentrated  and 
generally  contains  albumen.    There  is  moderate  leucocytosis. 

Under  these  manifestations  of  a  severe  constitutional  infection,  death  occurs 
in  some  cases  as  early  as  two  to  three  days  (pestis  siderans).  As  a  rule,  how- 
ever, certain  local  affections  especially  characteristic  of  the  plague  accompany 
the  general  symptoms.  According  to  their  particular  localization,  the  follow- 
ing three  principal  forms  are  differentiated : 

1.  Glandular  plague  (bubonic  plague)  probably  develops  more  especially 
in  those  cases  in  which  the  bacilli  have  entered  through  small  skin  wounds 
and  then  spread  along  the  lymphatic  channels.  On  abKout  the  third  or  fourth 
day  of  sickness  the  lymphatic  glands  and  the  periglandular  tissues  in  the  in- 
guinal region,  in  the  upper  femoral  triangle,  in  the  axillae,  in  the  neck,  lower 
jaws,  and  elsewhere,  according  to  the  site  of  the  infection,  become  greatly 
swollen.  The  buboes  may  grow  to  the  size  of  a  fist ;  in  addition,  the  surround- 
ing tissues  also  show  inflammatory  oedema.  In  the  favorable  cases  the  ade- 
nitis retrogresses,  but,  as  a  rule — if  death  does  not  ensue  earlier  because  of  the 
severity  of  the  general  infection — suppuration  and  rupture  of  the  buboes  occur. 
In  these  processes  secondary  infection  with  pus  cocci  (staphylococci  and 
others)  probably  plays  a  prominent  part. 

2.  Dermal  plague  is  very  much  rarer  than  glandular  plague.  It  is  char- 
acterized by  the  appearance  of  "  plague  pustules  "  or  "  plague  boils  " — i.  e., 
purulent  vesicles — circumscribed  hemorrhagic  cutaneous  necroses,  and  furun- 
culous  and  carbunculous  inflammations  of  the  skin.  In  mild  and  favorable 
cases  these  inflammations,  too,  may  become  absorbed.  But  usually  the  ad- 
vancing suppurative  processes  lead  to  ulcerative  necrosis  of  the  tissues. 

3.  Pulmonary  plague  is  probably  due  to  direct  inhalation  of  plague  bacilli. 
Under  the  clinical  picture  of  a  severe  and  often  hemorrhagic  pulmonary  inflam- 
mation (plague  pneumonia)  it  almost  unexceptionally  runs  a  lethal  course. 
The  presence  of  numerous  plague  bacilli  in  the  expectoration  has  already  been 
mentioned.  This  form  of  plague  occurs  more  especially  in  persons  already 
having  pulmonary  affections.  Phthisical  patients  often  die  during  a  plague 
epidemic.  Aside  from  this  fact,  many  epidemics  are  distinguished  by  the  fre- 
quent occurrence  of  pulmonary  localization. 

These  three  forms  of  plague  show,  naturally,  manifold  combinations  and 
transitions,  so  that  the  total  course  of  the  disease  may  vary  very  much.  Aside 
from  the  diversity  of  the  localization,  the  severity  of  the  infection  also  differs. 
There  are  mild  and  abortive  types,  severe  and  fully  developed  cases,  and  cases 
of  the  gravest  infection  with  rapidly  fatal  termination  ere  the  development 
of  local  manifestations  can  occur.  (Pestis  siderans,  see  supra).  Complica- 
tions with  septic  infections,  meningitis,  general  hemorrhagic  diathesis,  etc., 
also  take  place.  If  the  disease  lasts  for  some  time,  marked  remissions  can 
often  be  seen  on  the  third,  sixth,  and  ninth  days  of  the  sickness.    The  malady 


126  ACUTE  GENERAL  INFECTIOUS   DISEASES 

then  seems  to  be  composed  of  several  relapses.  Occasionally  there  may  be 
an  actual  recurrence  of  the  plague.  Sequelae  of  various  kinds  (paralysis,  sec- 
ondary inflammation)   are  but  rarely  observed. 

Prognosis. — The  prognosis  of-  plague  is  very  unfavorable.  The  mortality 
may  reach  fifty  to  sixty  per  cent,  or  even  seventy  to  eighty  per  cent.  Death 
usually  occurs  in  the  first  six  to  eight  days  of  the  disease.  If  the  disease  takes 
a  longer  course,  weeks  may  pass  before  convalescence  begins,  or  death  may 
occur  even  at  a  later  period  through  general  debility.  We  need  not  add  any- 
thing regarding  the  pathologico-anatomical  findings,  as  they  are  evident  as 
regards  their  general  features,  at  least,  from  what  has  been  said  of  the  clinical 
facts. 

Prophylaxis. — The  general  hygienic  and  sanitary  regulations  for  the  com- 
bating of  plague  need  not  be  entered  into  here.  The  efforts  to  find  a  method  of 
prophylactic  inoculation  against  plague  (Haffkine)  have  so  far  yielded  but 
little  satisfactory  results.  Much  cannot  be  expected  in  this  direction,  as  even 
recovery  from  plague  does  not  confer  immunity  against  a  second  attack. 

Treatment. — The  treatment  of  plague  must  still  be  guided  by  the  prin- 
ciples applying  to  all  severe  infectious  diseases.  We  know  no  specific  remedy, 
although  modern  experimental  therapy  is  assiduously  at  work  on  the  problem 
of  producing  an  antitoxin.  For  the  present,  treatment  consists  chiefly  in  pro- 
viding the  best  attainable  general  conditions  (air,  nourishment,  location,  etc.) 
and  in  giving  due  attention  to  the  heart  and  respiration  and  the  individual 
symptoms  of  the  case.  Regarding  surgical  procedures  in  plague  buboes,  plague 
carbuncles,  etc.,  the  opinions  of  experienced  physicians  are  very  divergent. 
Generally  speaking,  an  expectant  attitude  seems  more  commendable  than  pre- 
mature incision  and  extirpation. 


CHAPTER   XVIII 

EPIDEMIC    CEREBROSPINAL    MENINGITIS 

{Spotted  Fever.     Cerebrospinal  Fever) 

^Etiology. — The  epidemic  form  of  cerebro-spinal  meningitis  has  been 
known  only  since  the  beginning  of  the  nineteenth  century.  The  first  epidemics 
were  observed  in  southern  France  and  in  Geneva.  Smaller  ones  occurred  in 
Germany  in  1822  and  1853 ;  but  it  was  not  till  1863  that  the  disease  became 
at  all  frequent  among  us.  Since  that  date  there  have  been  more  or  less  ex- 
tensive epidemics  almost  every  year  in  the  southern  and  central  portions  of 
Germany.  In  1904  and  1905  an  unusually  widespread  and  malignant  epidemic 
occurred  in  upper  Silesia,  In  1906  and  1907  the  disease  showed  itself  espe- 
cially in  the  Rhine  Province. 

Most  of  the  epidemics  appear  in  the  winter  and  spring.  We  do  not  know 
any  particular  factors  which  promote  the  disease.  It  often  seems  to  .be  de- 
cidedly endemic.  Barracks,  workhouses,  and  the  like  have  been  marked  by 
tolerably  extensive  epidemics.  The  spreading  of  the  disease  to  hitherto  un- 
affected areas  by  patients  is  possible,  but  the  danger  is  not  very  great  (vide 
infra).    The  poorer  classes,  with  their  unfavorable  housing  and  their  lack  of 


— 

V 

*    - 
■  ■*. 

EPIDEMIC   CEREBRO-SPINAL   MENINGITIS  127 

cleanliness,  are  most  exposed  to  the  disease.     Children  and  young  adulte 
the  most  frequent  victims,  but  now  and  then  elderly  persons  are  attacked.    Sex 
cannot  be  shown  to  have  much  influence. 

The  direct  cause  of  epidemic  meningitis  i-  the  Diplococcus  intracellularis 
meningitidis  (meningococcus)  first  described  by  Weichselbaum.  The  menin- 
gococci are  best  found  in  the  spinal 
fluid   obtained  by  lumbar  puncture;      ft 

they  lie  in  pairs,  in  shape  like  break-  —  «- 

fast  rolls,  either  in  the  leucocytes  or 
alongside  of  them,  and  in  appear- 
ance are  very  much  like  the  gono- 
cocci.  The  meningococci  have  also 
been  found  in  the  blood  and  the 
fluid   of  affected  joints.     Eegarding  y* 

their  existence  in  the  nasal  cavity, 
see  below.   They  may  be  easily  grown  * 

on  Loffler's  blood  serum.     They  are  / 

of  low  vitality;  desiccation,  sunshine,  ^* 

cold,  and  the  like  readily  kill  them.  FlG"  f -"Meningococcus  intracellularis  in  spi- 

Lpp-,  .  j,  nal   fluid.      a.  polynuclear   leucocytes   with 

Of    fundamental    importance    for  meningococci;  6,  endothelial  cells, 

the  question  as  to  the  kind  of  infec- 
tion and  the  spread  of  the  disease  is  the  fact  that  the  meningococcus  is  very 
frequently  found  in  the  secretion  of  the  nose  and  the  nasopharynx  during  the 
first  days  of  the  disease.  The  suspicion  is  therefore  natural  that  the  infection, 
as  a  rule,  enters  the  body  through  the  nostrils  or  the  tonsils  (pharyngeal  or 
faucial).  Whether  they  pass  thence  through  the  lymphatic  channels  directly 
into  the  meninges,  or,  what  I  consider  more  probable,  only  get  there  by  way 
of  the  general  blood  stream,  is  not  determined.  The  low  vitality  of  the  germ 
(vide  supra)  explains  the  fact  that  there  is  danger  of  severe  visitation  of  the 
disease  only  where  many  persons  are  living  together  in  close,  damp  quarters 
under  unfavorable  external  conditions.  In  hospitals  and  in  good  apartments 
where  sufficient  caution  is  exercised  the  danger  of  contagion  is  very  remote.  A 
prominent  role  in  the  spread  of  the  disease  is,  in  all  probability,  pla)red  by  the 
"  cocci  carriers."  For  it  has  been  shown  that  many  persons  who  are  in  con- 
tact with  meningitis  patients  harbor  meningococci  in  their  nares  without  them- 
selves being  sick.  Probably  the  transmission  and  spread  of  the  disease  occur 
to  a  greater  measure  through  these  healthy  cocci  carriers  than  through  bed- 
ridden, isolated  meningitis  patients. 

Xot  infrequently  single  sporadic  cases  of  primary  purulent  meningitis  or 
very  small  epidemics  occur.  The  aetiology  of  these  cases  can  be  determined 
only  by  bacteriological  examination.  Occasionally,  sporadic  cases  are  also  shown 
to  belong  to  the  epidemic  form  by  the  finding  of  the  meningococcus.  Often, 
however,  sporadic  cases  are  due  to  other  infectious  agents,  especially  the  pneu- 
mococcus  (vide  the  chapter  on  croupous  pneumonia),  the  streptococcus,  the 
so-called  streptococcus  mucosus,  and  others. 

Pathological  Anatomy. — The  autopsy  discloses  an  acute  purulent  cerebro- 
spinal leptomeningitis.  It  is  only  in  rapidly  fatal  cases  that  slight  and  in- 
cipient lesions  have  been  met  with.  As  a  rule,  the  extent  and  intensity  of  the 
objective  lesions  correspond  to  the  severity  of  the  symptoms.     In  the  brain 


128  ACUTE   GENERAL  INFECTIOUS   DISEASES 

the  purulent  inflammation  attacks  the  convexity  as  well  as  the  base.  It  is 
usually  most  marked  along  the  larger  blood  vessels  and  in  the  fissures  of  the 
cortex.  Of  the  spinal  cord  the  posterior  surface  suffers  most.  Frequently  the 
lumbar  portion  is  more  affected  than  the  parts  above.  It  is,  however,  excep- 
tional for  the  disease  to  be  limited  to  the  meninges ;  it  is  prone  to  extend  into 
the  underlying  parenclryma.  The  microscope  reveals  clumps  of  pus  corpuscles 
about  the  blood  vessels,  where  they  penetrate  into  the  tissues,  and  not  infre- 
quently there  are  numerous  centers  of  genuine  encephalitis.  These  latter  may 
be  visible  to  the  naked  eye.  Exceptionally  there  may  even  be  cerebral  abscesses 
of  considerable  size.  The  vessels  are  distended  with  blood,  clear  into  the  cen- 
tral ganglia,  and  ecchymoses  are  frequent.  The  cerebral  ventricles  are  usually 
enlarged,  and  filled  with  a  cloudy  serum,  or  even  with  pus.  It  is  plain  that 
these  lesions  of  the  cerebro-spinal  parenchyma  greatly  modify  the  clinical  pic- 
ture, and  that  they  must  frequently  have  more  to  do  with  the  severity  of 
the  symptoms  than  has  the  leptomeningitis  itself. 

Clinical  History. — Prodromata  are  relatively  rare,  and  if  present  they  are 
not  severe,  being  confined  to  general  malaise,  with  slight  headache,  and  pain 
in  the  limbs.  Usually  the  disease  begins  rather  suddenly;  there  is  intense 
headache,  often  felt  mainly  in  the  occiput,  pain  and  stiffness  in  the  back  of 
the  neck,  and  great  general  discomfort.  It  is  not  rare  for  vomiting  to  occur 
at  first.  ATery  often  there  are  among  the  early  symptoms  such  important  men- 
tal disturbances  as  stupor  or  delirium.  There  is  usually  fever  from  the  first. 
An  initial  rigor  may  occur,  but  it  is  not  the  rule. 

The  intensity  of  these  first  symptoms  is  not  always  the  same.  Subsequently 
to  them  the  course  of  the  disease  may  vary  greatly.  First  there  are  very 
acute,  violent  forms,  termed  "  explosive  "  (meningitis  cerebro-spinalis  siderans, 
meningite  fondroyante) ,  in  which  the  cerebral  symptoms  are  very  severe,  and 
the  patient  survives  only  a  few  days  or  even  hours.  Again,  there  are  abortive 
cases,  which  also  begin  with  apparently  most  dangerous,  violent  symptoms, 
but  after  a  few  days  present  a  strikingly  raj}id  and  complete  improvement. 
The  majority  of  cases  last  about  two  to  four  weeks.  In  severe  cases  death  may 
come  as  early  as  the  first  week.  The  disease  is  often  protracted  to  six  or -eight 
weeks'  duration,  or  even  longer,  and  may  end  in  death  after  all.  Cases  that 
last  a  good  while  sometimes  exhibit  a  remarkably  intermittent  character.  Im- 
provement and  relapses  are  very  characteristic  of  meningitis.  Finally,  there 
are  a  considerable  number  of  mild  cases  in  which  none  of  the  symptoms  is 
very  pronounced,  and  recovery  is  relatively  early. 

The  symptoms  of  the  disease  may  be  divided  into  (1)  the  severe  general 
symptoms,  referable  to  the  brain  and  spinal  cord;  (2)  the  more  localized, 
nervous  sjanptoms;  and  (3)  the  results  of  the  constitutional  infection,  includ- 
ing fever  and  sjmiptoms  in  other  parts  of  the  body. 

1.  Among  the  less  definite  cerebral  symptoms  headache  is  important.  It  is 
usually  terribly  severe.  It  is  chiefly  occipital,  but  sometimes  is  frontal  or  tem- 
poral. Like  most  of  the  symptoms  of  meningitis,  the  headache  undergoes  very 
frequent  changes  in  intensity  during  the  course  of  the  disease.  For  a  time  it 
may  remit,  only  to  recur  with  fresh  severity.  .Marked  vertigo  and  a  sense  of 
fullness  in  the  head  may  accompany  it. 

The  pain  in  the  head  is  reenforced  by  intense  pain  in  the  nape  of  the  neck 
and  back,  due  to  the  spinal  meningitis.     There  is  almost  always  considerable 


Kl'IDKMIC   CKRKBRO  SPINAL   MENINGITIS 


L29 


tenderness  along  (lie  whole  spinal  column.    The  erector  spina?  ie  contracted 
malting  the  back  straighl  and  rigid,  or  even  producing  opisthotonos;  and  the 
head  is  bent  backward  by  the  reflex  contraction  of  the  neighboring  muscles. 
This  lias  gained    tor  the  disease  the  German   name  " Genickstarre "    (stiff- 
neck).     (C/.  Fig.  2l>.)     If  an  attempt 
be  made  at  passive  flexion  of  the  bead, 
violent  pains  at  once  ensue. 

In  most  of  the  severe  cases  intelli- 
gence is  blunted;  we  find  all  degrees  of 
disturbance,  from  slight  drowsiness  to 
delirium  on  the  one  hand,  or  deep  coma 
on  the  other.  Some  cases  begin  with 
marked  maniacal  excitement.  These 
symptoms  likewise  may  undergo  fre- 
quent variation  in  their  intensity. 
General  convulsions  occur  in  very  se- 
vere cases  alone,  and  are  of  evil  omen. 

The  vomiting  is  also  to  be  regarded 
as  of  cerebral  origin.  It  frequently  is 
an  early  symptom,  but  ma}^  be  deferred. 

2.  Symptoms  referable  to  the  indi- 
vidual cerebral  nerves  are  manifold  and 
variable.  The  most  frequent  disturb- 
ances are  in  the  nerves  that  supply  the 
muscles  of  the  eye.  They  include  stra- 
bismus; nystagmus,  or  slow  move- 
ments independent  of  volition;  uni- 
lateral or  bilateral  ptosis;  slow  reaction 
of  the  pupils,  or  inequality  of  them,  or 
myosis  or  mydriasis.  In  the  area  of 
distribution  of  the  facial  there  is  often 
a  noticeable  contraction  of  the  muscles, 
giving  the  face  a  peculiar,  painfully 
distorted    look.     Convulsive,    irritative 

conditions  in  the  muscles  of  mastication  cause  grinding  of  the  teeth, 
sistent  trismus  may  occur,  and  is  usually  a  bad  sign. 

Disturbance  of  the  nerves  of  special  sense  is  frequent.  Deafness  may  be 
due  to  the  stupor,  but  is  often  the  result  of  an  extension  of  the  inflammation 
to  the  acoustic  nerve.  The  purulent  inflammation  may  be  propagated  as  far  as 
the  labyrinth,  or  even  into  the  middle  ear.  Tinnitus  aurium  is  also  frequent. 
Disturbances  of  vision  are  far  less  frequently  observed,  but  optic  neuritis  has 
been  repeatedly  found  by  the  ophthalmoscope.  Severe  metastatic  ophthalmia 
and  irido-choroiditis  have  been  also  observed.  They  are  probably  clue  to  ex- 
tension of  the  inflammation  along  the  sheath  of  the  optic  nerve  or  to  a  hema- 
togenous infection.  Conjunctivitis  sometimes  occurs,  but  is  probably  caused 
by  external  injuries  rendered  possible  by  the  imperfect  closure  of  the  lids,  or 
the  diminished  sensitiveness  of  the  parts.  We  have  several  times  found  the 
sense  of  smell  diminished. 

Of  the  disturbances  in  the  area  of  distribution  of  the  spinal  nerves,  the 


Fig.  23.- 
ingitis. 


-Severe  case  of  cerebrospinal  men- 
Stiff  neck.     General  emaciation. 


Per- 


130  ACUTE  GENERAL  INFECTIOUS  DISEASES 

most  value  in  diagnosis  is  possessed  by  the  cutaneous  hyperesthesia.  It  is 
apt  to  be  particularly  severe  in  the  legs,  and  it  may  be  so  extreme  that  the 
light  touch  of  a  finger  or  a  needle  causes  great  pain.  Sometimes  there  is  a 
slight  twitching  in  the  muscles  -of  the  extremities.  This  has,  however,  no 
special  significance.  There  are  often  rigidity  and  stiffness  of  the  muscles.  If 
the  trunk  of  the  patient  be  passively  raised  up  in  bed,  the  legs  usually  do  not 
remain  extended  but  are  involuntarily  flexed  (Kernig's  sign).  As  might  be 
expected,  there  is  no  invariable  rule  about  the  reflexes.  The  cutaneous  re- 
flexes are  usually  well  marked,  and  the  tendon  reflexes  may  be;  but  in  some 
cases  we  have  found  the  tendon  reflexes  markedly  diminished  or  even  abol- 
ished. Such  a  condition  is  probably  due  to  some  lesion  of  the  fibers  of  the 
posterior  nerve  roots. 

All  of  the  nervous  symptoms  above  enumerated  result  from  one  of  two 
causes— either  the  roots  of  the  nerves  are  affected  by  the  purulent  exudation, 
or  the  inflammation  extends  inward  to  the  central  organs  themselves.  This 
extension  is  the  explanation  also  of  other  symptoms  sometimes  observed — viz., 
hemiplegia,  paraplegia,  partial  convulsions,  and  aphasia. 

3.  In  addition  to  all  these  nervous  disturbances,  we  see  also  symptoms 
referable  to  other  parts  of  the  body.  Of  this  class  there  is  one  cutaneous 
affection  which  is  a  very  valuable  aid  to  diagnosis.  Herpes  labialis  or  herpes 
facialis  is  apt- to  appear  soon  after  the  beginning  of  the  meningitis.  It  is  seen 
in  more  than  half  the  cases,  and  as  frequently  in  severe  as  in  mild  attacks. 
Other  eruptions  occur  now  and  then — e.  g.,  roseola,  urticaria,  or  petechias. 
Sometimes  they  are  so  symmetrically  distributed  upon  the  two  halves  of  the 
body  as  to  suggest  the  idea  of  a  nervous  origin. 

The  digestive  system  seldom  displays  severe  symptoms  beyond  the  vomiting 
already  mentioned.  Anorexia  and  constipation  are,  indeed,  usually  present,  as 
in  many  grave  diseases.  We  have  seen  mild  dysentery  a  few  times.  Now  and 
then  a  slight  jaundice  has  been  noticed.  The  spleen  is  often  somewhat  swollen, 
but  very  rarely  attains  great  size. 

Swelling  of  the  joints  has  been  observed  quite  often;  it  is  much  more  fre- 
quent in  some  epidemics  than  in  others.  The  enlargement  may  be  an  early  or 
a  later  symptom.     It  does  not  usually  prove  serious. 

The  urinary  apparatus  is  seldom  affected.  The  urine  may  contain  some 
albumen  and  a  few  casts.  Polyuria  is  an  interesting  symptom,  probably  of 
nervous  origin.  It  is  more  apt  to  occur  in  the  latter  part  of  the  disease.  In  a 
number  of  cases  sugar  has  been  found  in  the  urine.  Cystitis  is  a  secondary 
disorder  which  is  not  very  rare,  particularly  in  severe  cases  when  the  catheter 
has  been  used. 

Pulmonary  and  bronchial  symptoms  are  likewise  secondary.  They  occur 
very  often  in  bad  cases.  It  is  evident  how  easily  the  stupor  of  the  patient 
may  lead  to  the  inhalation  of  solid  matter,  with  consequent  bronchitis  and 
lobular  pneumonia. 

Lesions  of  the  circulatory  system  are  rare.  Acute  endocarditis  has  been 
observed  only  a  few  times.  The  pulse  is  usually  somewhat  accelerated,  seldom 
rendered  slow.  Very  frequently  the  pulse  rate  is  remarkably  variable,  un- 
doubtedly because  of  variation  in  the  supply  of  nervous  force.  Slight  irregu- 
larities in  the  pulse  are  also  common.  In  the  blood  we  find  quite  a  marked 
leucocytosis. 


EPIDEMIC  CEREBROSPINAL   MENINGITIS  ]:;] 

The  fever  in  epidemic  meningitis  conforms  to  qo  single  iyi><'-  It  does 
not  correspond  at  all  to  the  severity  of  the  other  symptoms;  the  worsi  cases 
may  run  their  course  with  Little  or  no  fever.  In  most  instances  the  fever  lias 
irregular  remissions.     It  seldom  exceeds   104°  F,   (40°  C).     Sometimes  the 

fever  exhibits  a  decidedly  intermittent  charaeter.  It  is  in  these  cases  par- 
ticularly that  we  find  the  variation  in  the  intensity  of  all  the  symptoms  of 
which  mention  has  been  made  repeatedly.  The  variations  in  the  temperature 
do  not,  however,  always  run  parallel  with  the  changes  in  the  other  Bymptoms. 
In  mild  cases  the  fever  is  usually  moderate  and  brief.  The  abortive  attacks 
may  present  high  temperatures  at  first,  but  these  quickly  abate.  Id  ease  of 
a  fatal  issue  there  is  sometimes  hyperexia  before  death,  reaching  108°  to  109 J 
F.  (42°  to  43°  C).  In  the  severer  but  not  fatal  cases  the  fever  declines  -lowly 
but  irregularly.  The  fever  may  be  over  long  before  the  other  symptoms 
disappear. 

In  many  cases  there  is  exceedingly  rapid  and  severe  emaciation.  The 
patients,  especially  children,  become  wasted  to  skeletons  (Fig.  23).  Undoubt- 
edly the  fever  and  defective  assimilation  of  food  are  the  greatest  factors,  but 
the  simultaneous  action  of  neurotrophic  influences  is  undeniable. 

It  is  impossible  to  portray  all  the  forms,  symptoms,  and  courses  the  disease 
may  have.  The  chief  varieties  have  been  already  mentioned;  but  in  reality 
these  are  only  types  which  run  into  one  another  without  sharply  denned  border 
lines.  It  is  in  itself  a  characteristic  of  epidemic  meningitis  that  most  of  the 
more  tedious  cases  have  a  variable,  uncertain  course.  We  may  even  meet  with 
a  complete  intermission  of  all  the  symptoms,  lasting  for  quite  a  while,  so  that 
the  return  of  the  trouble  may  fairly  be  called  a  relapse. 

Sequelae. — Sequela?  are  not  rare  after  severe  cases.  Persistent  deafness  is 
most  frequent.  It  results  from  the  complications,  already  mentioned,  which 
affect  the  labyrinth  and  the  middle  ear.  Little  children  may  become  deaf  and 
dumb.  Again,  vision  may  be  deranged,  because  of  retinitis,  atrophy  of  the 
optic  nerve,  or  corneal  opacities,  etc.  It  is  not  very  rare  for  meningitis  to 
leave  grave  nervous  disorders  behind  it.  These  are  frequently  the  symptoms 
of  a  chronic  hydrocephalus.  We  may  observe  headache,  sudden  unconscious- 
ness, or  even  convulsions,  mental  impairment,  and  weakness  and  ataxic  un- 
certainty of  the  extremities.  Or  there  may  be  localized  disturbances  due  to 
permanent  injury  of  limited  portions  of  the  brain  or  spinal  cord,  such  as 
hemiplegia,  paraplegia,  and  aphasia.  From  many  of  these  conditions  there 
may  be  a  gradual  recovery,  but  others  prove  incurable. 

Diagnosis. — The  diagnosis  of  cerebro-spinal  meningitis  is  not  difficult  in 
a  well-developed  case,  particularly  if  the  prevalence  of  an  epidemic  puts  us  in 
mind  of  the  disease.  Diagnosis  is  more  difficult  in  sporadic  cases,  and  most 
difficult  of  all  when  the  patient  does  not  come  under  observation  till  he  is 
very  ill  and  when  we  cannot  obtain  the  previous  history.  Important  factors 
are  the  abrupt  onset,  the  speedy  appearance  of  grave  cerebral  symptoms,  the 
characteristic  headache  and  pain  in  the  back,  the  stiffness  of  the  neck,  and 
the  herpes  labialis. 

If  wc  find  evident  symptoms  of  meningitis,  we  have  still  to  decide  whether 
the  case  is  one  of  primary  epidemic  disease,  or  secondary,  due,  perhaps,  to 
extension  from  some  other  part.  Bearing  this  last  possibility  in  mind,  we 
should  examine  the  ears  carefully;  for,  as  is  well  known,  chronic  otitis  media 


132  ACUTE  GENERAL   INFECTIOUS   DISEASES 

may  set  up  a  purulent  meningitis.  Again,  it  may  be  very  difficult  to  exclude 
a  tubercular  meningitis.  Here  we  should  consider  other  circumstances  that 
might  render  tuberculosis  probable,  such  as  the  general  condition  of  the  pa- 
tient, heredity,  previous  pleurisy/the  results  of  thoracic  examination,  or  scrofu- 
lous disease  of  the  bones  or  joints.  The  existence  of  herpes  points  toward  epi- 
demic meningitis,  for  it  is  exceptional  in  the  other  forms  of  the  disease.  It 
is  sometimes  difficult  to  distinguish  between  meningitis  and  severe  cases  of 
other  acute  infectious  diseases — e.  g.,  typhoid  fever  and  septic  diseases.  Here 
we  must  weigh  all  the  circumstances  carefully. 

Lumbar  puncture  has  greatly  aided  the  diagnosis  of  meningitis.  This  was 
introduced  by  Quincke,  and  is  now  generally  employed.  As  Quincke  first 
showed,  we  can  usually  reach  the  subarachnoid  space  of  the  cauda  equina  with- 
out difficulty  between  the  third  and  fourth  lumbar  vertebra?  with  an  aspirating 
needle  about  8  cm.  long.  The  patient  should  lie  on  one  side.  In  this  way 
we  can  obtain  more  or  less  of  any  meningitic  exudation  that  may  be  present. 

In  epidemic  meningitis  the  spinal  fluid  is  generally,  though  not  always,  dis- 
tinctly cloudy,  and  deposits  a  more  or  less  marked  sediment  of  pus  corpuscles, 
which,  upon  microscopical  examination,  are  seen  to  be  polynuclear  leucocytes. 
As  a  rule,  lymphocytes  are  not  present,  in  contrast  with  tubercular  meningitis. 
The  bacteriological  examination  of  the  fluid  with  the  demonstration  of  menin- 
gococci (vide  supra)  or  tubercle  bacilli,  etc.,  is  of  decisive  importance. 

Prognosis. — The  prognosis  depends  chiefly  upon  the  severity  of  the  cerebral 
symptoms.  Yet  we  should  be  guarded  in  our  utterances,  even  when  the  case 
seems  mild,  or  has  apparently  made  the  first  steps  toward  convalescence.  The 
disease  sometimes  changes  for  the  worse  at  a  late  period.  In  general  the 
mortality  is  about  thirty  to  forty  per  cent.  Probably  this  estimate  does  not 
take  into  account  many  very  mild  cases.  In  the  last  extremely  malignant 
epidemic  in  Upper  Silesia  the  mortality  rose  even  to  sixty  to  seventy  per  cent. 

Treatment. — In  the  last  extensive  epidemics  many  attempts  have  been 
made  to  find  a  specific  treatment  for  meningitis.  The  transmission  of  menin- 
gitis to  animals  has  not  yet  been  successful.  But  the  blood  serum  of  animals 
previously  injected  with  living  or  dead  cultures  agglutinates  meningococci. 
Such  sera  have  frequently  been  used  for  therapeutic  purposes  ( Jochmann,  Kolle 
and  Wassermann,  and  others).  The  injections  are  given  sometimes  subcu- 
taneous^, sometimes  after  preparatory  lumbar  puncture,  directly  into  the 
spinal  canal.  Definite  curative  results  have  not  been  obtained,  and  under 
these  circumstances  the  treatment  of  epidemic  meningitis  must  still  be  mainly 
symptomatic. 

[Eecent  results  are  better.  Of  400  cases  treated  by  Flexner's  serum,  295 
recovered.  Netter  reported  a  mortality  of  only  twenty  per  cent  in  the  recent 
epidemic  in  Paris.    At  Evreux,  of  18  soldiers  treated  with  serum,  only  2  died.] 

A  valuable  remedy  is  cold  applications.  Ice  bags  are  placed  upon  the  head, 
and,  if  possible,  along  the  spine.  There  are  long  and  narrow  rubber  bags  for 
the  latter  purpose.  These  applications  are  borne  well  by  most  patients  and 
afford  decided  relief.  The  local  abstraction  of  blood  has  also  an  undeniably 
beneficial  influence,  however  difficult  this  may  be  to  explain.  Leeches  are  put 
behind  the  ears,  and  cupping  glasses  on  the  back  of  the  neck  and  along  the 
spine.  Mercurial  ointment  is  often  rubbed  in,  not  only  locally  but  also  in  the 
same  way  as  in  treating  syphilis.     Its  efficacy  is  doubtful.     The  narcotics  are 


SEPTIC   AND   PYEMIC    DISEASES  133 

of  great  value.     The  best  is  morphin  given  subcutaneously.     U  the 

pain,  and  often  affords  the  uneasy  and  delirious  patient  res!  and  sleep. 
Chloral,  bromid  of  potassium,  antipyrin,  sodium  salicylate,  etc.,  may  also  be 
employed.  Iodid  of  potassium  is  often  given  internally,  to  the  amounl  of 
22.5  to  30  gr.  (gin.  1.5  to  2)  in  a  day,  especially  in  cases  with  a  slow  course. 
Iodid  of  sodium  has  been  particularly  recommended  in  daily  amounts  of  15 
to  22.5  gr.  (gm.  1  to  1.5)  in  solution.  [Urotropin  has  recently  been  recom- 
mended.] The  evacuation  of  a  part  of  the  menihgitic  exudation  by  lumbar 
puncture  (vide  supra)  is  sometimes  followed  by  a  temporary  improvement  of 
the  symptoms.  Some  physicians  earnestly  advocate  lumbar  puncture  repeated 
every  four  or  five  days.  The  author  can  corroborate  the  favorable  symptomatic 
influence  of  lumbar  puncture  in  some,  though  not  all,  cases,  but,  after  the 
experiences  of  the  last  great  epidemic,  must  warn  against  exaggerated  expec- 
tations. 

The  fever  hardly  ever  requires  special  treatment.  Quinin  exerts  no  in- 
fluence in  the  intermittent  type.  Antipyrin  is  better  borne,  and  it  also,  like 
the  other  nervines,  sometimes  relieves  the  nervous  symptoms.  Cool  baths  are 
not  to  be  recommended,  but  warm  and  hot  baths  or  hot  packs  sometimes  seem 
to  be  of  decided  benefit.  Local  complications — e.  g.,  affecting  the  eye  or  the 
ear — require  special  treatment.  The  swelling  of  the  joints  which  sometimes 
occurs  we  have  thought  to  be  somewhat  relieved  by  salicylates,  aspirin,  etc. 


CHAPTEE   XIX 

SEPTIC    AND    PYEMIC    DISEASES 

(Spontaneous  Septico-pycemia) 

The  septic  and  pysemic  processes  which  follow  serious  injuries  or  opera- 
tions belong  to  surgery;  but  analogous  diseases  occur  in  persons  who  are 
apparently  in  perfect  condition.  They  take  the  form  of  an  extremely  severe 
acute  infectious  disease,  usually  fatal.  There  can  scarcely  be  a  doubt  that 
in  almost  all  these  cases  there  is  some  small  break  in  the  continuity  of  the 
external  skin  or  the  mucous  membrane  which  affords  an  entrance  for  the  in- 
fectious material ;  but,  since  the  infection  itself  is  wholly  unnoticed,  the  gen- 
eral disease  seems  a  primary  affection,  and  its  correct  interpretation  often 
occasions  the  physician  considerable  difficulty.  Even  if  the  septic  infection 
be  correctly  recognized,  it  is  sometimes  impossible  to  determine  the  point  of 
origin.  Eor  such  cases  Leube  has  introduced  the  name  of  "  cryptogenic " 
septico-pyaemia.  We  must  add,  however,  that,  in  many  cases,  at  least,  a  care- 
ful inquiry  and  examination  will  reveal  the  origin  of  the  infection.  In  many 
cases,  however,  a  complete  explanation  of  the  occurrence  of  the  infection  is 
given  only  by  the  autopsy,  and  the  origin  of  some  cases  remains  obscure  even 
after  a  careful  autopsy.  Not  infrequently  a  general  septic  infection  follows 
some  other  disease,  as  scarlatina,  diphtheria,  or  one  such  as  erysipelas  or 
furunculosis,  which,  though  itself  due  to  pus  cocci,  is  at  first  localized.  In 
such  cases  we  speak  of  a  secondary  sepsis. 


134  ACUTE   GENERAL  INFECTIOUS   DISEASES 

iEtiology. — The  causes  of  pyamiic  and  septic  affections  are  chiefly  the 
same  pus  cocci  which  produce  many  circumscribed  inflammations  and  suppu- 
rations, especially  the  Streptococcus  pyogenes,  the  Staphylococcus  pyogenes 
albus,  and  the  Staphylococcus  pyogenes  aureus.  But  pneumococci,  B.  coli, 
gonococci,  meningococci,  B.  pyocyaneus,  proteus,  and  other  varieties  may  also 
lead  to  a  general  septic  infection.  A  clinical  differentiation  of  septic  affec- 
tions, according  to  the  special  kind  of  disease  produced,  is  not  strictly  prac- 
ticable. But,  in  general,  it  may  be  said  that  the  graver  cases  of  septic 
infection  with  extreme  constitutional  intoxication,  hemorrhage,  bacterial 
foci,  etc.,  but  without  real  multiple  suppurations,  are  due  especially  to  the 
streptococci.  The  staphylococci  show  a  decided  tendency  to  form  metastatic 
abscesses.  Following  the  old  usage,  cases  with  multiple  pus  foci  are  termed 
pysemia. 

It  is  very  important  for  the  correct  understanding  of  all  these  condi- 
tions to  bear  in  mind  that,  in  different  cases,  different  organs  or  parts  of  the 
body  may  become  the  chief  seat  for  the  localization  of  the  micrococci.  Hence 
severe  local  disorders  may  arise,  which,  of  course,  may  give  diverse  aspects  to 
the  clinical  picture  according  to  the  special  localization.  This  is  the  reason 
why  many  of  these  affections  were  formerly  regarded  as  separate  diseases, 
although  in  reality  they  were  only  different  localizations  and  forms  of  the 
same  infectious  process.  Among  these  affections  were  the  so-called  "  acute 
osteomyelitis  "  almost  always  caused  by  the  Staphylococcus  pyogenes  aureus, 
"  malignant  endocarditis,"  certain  forms  of  "  malignant  erysipelas,"  etc.  In 
their  clinical  aspect  these  differences  are,  of  course,  still  of  great  importance, 
but  the  agtiological  connection  of  all  these  cases  must  always  be  emphasized, 
because  only  by  putting  a  proper  stress  upon  this  point  can  we  obtain  a  correct 
understanding  of  all  the  combinations  manifested  in  the  clinical  course  of  the 
disease. 

Before  we  consider  the  details  of  the  anatomical  changes  in  septic  affec- 
tions, we  would  mention  those  circumstances  (exciting  causes)  which,  we 
know  by  experience,  most  commonly  cause  or  render  possible  the  occurrence 
of  septic  infection.  The  following  are  chiefly  to  be  considered:  1.  The  puer- 
peral processes  take  the  first  place.  Both  after  delivery,  and  still  more  fre- 
quently after  abortion,  the  raw  surface  of  the  uterus  may  be  the  door  of 
entrance  for  the  septic  poison.  Artificial,  criminal  abortion,  often  performed 
with  great  carelessness,  not  rarely  leads  to  septic  infection.  The  physician 
must,  therefore,  always  bear  this  possibility  in  mind.  A  gross  pathological 
change  is  not  necessarily  to  be  seen  in  the  uterus .  itself  or  in  its  appendages. 
We  do  find,  often  enough,  diphtheritic  and  gangrenous  inflammation  at  the 
place  where  the  placenta  was  inserted,  or  purulent  thrombi  in  the  veins  of 
the  uterus  and  of  the  pelvis,  etc. ;  but  in  other  cases  the  uterus  is  merely  a 
gate  of  entrance  for  the  poison,  remaining  itself  normal.  2.  The  septic 
poison  may  also  be  absorbed  through  slight  abrasions  of  the  skin,  injuries, 
felons,  whitlows,  etc.;  and  these  may  be  almost  completely  healed  by  the 
time  the  severe  symptoms  of  disease  are  developed.  Bedsores  belong  in  this 
category.  3.  Ulcers  of  the  mucous  membranes  may  give  rise  to  infection. 
Septic  infections,  unfortunately,  not  infrequently  develop  from  sore  throats 
of  all  kinds.  At  other  times  the  infection  starts  from  the  nose  or  ear  (mid- 
dle-ear abscess).     The  most  frequent  intestinal  causes  are  ulcerative  proc- 


septic;  and  pyemic  diseases  135 

esses  in  the  vermiform  appendix  and  the  many  Conns  of  cholecystitis  (usually 
through  II.  coll).  From  the  urethral  mucosa  a  gonococcus  sepsie  infrequently 
develops.  Often  the  urinary  passages  give  rise  to  an  infection  with  B.  coli 
or  staphylococci.  I.  A  peculiar  position  among  septic  diseaseg  ie  held  by 
acute  endocarditis,  which  often  develops  on  the  basis  of  an  old  chronic  endo- 
carditis. Tiiis  form  of  sepsis  will  be  specially  discussed  later  on.  5.  Lastly, 
we  sometimes  find  no  other  source  Tor  general  sepsis  than  a  suppurating  dis- 
ease of  the  bones,  joints,  or  other  parts,  previously  existing.  We  must  here 
suppose  that  some  connection  was  formed  between  the  original  pus  cavity 
and  the  blood  or  lymph  channels,  and  that  thus  the  micrococci  entered  the 
general  circulation  and  were  enabled  rapidly  to  increase. 

Pathological  Anatomy. — The  most  striking  feature  at  the  autopsy  of 
cases  is  that  there  is  never  found  a  lesion  of  one  organ  exclusively.  Several, 
or  it  may  be  almost  all,  of  the  organs  exhibit  numerous  limited  foci  of  disease. 
The  lesions  sometimes  consist  for  the  most  part  of  multiple  abscesses,  some- 
times of  numerous  ecchymoses,  and  sometimes  of  combinations  of  the  two. 
The  abscesses  are  found  chiefly  in  the  lungs,  kidneys,  liver,  spleen,  muscles, 
heart,  brain,  and  thyroid  gland.  Quite  extensive  purulent  inflammation  is 
also  found.  This  attacks  the  joints  or  causes  phlegmon  of  the  muscles  or 
skin  by  preference,  but  it  also  attacks  the  pleura,  the  meninges,  and  the  eye, 
where  it  causes  purulent  choroiditis,  panophthalmitis,  and  purulent  degen- 
eration of  the  vitreous.  Purulent  phlebitis  also  occurs.  The  ecchymoses  are 
most  frequent  upon  the  surface  of  the  body,  the  serous  membranes  (peri- 
cardium, pleura),  the  retina,  the  conjunctiva,  the  brain,  the  pelvis  of  the 
kidney,  etc.  Besides  these  multiple  abscesses  and  ecchymoses,  there  is  fre- 
'quently  another  disorder,  which  seems  to  be  the  very  focus  of  the  disease, 
viz.,  acute  ulcerative  endocarditis  (cf.  the  appropriate  chapter).  This  usu- 
ally attacks  the  mitral  valve,  more  rarely  the  valves  of  the  aorta,  and  quite 
exceptionally  the  valves  of  the  right  side  of  the  heart.  Finally  come  a  num- 
ber of  changes  common  to  all  severe  constitutional  infectious  diseases — acute 
splenic  tumor,  "  cloudy  swelling "  of  the  liver  and  kidneys,  a  dryness  and 
dark-red  color  of  the  muscles,  etc. 

In  regard  to  the  special  origin  of  all  these  symptoms  we  may  certainly 
refer  the  abscesses,  the  purulent  inflammation,  and  the  endocarditis  to  the 
immediate  presence  of  the  micrococci  themselves,  while  the  parenchymatous 
degenerations  of  different  organs,  the  hemorrhages,  and  probably  the  splenic 
enlargement  and  the  diffuse  acute  nephritis,  are  to  be  regarded  as  due  to 
toxic  action.  Microscopic  examination  of  the  internal  organs  gives  us  a  very 
instructive  insight  into  the  morbid  process.  This  often  reveals  the  presence 
of  many  tiny  foci  of  disease,-  in  the  center  of  which  we  often  see  a  little 
blood  vessel  completely  filled  with  micrococci  ("micrococcus  embolus").  As 
Weigert  first  found,  the  primary  action  of  a  little  focus  of  micrococci  upon 
the  surrounding  tissues  consists,  of  a  circumscribed  cell  necrosis,  a  small 
focus  of  "  coagulation-neerotic  "  cells  without  nuclei.  This  may  be  followed 
later  by  circumscribed  suppuration. 

Clinical  History. — It  is  our  intention  to  discuss  below  those  cases  chiefly 
which  are  of  interest  to  the  physician  rather  than  the  surgeon — i.  e.,  where  the 
septico-pysemia  is  an  apparently  primary,  acute,  and  grave  disease.  Many  of 
the  essential  traits  of  this  type  of  disease  are  identical  with  those  of  the  pyasmia 


136 


ACUTE   GENERAL   INFECTIOUS   DISEASES 


which  complicates  the  effects  of  serious  wounds  or  the  inflammation  subsequent 
to  childbirth.  But  it  is  precisely  the  apparent  absence  of  a  cause  which  ren- 
ders many  cases  of  this  form  of  sepsis  so  obscure  and  difficult  to  understand. 
Besides,  the  patient  is  often  in  a  stuporous  condition  when  the  physician  is 
called;  and  this  adds  greatly  to  the  difficulties  of  a  correct  judgment. 

The  beginning  of  the  disease  is  usually  rather  abrupt.  An  apparently 
healthy  person  is  attacked  with  febrile  symptoms,  headache,  and  "  rheumatic  " 
pains  in  the  muscles,  joints,  and  loins.  There  may  also  be  gastro-intestinal 
symptoms  of  considerable  severity,  including  vomiting  and  diarrhea.  Usu- 
ally the  patient  feels  ill  enough  to  take  speedily  to  his  bed.  The  symptoms 
now  increase  rapidly,  and  develop  into  a  severe  illness  which  may  resemble 
either  a  bad  case  of  typhoid  fever  or  miliary  tuberculosis.  Or  the  cerebral 
symptoms,  such  as  headache,  stupor,  and  delirium,  may  become  so  prominent 
that  the  attack  seems  like  meningitis.  If  the  trouble  in  the  joints  (vide  in- 
fra) predominates  and  there  are  signs  of  endocarditis,  the  disease  may  at 
first  be  taken  for  a  violent  attack  of  acute  articular  rheumatism. 

Taking  up  the  separate  symptoms,  we  shall  first  name  those  which  belong  to 
every  severe  acute  infectious  disease  and  have  nothing  characteristic  about 
them.  In  this  list  belong  the  general  prostration,  the  anorexia,  the  mental 
disturbance,  the  stupor  and  delirium,  the  headache,  the  subjective  symptoms 
of  fever,  the  dryness  of  the  tongue,  and  finally  the  acute  splenic  tumor  which 
can  often  be  made  out.  There  are,  however,  other  and  more  characteristic 
symptoms;  and  it  is  chiefly  upon  these  that  the  diagnosis  rests,  provided  we 
can  make  one  at  all.    These  are : 

1.  The  Course  of  the  Fever. — In  many  eases,  it  must  be  confessed,  this 
is  not  at  all  characteristic.     It  may  even  be  so  like  that  of  typhoid  fever,  at 


J 

IHHinHM 

111 

39.0    IM 

■ihmhi 

38.0    1  Bi 

inmnnni 
wmmami 

II 

37.0°  I 

36.0°  \m\ 

mmamm 

Fig.  24. — Fever  curve  in  pygemic  infection.     The  marked  elevations  in  temperature  were  always 
ushered  in  by  a  chill.     (Erlangen  Medical  Clinic.) 

least  for  some  time,  as  to  lead  to  a  wrong  diagnosis.  In  other  cases,  however, 
the  temperature  curve  does  aid  us  greatly — viz.,  when  it  represents  an  inter- 
mitting fever  with  marked  elevations,  reaching  106°  F.  (41°  C.)  and  higher, 


SEPTIC   AM )   PYEMIC    DISEASES  137 

and  often  accompanied  by  a  chill,  and  with  subsequent  deep  depressions. 
The  curve  may  thus  come  to  resemble  closely  thai  of  ;i  quotidian  or  even  ter- 
tian intermittent  lever.  This  true  "pyaemic"  fever,  in  which  the  rise  in 
temperature  is  usually  associated  with  a  severe  chill,  occurs  chiefly  in  the 
cases  with  multiple  abscesses.  Sometimes,  again,  the  course  of  the  fever  is 
made  up  of  similar  paroxysmal  elevations,  separated  by  periods  of  ordinary 
remitting  fever. 

Generally  streptococcus  infections  have  a  more  irregularly  remit  lent  or, 
in  severe  cases,  an  almost  continuous   fever.      Intermittent    attacks   of    Ei 
occur  especially  in  infections  with  staphylococci,  bacteria  coli,  and  gonococci. 

2.  Cutaneous  Symptoms. — These  are  very  frequent,  and  a  great  aid  to 
diagnosis.  The  hemorrhages  into  the  skin  are  of  chief  importance.  They 
may  be  either  punctiform  petechias  or  more  extensive  ecchymoses.  Of  other 
cutaneous  appearances,  the  first  in  relative  frequency  is  an  erythema  resem- 
bling scarlatina.  It  is  not  improbable,  as  we  have  already  said,  thai  many 
cases  which  have  been  described  as  severe  scarlet  ['c\c\-  occurring  during  child- 
bed were  in  reality  septic  disease.  We  also  sometimes  see  eruption-  resembling 
erythema  exudativum  multiforme  or  erythema  nodosum,  and  also  in  some 
cases  roseola,  pustular  eruptions,  and  herpes.  Extensive  inflammations  of  the 
skin,  like  erysipelas,  are  especially  characteristic  of  certain  cases.  They  are 
seen  on  the  lateral  surfaces  of  the  thorax,  the  back,  the  thighs,  etc.,  and  often 
end  in  phlegmonous  suppuration.  When  they  occur  we  can  usually  make  a 
very  positive  diagnosis  of  septic  infection. 

3.  Circulatory  Disturbances. — An  ability  to  recognize  the  cardiac  lesions 
would  be  very  desirable;  but  often  this  is  impossible  before  death.  Endo- 
cardial murmurs  are  often  wanting,  even  in  cases  where  the  autopsy  discloses 
abundant  exudation  and  ulcers  upon  the  valves.  Still,  in  some  cases  of  this 
sort  we  have  found  the  heart  sounds  noticeably  deficient  in  clearness.  Some- 
times we  hear  very  loud  or  low,  blowing  sounds.  The  cardiac  dullness  is  often 
quite  normal,  in  other  cases  somewhat  increased.  In  some  cases  fibrinous  or 
purulent  pericarditis  develops.  Functional  disturbances  of  the  heart's  action 
are  almost  always  present.  The  heart's  action  is  excited  and  very  rapid  (120 
to  140  or  more),  or  in  rare  cases  abnormally  slow.  Irregularity  and  inequality 
of  the  pulse  are  common.  The  tension  of  the  pulse  is  usually  low,  and  the 
frequent  pallor  and  mild  cyanosis  of  the  patient  point  to  a  diminished  energy 
in  the  heart's  action  and  impaired  vascular  tone.  All  these  disturbances  are 
due  partly  to  the  effect  of  the  toxins,  and  partly  to  an  acute  (circumscribed) 
myocarditis.  In  the  blood  there  is,  almost  without  exception,  more  or  less 
marked  leucocytosis  and  a  diminution  in  the  number  of  red  corpuscles,  which 
in  the  severe  cases  may  lead  to  a  most  profound  anasmia.  The  demonstration 
of  the  pathogenic  organisms  in  the  blood,  is  of  the  greatest  importance.  ( Vide 
infra,  "Diagnosis.") 

4.  Cerebral  Symptoms. — The  grave  cerebral  symptoms  are  for  the  most 
part  quite  analogous  to  those  of  other  severe  acute  infectious  diseases.  They 
may  be  present,  and  yet  no  marked  objective  cerebral  lesions  may  be  found 
after  death.  In  other  cases  they  have  an  anatomical  basis — in  purulent  menin- 
gitis, hemorrhagic  pachymeningitis,  cerebral  hemorrhage,  or  abscess.  These 
conditions,  just  enumerated,  may  excite  focal  cerebral  symptoms — e.g.,  hemi- 
plegia. 


138  ACUTE   GENERAL  INFECTIOUS   DISEASES 

5.  Affections  of  the  Joints. — Affections  of  the  joints  are  comparatively  fre- 
quent, and  of  great  value  in  diagnosis.  We  may  find  serous,  or  more  likely 
purulent  inflammation,  or  even  peri-articular  abscesses.  If  they  appear  early 
in  the  attack,  they  may,  as  we  have  said,  lead  to  an  erroneous  diagnosis  of 
acute  articular  rheumatism.  Suppurative  processes  affecting  the  periosteum 
and  the  marrow  of  the  bones  not  infrequently  accompany  the  joint  affections. 
Only  in  rare  cases  do  the  bones  remain  wholly  unaffected,  as  is  evident  from 
the  frequent  occurrence  of  pain  in  the  long  bones.  If  there  is  decided  sup- 
puration in  the  bones  we  speak  of  an  acute  osteomyelitis.  This  is  seen  espe- 
cially in  the  lower  extremities.  It  is  almost  always  occasioned  by  the  Staphy- 
lococcus aureus.  In  earlier  times  such  cases  were  termed  bone-typhoid. 
Finally,  abscesses  and  extensive  phlegmonous  suppuration  in  the  muscles  are 
not  uncommon. 

6.  Renal  Changes. — Renal  changes  are  very  frequent,  but  abscesses  and 
hemorrhages  may  be  numerous  in  the  kidneys,  or  hemorrhages  in  the  mucous 
membrane  of  the  pelvis  of  the  kidney,  without  materially  altering  the  char- 
acter of  the  urine.  In  most  cases,  however,  an  acute  septic  nephritis  is  con- 
joined with  the  infarctions  and  abscesses,  and  then  the  urine  exhibits  all  the 
characteristics  of  acute  Bright's  disease,  having  a  small  or  large  amount  of 
albumen,  red  and  white  blood  corpuscles,  epithelium,  and  casts. 

7.  Pulmonary  Symptoms. — The  pulmonary  sym2?toms  are  in  part  second- 
ary. Bronchitis  and  lobular  pneumonia  develop  as  in  all  other  severe  con- 
stitutional diseases.  Embolic  foci  of  pneumonia  and  the  pulmonary  abscesses, 
as  such,  rarely  produce  distinct  objective  physical  symptoms,  but  frequently 
there  is  a  striking  dyspnoea  which  is  out  of  proportion  to  the  insignificance 
of  the  physical  symptoms.  Empyema  is  a  not  infrequent  result  of  infection 
of  the  pleura,  due  to  the  foci  of  disease  which  are  situated  upon  the  outer 
surface  of  the  lungs,  or  perhaps  sometimes  to  the  condition  of  the  blood.  If 
the  aspirating  needle  shows  the  actual  existence  of  empyema,  this  fact  may 
make  the  diagnosis  of  the  constitutional  disease  much  easier.  A  fibrinous 
pleurisy  of  slight  degree  is  often  found  at  the  autopsy,  and  it  may  be  diag- 
nosticated during  life  by  the  detection  of  a  slight  pleuritic  friction  rub. 

8.  Abdominal  Symptoms. — Of  the  abdominal  symptoms  we  have  already 
mentioned  the  acute  splenic  tumor.  It  is  almost  impossible  to  diagnosticate 
infarctions  and  abscesses  in  the  spleen.  If  the  spleen  is  enlarged  and  notice- 
ably painful,  we  may  suspect  their  existence.  There  are  sometimes  quite 
severe  intestinal  symptoms,  such  as  a  profuse  "  septic  diarrhea/'  in  cases  where 
the  autopsy  does  not  show  any  particularly  grave  lesions.  Still,  intestinal 
ecchymoses  and  intestinal  diphtheria  have  sometimes  been  observed.  We 
should  mention  that  often  the  skin  has  a  faint  jaundiced  hue.  This  is  some- 
times the  result  of  duodenal  catarrh,  but  more  frequently  it  is  to  be  re- 
garded as  a  "  hepato-hematogenous  "  jaundice  due  to  a  decomposition  of  the 
blood. 

9.  Ocular  Disturbances. — The  purulent  inflammations  of  the  eye,  which  are 
probably  of  embolic  origin  and  which  may  develop  into  diffuse  septic  panoph- 
thalmitis, have  been  known  for  some  time.  Lately,  Litten  and  others'  have 
called  attention  to  more  minute  changes  in  the  fundus  of  the  eye.  These  are 
revealed  through  the  ophthalmoscope,  and  have  great  diagnostic  value.  Chief 
among  them  is  retinal  hemorrhage,  which  is  sometimes  accompanied  by  a  white 


SEPTIC   AND   PYEMIC   DISEASES  139 

spot  in  the  center,  corresponding  to  a  necrosis  of  the  retina  in  that  place;  but 
there  may  be  similar  white  spots  without  hemorrhage. 

Course  of  the  Disease  and  Prognosis. —  In  severe  general  septic  infection, 
death  sometimes  occurs  in  a  few  days.  In  other  cases  the  disease  continues 
longer,  the  symptoms  lasting  two  or  three  weeks  or  even  more,  [mprovemenl 
sometimes  lakes  place,  followed  by  a  relapse.  Here,  too,  the  resull  is  often 
fatal,  although  the  infection  may  finally  be  completely  overcome.  We  may  also 
accept  as  certain  that  there  are  mild,  curable  forms  of  septic  disease.  In  these 
the  signs  of  general  infection  may  predominate,  such  as  fever  with  general 
intoxication,  cardiac  weakness,  pains  in  the  joints,  albuminuria  or  exanthe- 
mata, or,  in  other  cases,  the  chief  symptoms  may  be  due  to  a  special  localiza- 
tion of  the  germs  or  their  toxins  (acute  endocarditis,  septic  nephritis,  septic 
inflammation  of  the  serous  membranes,  septic  enteritis,  etc.).  As  we. shall  see 
later,  the  so-called  hemorrhagic  diseases,  as  also  acute  articular  rheumatism, 
acute  endocarditis,  erythema  exudativurn,  and  oilier  diseases  have  many  close 
connections  with  the  milder  forms  of  septic  infections. 

Diagnosis. — It  is  self-evident  that  a  disease  which  combines  symptoms  so 
manifold  and  so  ambiguous  must  be  very  difficult  to  recognize.  Especially  in 
the  prebacteriological  times  was  the  diagnosis  of  sepsis  often  impossible.  To- 
day the  advance  in  bacteriological  blood  examination  has  very  greatly  perfected 
our  diagnostic  technic  for  acute  infectious  diseases.  On  the  basis  of  bacterio- 
logical blood  findings,  it  is  not  only  possible  in  most  cases  to  make  a  diagnosis 
of  septicaemia,  but  also  to  determine  the  special  kind  of  infectious  agent 
(streptococci,  staphylococci,  B.  coli,  pneumonococci,  etc.).  JSTone  the  less,  for 
obvious  reasons,  this  method  of  diagnosis  cannot  at  present  be  generally  em- 
ployed in  medical  practice,  and  therefore  the  purely  clinical  diagnostic  means, 
though  often  far  less  certain  in  their  results,  still  retain  their  value.  We 
will  recapitulate  the  chief  diseases  to  be  excluded.  A  case  may  greatly  resem- 
ble typhoid  fever  when  there  is  persistent  prostration,  diarrhea,  an  eruption 
like  roseola,  and  an  enlarged  spleen.  In  discriminating,  we  should  consider 
with  great  care  the  possible  aetiology — e.  g.,  external  injuries,  etc. ;  we  should 
remember  that  most  septic  affections  begin  rather  more  abruptly;  and  we 
should  look  for  swelling  of  the  joints,  cutaneous  ecchymoses,  nephritis,  phleg- 
monous suppurations,  an  intermitting  form  of  fever,  and  septic  disease  of  the 
retina.  Leucocytosis  is  a  very  valuable  sign,  since  it  is  almost  always  absent 
in  typhoid  fever,  but  a  positive  result  from  WidaPs  serum  reaction  renders  a 
diagnosis  of  typhoid  very  probable.  It  is  all  the  more  possible  for  the  disease 
to  resemble  meningitis,  because,  as  we  have  said,  meningeal  disturbance  may 
be  one  of  the  symptoms  of  the  sepsis  and  color  the  whole  picture.  Here  the 
characteristic  symptoms  of  septic  poisoning  already  mentioned  would  be  of 
some  value  in  diagnosis,  and  the  physical  signs  of  endocarditis  or  of  a  greatly 
enlarged  spleen  would  be  worth  still  more.  The  final  decision  will  often 
depend  upon  the  result  of  lumbar  puncture.  There  may  be  much  difficulty  in 
the  differential  diagnosis  between  acute  sepsis  and  acute  miliary  tuberculosis. 
Here  we  should  consider  carefully  each  separate  symptom,  and,  above  all,  the 
aetiology,  searching  for  something  that  would  explain  the  occurrence  of  sepsis 
on  the  one  hand,  or  of  acute  miliary  tuberculosis  ( q.  v. )  on  the  other.  If  we 
found  miliary  tubercles  in  the  choroid  by  means  of  the  ophthalmoscope,  or 
tubercle  bacilli  in  the  sputum  or  in  the  blood  (which  is,  of  course,  not  always 


140  ACUTE   GENERAL  INFECTIOUS   DISEASES 

possible),  all  doubt  would  vanish.  A  marked  diazo-reaction  of  the  urine,  too, 
argues  for  acute  tuberculosis.  At  the  beginning  of  a  septic  attack  the  rigors 
may  arouse  suspicions  of  intermittent  fever.  Usually  the  early  appearance  of 
other  symptoms  corrects  this  idea ;  but,  if  not,  the  powerlessness  of  quinin  will. 
If  a  severe  acute  nephritis  has  developed  itself  in  a  septic  case,  all  the  symp- 
toms may  be  erroneously  referred  to  ursemia ;  but  persistent  observation 
will  usually  lead  us  to  the  right  conclusion.  As  to  the  conditions  of  great 
prostration  resembling  acute  sepsis,  which  occur  in  acute  (primary)  ulcera- 
tive endocarditis  and  in  severe  articular  rheumatism,  see  the  appropriate 
chapters. 

In  general,  the  diagnosis  of  acute  sepsis  and  septico-pyasmia  can  rarely  be 
settled  during  the  first  days  of  the  disease,  but  on  further  observation  and  with 
due  attention  a  tolerably  definite  diagnosis  can  usually  be  made.  The  chief 
elements  for  diagnosis  are  a  careful  consideration  of  the  aetiology  (previous 
circumscribed  suppurations,  sore  throat,  etc.)  and  attention  to  the  whole 
clinical  picture,  as  well  as  to  any  individual  symptoms  especially  characteristic 
of  septic  infection  (purulent  inflammation  chills  and  fever,  cutaneous  and 
retinal  hemorrhages,  nephritis,  joint  swellings,  splenic  tumor,  pale,  icteric 
complexion,  marked  leucocytosis,  etc.). 

If  there  be  persistent  high  intermittent  fever  with  chills,  without  any 
demonstrable  local  affection  and  an  often  fairly  good  general  condition  for  a 
long  time,  we  must  susjDect  a  hidden  pus  focus  in  the  body.  This  point  must 
always  be  carefully  borne  in  mind  because  of  the  possibility  of  surgical  treat- 
ment. Examine  most  thoroughly  and  give  due  attention  to  the  subjective 
complaints  of  the  patient  (pain,  sensitiveness  to  pressure,  etc.).  Concealed 
suppurative  processes  in  the  abdominal  cavity  (subphrenic  or  perinephritic 
abscesses)  are  especially  apt  to  be  overlooked. 

Treatment.- — The  treatment,  aside  from  cases  in  which  surgical  interven- 
tion is  indicated,  is  merely  symptomatic.  Of  course  we  try  again  and  again 
to  cut  short  the  attacks  of  fever  by  large  doses  of  quinin,  antipyrin,  pyramidon, 
etc.,  but  never  with  lasting  success.  With  marked  swelling  of  the  joints  we 
may  try  the  salicylates.  Of  other  remedies,  cardiac  stimulants  (alcohol,  cam- 
phor, caffein)  are  most  frequently  employed,  and  narcotics  if  necessary.  At 
times  the  repeated  subcutaneous  infusion  of  sterile  physiological  saline  solu- 
tion is  most  appropriate,  especially  when  cardiac  strength  is  failing  and  vas- 
cular tension  lessening.  Great  stress  is  to  be  laid  on  keeping  up  the  physical 
strength  by  careful  nourishment.  Specific  treatment,  promising  as  its  future 
may  be,  has  not  yet  attained  positive  success.  Others  and  we  ourselves  have 
not  seen  indubitable  results  from  the  various  antistreptococcic  sera,  any  more 
than  from  the  chemical  preparations  recommended  (argentum  colloidale  named 
"  collargol,"  twenty-five  per  cent  iodipin  subcutaneously,  5  to  10  c.c.  =  H\lxxv 
to  3ijss.).  None  the  less,  these  remedies  will  frequently  be  resorted  to  in 
practice. 

Circumscribed  suppurative  processes,  which  may  develop  (vide  supra),  of 
course  demand  appropriate  surgical  treatment  (empyema,  phlegmons,  deep- 
seated  abscesses,  etc.).  The  recent  efforts  to  treat  puerperal  fever  and  other 
septico-pyasmic  infections  arising  from  the  uterus  by  tying  off  the  afferent 
veins,  can  only  be  briefly  mentioned  here.  [What  is  said  of  specific  sera  ap- 
plies also  to  vaccinations  with  sterilized  bacteria,  preferably  obtained  by  blood 


TETANUS  141 

culture.  In  an  acute  and  severe  case  of  sepsis  there  is  scarcely  any  hope  of 
their  doing  good;  in  a  milder  and  more  chronic  infection  the  possibility  of 
benefit  is  a  trifle  greater.] 


CHAPTEE    XX 

TETANUS 

{Lockjaw) 

Tetanus  is  an  acute  infectious  disease  whose  chief  symptom  is  the  occur- 
rence of  severe,  extensive,  tonic  ("tetanic")  muscular  spasms.  The  specific 
cause  of  tetanus,  the  tetanus  bacillus,  was  first  discovered  by  Xicolaier  in 
garden  earth,  and  examined  more  closely  in  pure  culture  by  Kitasato.  Rosen- 
bach  first  cultivated  the  same  bacilli  from  the  secretion  of  the  wound  of  a  man 
who  died  of  traumatic  tetanus.  Since  then  the  specific  significance  of  the 
tetanus  bacillus  has  been  positively  confirmed  beyond 
any  doubt  by  numerous  investigations.     These  bacilli  '»-      *    — 

are    slender   motile   rods,    distinguished    by   a   little  \i    ,    f^  V  *f 

head  spore  at  one  end  (vide  Fig.  25).    These  spores         /  &-        S\ 

are  remarkable  for  their  resistance  to  external  in-       -  k  N      I   f>    ^*\P 

fluences  (heat  and  desiccation).     The  tetanus  bacilli  <{  ,     "^       \>  <( 

grow    only    anaerobically — i.  e.,    under    the    greatest  /    __     <v^  ^  ^ 

possible  exclusion  of  oxygen.     Their  growth  is  there-  .  ^     A 

fore  facilitated  by  the  presence  of  other  bacilli  which 

consume  oxygen.  If  a  small  quantity  of  bacilli  is  Fig.  25. — Tetanus  bacilli, 
injected  under  the  skin  of  mice,  rabbits,  or  guinea 

pigs,  the  animals  die  under  the  most  violent  tetanic  spasms  in  from  twenty- 
four  to  thirty-six  hours.  Since  the  development  of  the  bacteria  remains  lim- 
ited to  the  seat  of  the  wound  or  the  injection,  it  is  a  priori  probable  that  the 
spasms  are  not  excited  immediately  by  the  bacilli,  but  by  a  chemical  poison 
produced  by  them  during  life.  In  fact,  Brieger  has  lately  succeeded  in  pro- 
ducing several  alkaloid-like  substances  from  tetanus  cultures,  so-called  toxins, 
which  he  terms  tetanin,  tetanotoxin,  and  spasmotoxin.  All  these  substances 
are  violent  poisons,  and,  like  strychnin,  provoke  the  most  violent  tetanic 
spasms  in  the  animals  experimented  on. 

According  to  the  investigations  of  H.  Meyers,  the  tetanus  toxins  are  first 
absorbed  by  the  peripheral  nerves  and  thence  migrate  up  to  the  central  organs. 

In  regard  to  the  method  of  infection  in  man,  it  occurs  by  far  most  fre- 
quently through  open  wounds  (operation  wounds,  or  small  accidental  injuries). 
Since  the  tetanus  bacilli  are  found  chiefly  in  the  soil,  we  can  readily  under- 
stand that  injuries  of  the  feet  in  persons  who  go  barefoot,  or  injuries  of  the 
hands  in  gardeners,  farmers,  etc.,  most  frequently  give  rise  to  tetanus.  In 
view  of  the  wide  prevalence  of  the  tetanus  bacilli,  the  rareness  of  tetanus  in 
human  beings  is  striking.  This  is  probably  explained  by  the  anaerobic  require- 
ment for  growth.  Therefore,  the  most  danger  exists  in  somewhat  deep  wounds, 
situated  beneath  the  skin,  that  are  rendered  unclean  by  garden  earth  (stab 
wounds  [blank-cartridge  wounds],  long  wooden  splinters,  etc.).     The  fact  is 


142  ACUTE   GENERAL  INFECTIOUS   DISEASES 

of  practical  importance  that  the  tetanus  bacilli  are  not  infrequently  found  in 
the  caecum  of  herbivorous  animals  (horses  and  cows).  Therefore,  earth  mixed 
with  dung  is  especially  infectious.  Horses  frequently  suffer  from  tetanus. 
Formerly,  in  place  of  traumatic  tetanus,  the  term  idiopathic  tetanus  was  em- 
ployed where  no  external  injury  could  be  detected  as  a  point  of  infection. 
[Commercial  gelatin  may  contain  tetanus  bacilli,  and  therefore  should  be  thor- 
oughly sterilized  before  it  is  used  for  therapeutic  injections  for  bleeding.] 
Aside  from  small,  unnoticed  external  injuries,  infection  may  take  place 
through  the  mucous  membranes  (pharynx).  If,  as  is  often  the  case,  the 
affection  is  preceded  by  a  severe  cold  or  wetting,  we  speak  of  a  rheumatic 
tetanus.  Tetanus  neonatorum  is  undoubtedly  an  ordinary  wound  tetanus, 
almost  always  arising  from  an  infection  of  the  umbilicus. 

In  Germany  [and  temperate  latitudes  generally]  tetanus  is  a  compara- 
tively rare  disease.  Men  are  much  oftener  attacked  than  women.  Tetanus  is 
much  more  common  in  the  tropics  than  in  our  climate.  The  frequency  of  the 
disease  in  negroes  is  well  known.  Tetanus  is  also  not  equally  frequent  at  all 
times.  Endemics  and  epidemics  of  tetanus  have  often  been  observed,  espe- 
cially in  time  of  war.  These  have  arisen  in  part  from  the  unfavorable  influ- 
ence of  certain  external  conditions,  such  as  poor  care,  bad  weather,  sleeping 
on  the  wet  ground,  etc. 

Clinical  History. — In  so-called  "  rheumatic  "  tetanus  the  symptoms  usually 
begin  soon  after  exposure  to  the  exciting  cause.  There  may  be,  however,  an 
interval  during  which  the  patient  feels  perfectly  well,  or  at  most  has  only 
certain  mild  and  indefinite  premonitory  symptoms,  such  as  languor  and  head- 
ache.    Similar  prodromata  may  occur  in  the  apparently  idiopathic  cases. 

Traumatic  tetanus  seldom  begins  immediately  after  the  injury  has  been 
received.  Several  days  or  even  weeks  may  intervene  previous  to  the  outbreak 
of  the  disease.  Here,  too,  there  may  be  mild  prodromata  for  a  brief  period 
preceding  the  graver  phenomena.  The  patient's  wound  presents,  as  a  rule,  no 
specific  appearances.  Tetanus  may  be  associated  with  either  slight  or  severe 
injuries,  whether  treated  carelessly  or  kept  apparently  aseptic. 

The  symptoms  of  the  disease  proper  are  the  same  in  both  rheumatic  and 
traumatic  tetanus.  They  usually  begin  gradually.  Ordinarily,  the  first  thing 
noticed  is  a  feeling  of  rigidity  and  tension  in  the  muscles  of  the  face,  lower 
jaw,  and  back  of  the  neck.  The  stiffness  spreads  by  degrees  to  the  muscles  of 
the  back  and  abdomen.  The  disease  is  sometimes  completely  developed  in  a 
few  hours,  but  sometimes  not  till  after  several  days. 

The  persistent  tension  of  the  facial  muscles  gives  the  countenance  a  strange 
immobility  (vide  Fig.  26).  The  brow  is  usually  wrinkled,  and  the  corners  of 
the  mouth  are  often  drawn  back  in  a  "  sardonic  grin,"  or  the  face  has  a  tear- 
ful expression  from  the  deepening  of  the  nasolabial  folds  and  the  drawing 
down  of  the  corners  of  the  mouth.  Most  prominent  of  all  is  the  tonic  spasm 
of  the  masseters,  or  trismus.  The  teeth  are  so  firmly  pressed  together  that  it 
finally  becomes  impossible  to  open  the  mouth  more  than  a  few  millimeters. 
The  eyes  are  staring,  the  pupils  usually  contracted.  The  muscles  at  the  back 
of  the  neck  draw  the  head  somewhat  backward,  but  in  many  cases  it  can  still 
be  moved  quite  well,  although  in  other  cases  it  is  fixed  by  the  spasm.  The 
spinal  column  is  bent  forward,  so  that  the  trunk  is  convex  anteriorly,  permit- 
ting the  hand  to  be  passed  between  it  and  the  bed — opisthotonos.    The  muscles 


TETANUS 


143 


of  the  back  are  hard  and  contracted.    The  epigastrium  and  the  anterior  part 
of  the  abdomen  arc  flat.    The  abdominal  muscles  are  as  hard  as  a  board.    The 
lower  limbs  may  be  rigidly  extended  at  the  knee,  and  the  adductors  an 
contracted,  but,  as  a  rule,  the  feet  and  toes  arc  five  from  spasm.     The  arms 


Fig.  26. — Facies  in  tetanus.      The  mouth  cannot  be  opened  wider  on  account  of  the  existing 

trismus  (personal  observation). 


generally  can  be  quite  freely  moved,  but  the  movements  at  the  shoulder  are 
usually  decidedly  impaired.  Convulsive  dysphagia,  as  seen  in  hydrophobia, 
may  occur,  but  it  is  rare  {vide  infra). 

In  many  cases  the  continuous  tonic  spasm  is  occasionally  interrupted  by 
sudden  paroxysms,  during  which  all  the  affected  muscles  become  still  more 
tense.  In  severe  cases  this  gives  the  whole  body  a  violent  shock,  and  makes 
the  opisthotonos  even  more  pronounced.  In  a  very  bad  case  the  paroxysms  are 
very  frequent ;  in  a  mild  case  they  are  rare  or  almost  indistinguishable.  Some- 
times they  are  apparently  spontaneous,  and  sometimes  they  are  evidently  of 
reflex  origin,  being  superinduced  by  external  irritation,  often  quite  insig- 
nificant, such  as  a  slight  jar  of  the  body,  noises,  etc. 

As  to  other  nervous  derangements,  little  is  known  about  them — partly,  no 
doubt,  because  it  is  seldom  possible  to  make  an  extended  examination  of  the 
patient.  Sensation  is  said  to  have  been  impaired  in  some  instances,  but  in 
others  it  is  perfectly  normal.  The  muscles  affected  by  the  spasms  are  usually 
the  seat  of  severe  pain.  The  cutaneous  reflexes  are  almost  always  exaggerated. 
In  several  cases  which  we  saw  very  recently,  the  patellar  reflex  was  much 
10 


144  ACUTE   GENERAL  INFECTIOUS   DISEASES 

increased,  and  in  one  there  was  distinct  ankle  clonus.  Paralysis  is  extremely 
exceptional.  There  is  often  profuse  perspiration.  The  forehead  is  usually 
studded  with  many  beads  of  sweat.    The  intellect  remains  perfectly  unclouded. 

There  is  a  special  form  of  tetanus  which  must  be  briefly  mentioned.  It  was 
first  described  by  E.  Kose,  and  is  called  "  hydrophobic  tetanus,"  or  "  cephalic 
tetanus."  It  occurs  only  in  connection  with  injuries  situated  in  the  distribu- 
tion of  the  cranial  nerves — that  is,  in  the  face  and  head — and  is  characterized 
in  most  cases  by  violent  spasm  of  the  muscles  of  the  pharynx.  This  is  in  addi- 
tion to  the  other  ordinary  phenomena  of  tetanus.  The  disease  in  many  ways 
reminds  one  of  hydrophobia.  Another  characteristic  point  is  that  in  most 
cases  there  is  facial  paralysis  on  the  injured  side. 

Tetanus,  as  a  rule,  gives  rise  to  no  disturbances  referable  to  the  internal 
viscera.  In  one  case,  however,  in  the  Leipsic  hospital,  croupous  pneumonia  and 
acute  nephritis  came  on  a  few  days  before  the  end.  Often  there  are  dyspnoea 
and  a  most  harassing  sense  of  thoracic  oppression — symptoms  due  mainly  to 
the  convulsive  rigidity  of  the  muscles,  by  which,  the  thorax  is  constantly  main- 
tained in  the  position  it  normally  assumes  during  inspiration.  Expectoration 
is  impeded;  and,  finally,  there  may  be  such  an  accumulation  of  secretions  in 
the  mouth  and  air-passages  as  to  cause  a  secondary  diffuse  bronchitis,  or  an 
inhalation  pneumonia.  Another  occasional  source  of  extreme  dyspnoea  is 
spasm  of  the  glottis. 

The  pulse  often  remains  normal  for  a  long  while/but  it  is  usually  accelerated, 
not  infrequently  reaching  120  or  160  beats  a  minute  in  severe  cases.  Such  a 
pulse  is  small,  and  may  be  somewhat  irregular.  The  temperature  is  at  first 
usually  normal,  or  slightly  elevated  (100°  to  102°  F.  [38°  to  39°  C.]).  Later 
it  is  almost  sure  to  rise,  and,  as  Wunderlich  pointed  out,  it  is  often  very  high 
shortly  before  death— for  instance,  107°  to  111°  F.  (42°  to  44°  C).  It  is  not 
rare  for  the  temperature  to  keep  on  rising  for  a  short  time  after  death.  No 
explanation  of  this  terminal  elevation  of  temperature  has  yet  been  furnished. 
It  cannot  be  the  result  of  the  increased  production  of  heat  occasioned  by  the 
muscular  spasm,  for  in  earlier  stages  the  most  violent  convulsions  are  unat- 
tended by  any  such  change.  Authorities  are,  therefore,  inclined  to  assume 
that  at  the  last  there  is  a  paralysis  of  the  centers  which  regulate  the  warmth 
of  the  body,  just  as  is  seen  in  other  severe  nervous  disorders,  such  as  menin- 
gitis, injury  to  the  cervical  portion  of  the  cord,  and  uraemia. 

Interesting  observations  have  been  made  with  regard  to  tissue-metamor- 
phosis during  tetanus.  The  excretion  of  urea  is  not  increased.  This  fact 
agrees  well  with  Voit's  view,  that  muscular  activity  has  no  relation  to  the 
breaking  down  of  albuminoids.  Senator  failed  to  find  any  increase  of  kreatin 
and  kreatinin  in  the  urine.  Probably  the  production  of  carbonic  dioxid  is 
abnormally  large  in  tetanus.  At  least,  physiological  considerations  would 
strongly  indicate  this,  although  it  has  not  yet  been  actually  demonstrated. 
Occasionally  traces  of  albumen  and  sugar  have  been  detected  in  the  urine. 
There  is  usually  obstinate  constipation,  probably  due  to  the  persistent  rigidity 
of  the  abdominal  muscles;  and,  indeed,  micturition  is  not  a  little  impeded 
from  the  same  cause. 

It  may  be  said,  in  regard  to  the  general  course  of  the  disease,  that  there  are 
severe  and  mild  forms  of  the  disease.  What  has  been  said  above  applies  mainly 
to  the  severe  form.    In  this,  all  the  symptoms  reach  their  extreme  violence  in  a 


TETANUS  145 

few  days,  the  paroxysms  occur  hr  quick  succession,  and  death  usually  ti 
place  within  a  week  or  two.  The  fatal  resull  is  brought  about  by  the  suspen- 
sion of  respiration  and  by  cardiac  failure.  Of  course,  the  extreme  difficulty  of 
taking  an  adequate  amount  of  food  has  an  unfavorable  influence.  The  bad 
cases  seldom  outlast  the  first  week.  If  they  do,  there  is  some  slighl  hope  of 
recovery;  the  paroxysms  may 'gradually  become  less  l'rcquenl  and  Less  severe, 
until  they  finally  cease  altogether.  The  severer  form,  however,  so  rarely  ends 
favorably  that  the  prognosis  is  always  very  grave.  The  mild  form,  on  the 
contrary,  usually  runs  a  much  more  favorable  course.  In  it,  all  the  symptoms 
are  from  the  first  much  less  severe.  Often  there  is  only  more  or  less  trismus, 
accompanied  by  no  marked  spasm  in  the  muscles  of  the  trunk,  if  any  at  all. 
There  is  little  constitutional  disturbance.  The  temperature  is  normal,  and 
the  prognosis  is  rather  favorable.  The  disease  may  sometimes  drag  on  for 
some  weeks,  but  it  often  ends  in  complete  recovery.  It  must  not  be  forgotten, 
however,  that  what  at  first  seems  a  mild  case  may  develop  into  the  severe 
form. 

The  anatomical  changes  in  the  nervous  system  in  fatal  cases  are  almost 
wholly  negative.  Further  investigations  are  necessary  to  determine  how  far 
the  finer  changes  in  the  motor  cells  of  the  spinal  cord,  which  have  repeatedly 
been  found  of  late,  are  of  pathological  significance.  Any  small  hemorrhages, 
etc.,  have,  if  they  be  present,  only  a  secondary  significance. 

Diagnosis. — In  most  cases,  tetanus  can  be  easily  recognized  from  the 
peculiar  convulsions  and  the  general  aspect  of  the  disease.  It  might  be  con- 
founded with  acute  meningitis,  for  this  may  cause  rigidity  of  the  neck  and 
back;  but  here  there  are  usually  certain  cerebral  symptoms  also  present,  such 
as  headache  and  impairment  of  consciousness;  and,  on  the  other  hand,  in 
tetanus,  trismus  is  an  almost  constant  phenomenon,  although  exceptional  in 
meningitis.  Strychnin  poisoning  produces  convulsions  similar  to  those  of 
tetanus,  but  they  generally  affect  the  extremities  in  a  more  marked  degree. 
Hydrophobia  is  distinguished  from  tetanus  by  the  aetiology,  the  absence  of  tris- 
mus, the  predominance  of  the  pharyngeal  convulsions,  and  the  greater  dis- 
tinctness of  the  individual  paroxysms.  The  hysterical  conditions  similar  to 
tetanus  can  usually  be  easily  distinguished  from  genuine  tetanus  by  the  dis- 
covery of  specific  hysterical  symptoms  (anaesthesia,  etc.). 

Where  trismus  is  the  only  symptom,  we  must  guard  against  mistaking  for 
tetanus  the  symptomatic  rigidity  of  the  jaws  which  occurs  with  severe  sore 
throat,  diseases  of  the  teeth,  or  inflammation  of  the  maxillary  articulation. 

Treatment. — The  attempts  to  cure  tetanus  by  means  of  an  antitoxic  serum 
(Behring,  Tizzoni)  are  most  interesting.  Horses  may  be  rendered  immune 
to  tetanus.  Their  blood  serum  then  contains  an  antitoxin  which  annuls  the 
action  of  the  tetanus  toxin  as  long  as  it  circulates  free  in  the  blood.  If  a  case 
of  tetanus  comes  under  treatment  during  the  first  thirty-six  hours,  the  pros- 
pects of  improvement  from  the  injection  of  serum  are  very  good.  One  hundred 
antitoxin  units  are  injected  (i.  e.,  a  vial  of  Behring's  antitoxin)  near  the  sus- 
pected site  of  infection.  The  injection  is  repeated  daily  for  several  days.  If 
serum  treatment  is  deferred,  the  chances  for  improvement  are  small,  as  then 
large  quantities  of  tetanus  toxin  are  already  taken  up  by  the  ganglion  cells, 
and  in  consequence  can  no  longer  be  influenced  by  the  antitoxin.  Of  course  a 
trial  of  antitoxic  treatment  will  be  made  whenever  possible. 


146  ACUTE   GENERAL  INFECTIOUS   DISEASES 

If  the  physician  cannot  obtain  an  antitoxic  serum,  he  must  look  to  the 
methods  of  treatment  heretofore  employed.  We  have  ourselves  treated  all  the 
cases  we  have  seen  in  the  last  few  years  with  salicylic  acid  (8  gr.,  gm.  0.5, 
every  hour),  and  we  believe  that  we  have  repeatedly  seen  a  favorable  influence 
from  this  remedy.  In  addition  we  like  to  make  use  of  routine  diaphoretic 
procedures,  which  the  patients  tolerate  well  because  they  usually  bring  relief 
from  their  painful  spasms.  Otherwise  narcotics  are  to  be  used.  Those  chiefly 
recommended  are  subcutaneous  injections  of  morphin,  opium  in  large  doses 
(if  desirable  combined  with  bromids),  and  chloral  hydrate,  of  which  30  gr. 
(gm.  2)  should  be  given  two  or  three  times  a  day,  and  the  amount  gradually 
increased.  If  deglutition  be  very  difficult,  the  chloral  may  be  given  by  enema. 
The  above  remedies  diminish  the  irritability  of  the  nervous  centers.  In 
curare  we  possess  a  means  of  lowering  the  excitability  of  the  terminations  of 
the  motor  nerves  in  the  muscles.  It  has  therefore  been  employed  by  many, 
but  by  few  with  success.  It  is  difficult  to  say  what  the  dose  of  curare  is,  inas- 
much as  the  strength  of  different  samples  varies.  The  best  way  is  to  deter- 
mine the  strength  of  the  solution  to  be  employed  by  experimenting  on  some 
animal.  Usually  a  one-per-cent  solution  of  curare  in  water  is  en^loyed,  and 
an  amount  equal  to  one  quarter  of  the  contents  of  a  Pravaz  syringe  is  in- 
jected, the  dose  being  gradually  and  cautiously  increased.  [Such  a  syringe 
contains  about  13  minims  (0.8  gr.).] 

It  is  very  desirable  to  put  the  patient  by  himself  in  a  darkened  and  quiet 
chamber.  Nourishment  should  be  liquid,  and  lukewarm  stimulants,  such  as 
alcohol  and  camphor,  should  be  given  from  the  first.  Protracted  warm  baths 
may  be  given  cautiously.  We  know  from  personal  observation  that  such  baths 
are  very  grateful  to  some  patients. 

It  need  hardly  be  said  that  in  traumatic  tetanus  the  primary  wound  should 
receive  careful  attention.  [Prophylactically,  suspicious  wounds  should  be  laid 
open  and  thoroughly  cleansed  antiseptically,  and  the  patient  given  serum.] 
Since  the  tetanus  bacilli  remain  limited  in  their  growth  to  the  seat  of  the 
wound,  it  may  be  indicated  in  the  beginning  of  tetanus,  if  possible,  to  ampu- 
tate the  wounded  part  or  to  excise  the  wound,  as  in  the  case  of  a  toe  injury. 
Of  course,  from  present  experience,  we  cannot  with  certainty  promise  success. 


CHAPTEE    XXI 

HYDROPHOBIA 

(Rabies  canina.  Lyssa) 

iEtiology. — A  peculiar  infectious  disease  sometimes  occurs  in  dogs,  and 
more  rarely  in  some  other  animals — viz.,  the  wolf,  fox,  cat,  etc.  Men  who 
are  bitten  by  the  animal  may  catch  the  disease,  and  thus  suffer  from  very 
severe  symptoms  originating  in  the  central  nervous  system. 

Two  forms  of  madness  are  distinguished  in  dogs — the  raving  madness  and 
the  quiet  madness.  Bollinger  describes  the  raving  form  as  beginning  with  pro- 
dromata,  the  melancholy  stage,  lasting  one  to  three  days.  The  animal  is  low- 
spirited,  timorous,  and  without  appetite.     Then  comes  the  stage  of  irritation 


HYDROl'llOJilA  147 

or  of  mania,  in  which  the  animal  is  possessed  with  an  impulse  to  bite.  U 
seems  determined  to  run  away  and  rove  about,  and  ii  utters  a  peculiar  howl. 
The  dog  will  not  touch  his  ordinary  food,  hut  he  often  swallows  Btraw,  hair, 
earth,  hits  of  wood,  etc.  In  the  third  or  paralytic  stage  paralysis  appears.  The 
dog  looks  lean  and  wretched,  and  always  dies  on  the  tenth  day  at  the  latest. 
in  what  is  called  the  quiet  madness  there  is  no  maniacal  stage  The  symptoms 
of  paralysis,  affecting  chiefly  the  hind  limbs  and  the  lower  jaw,  occur  earlier 
and  are  sooner  fatal.  Marked  pathological  changes  are  not  found.  There  are 
pulmonary  and  intestinal  catarrh  and  passive  congestion  of  the  viscera,  and 
the  stomach  often  contains  foreign  bodies  in  place  of  the  usual  partially  di- 
gested food. 

[On  the  Western  plains  hydrophobia  is  said  not  infrequently  to  follow 
skunk  bites.  The  bite  is  inflicted  during  sleep  on  persons  passing  the  night 
in  the  open  air  or  in  tents  to  which  the  animal  can  gain  access.] 

Rabies  is  transferred  to  the  human  being  almost  invariably  by  the  bite  of 
some  raving  animal,  and  this  animal  is  almost  always  a  dog;  much  more  rarely 
a  wolf  or  cat.  It  is  of  practical  importance,  and  it  has  been  repeatedly  con- 
firmed, that  the  bite  of  such  an  animal,  although  still  in  the  incubation  period 
of  hydrophobia,  can  convey  the  disease  to  man.  The  poison,  which  is  not  yet 
known  in  its  pure  form,  is  evidently  contained  in  the  saliva  or  slaver  or  in 
the  blood  of  mad  animals,  and  can,  by  means  of  these  substances,  be  success- 
fully inoculated  in  other  animals.  Pasteur  has  discovered  another  way  to  pro- 
duce the  disease  experimentally.  One  takes  minute  portions  of  the  brain, 
medulla  oblongata,  or  some  other  internal  viscus  of  a  mad  dog,  and  either 
injects  them  into  the  veins  of  a  healthy  animal,  or  trephines,  and  then  inserts 
them  beneath  the  meninges.  The  virulence  of  the  rabic  poison  when  thus 
manipulated  undergoes,  under  special  conditions,  very  peculiar  alterations, 
which  will  be  detailed  at  the  close  of  this  chapter. 

About  one  half  of  those  who  are  bitten  by  mad  animals  exhibit  no  subse- 
quent  symptoms.  Still,  this  can  scarcely  be  due  to  inherent  immunity  from  the 
disease,  and  it  must  result  chiefly  from  imperfect  infection.  Experience  has 
shown  that  infection  is  especially  apt  to  follow  when  through  the  bite  a  large 
quantity  of  the  saliva  of  the  diseased  animal  gets  into  the  wound  and,  at  the 
same  time,  small  nerve  branches  are  injured.  It  is  believed  that  the  poison 
reaches  the  nervous  centers  chiefly  through  the  nerve  channels,  and  to  a  lesser 
extent  by  way  of  the  blood  and  lymphatic  streams.  The  liability  to  infection 
is  in  direct  ratio  to  the  size  of  the  bite  and  its  proximity  to  the  brain.  Wounds 
of  the  head  are  therefore  the  most  dangerous,  and  next  to  them  come  wounds 
of  the  hands. 

The  duration  of  incubation  until  rabies  finally  breaks  out  seems  to  vary 
greatly.  As  a  rule  it  is  about  three  to  six  months,  but  observers  have  reported 
instances  both  of  shorter  and  of  much  longer  duration. 

Clinical  History. — The  disease  begins  with  a  general  feeling  of  indisposi- 
tion, anorexia,  headache,  and  uneasiness.  This  last  is  partially  explained,  to 
be  sure,  by  a  dread  of  what  is  impending.  If  the  bite  was  in  the  face,  fre- 
quent convulsive  sneezing  may  occur.  Even  now,  in  this  prodromal  stage,  a 
marked  aversion  to  liquids  is  a  usual  and  early  symptom.  The  attempt  to 
swallow  excites  slight  convulsive  disturbances.  Painful  sensations  may  arise 
once   more   in   the  bitten   place,   although   this   has   usually  been   cicatrized 


148  ACUTE   GENERAL   INFECTIOUS   DISEASES 

long    before;    and    the    neighboring    lymph-glands    are    often    found    to    be 
swollen. 

Only  a  day  or  two  later  the  second  hydrophobic  stage  begins.  The  especial 
characteristic  of  this  consists  in  the  peculiar  attacks  of  tonic  convulsions.  The 
pharynx  suffers  most,  but  convulsions  also  attack  the  muscles  of  respiration 
and  those  of  the  trunk  and  extremities.  Severe  dyspnoea  and  a  terrible  feel- 
ing of  anxiety  and  oppression  accompany  these  attacks,  so  that  one  who  has 
once  witnessed  the  sight  can  never  forget  it.  The  convulsions  always  seem  to 
be  reflex,  and  are  produced  by  the  slightest  causes,  particularly  by  any  attempt 
to  swallow,  or  sometimes  by  the  mere  sight  of  water.  They  recur  at  gradually 
diminishing  intervals,  and  last  from  a  few  minutes  to  half  an  hour.  The 
excitement  of  the  patient  may  reach  the  pitch  of  delirium  or  mania.  The 
pulse  is  at  first  full  and  rapid,  but  later  it  is  small  and  irregular.  The  tem- 
perature is  usually  only  slightly  elevated,  but  later  it  not  rarely  rises  to  39° 
to  40°  C.  (102°  to  104°  F.).  Shortly  before  death  hyperpyrexia  is  sometimes 
present.  There  is  great  thirst,  accompanied  by  burning  pain  in  the  throat. 
Usually  there  is  marked  salivation. 

This  condition  lasts  one  to  three  days.  Then  death  occurs,  ushered  in  by 
violent  convulsions.  Death  may  also  be  preceded  by  a  brief  third  stage  of 
paralysis,  during  which  there  are  no  convulsive  attacks.  Cases  of  recovery 
in  man,  if  they  ever  happen,  are  extremely  rare. 

The  autopsy  shows  very  little.  The  brain  and  medulla  especially  show  no 
gross  changes,  so  that  we  may  conclude  that  hydrophobia  is  chiefly  the  effect 
of  a  toxin.  The  microscope  has  repeatedly  detected  very  minute  hemorrhages, 
clusters  of  lymph-cells  around  the  blood  vessels,  etc.  There  have  been  only 
a  few  investigations  of  the  finer  microscopical  changes  in  the  motor  ganglion 
cells  of  the  medulla,  etc. 

Negri  was  the  first  to  discover  certain  peculiar  but  important  changes  in 
the  ganglion  cells,  chiefly  those  in  the  hippocampus  major.  They  contain  small 
round  bodies  with  honeycomb-like  structure,  in  whose  interior  there  are  often 

one  or  two  minute  vacuoles.  In '  sections 
stained  with  eosin-methylene-blue,  these  Negri 
bodies  appear  red  on  a  blue  background.  In  all 
probability  they  are  not  microorganisms,  but. 
the  outcome  of  special  cell  changes.  They  are, 
however,  of  great  diagnostic  significance,  since 
they  are  found  almost  constantly  and  exclu- 
sively in  human  as  well  as  in  animal  hydro- 
phobia. The  throat  may  present  the  signs  of 
Fig.  27.— Ganglion  cells  from  the  re-     catarrh.     The  lungs  are  congested,  and  often 

gion  of  the  hippocampus  major  n  mi      1  1    -  n   •      i      1  -j.i    j?  i    j. 

of  a  rabbit,  showing  Negri  bodies,     cedematous.    The  blood  is  dark,  with  few  clots.. 

The  heart,  liver,  and  spleen  are  normal. 
Diagnosis. — The  diagnosis  is  usually  easy,  particularly  if  we  know  of  the 
possibility  of  infection.  We  are  guided  by  the  convulsions  following  attempts 
to  swallow,  as  well  as  by  the  whole  group  of  symptoms.  Hydrophobia  is  dis- 
tinguished from  traumatic  tetanus  by  the  absence  of  trismus  and  of  the  char- 
acteristic tension  of  the  muscles  of  the  back  and  abdomen,  by  the  convulsions 
coming  in  separate  attacks,  and  by  the  usually  greater  length  of  incubation. 
Only  the  so-called  hydrophobic  tetanus   ( q.  v. )   bears  very  great  resemblance 


HYDROPHOBIA  149 

to  rallies.     II  should  be  mentioned  that  the  mere  dread  of  hydrophobia  may 
cause  an  easily  excited   person  to  have  the  nervous  symptoms  of  the  disi 
("hysterical  hydrophobia"),  but  of  course  without  disastrous  results.     Hys- 
teria, also,  may  give  rise  to  convulsions  on  swallowing  somewhat  resembling 
those  of  hydrophobia. 

Treatment. — However  hopeless  treatmenl  seem-,  we  musi  ai  least  try  to 
mitigate  the  patient's  suffering.  Narcotics  accomplish  this  besi — e.g.,  opium 
or  chloral,  or,  most  useful  of  all,  the  inhalation  of  chloroform.  Curare  has 
been  administered  repeatedly,  and  does  seem  to  lessen  the  violence  of  the  at- 
tacks. The  attempt  to  find  a  serum-therapy  for  hydrophobia  has  un fortu- 
nately not  been  thus  far  successful. 

Prophylaxis  is  extremely  important.  We  cannot  consider  in  detail  the 
regulations  (muzzling)  which  the  government  should  make  in  order  to  prevent 
the  spread  of  the  disease.  As  to  individual  prophylaxis,  every  suspicious  bite 
shordd  be  very  thoroughly  disinfected,  and  then  cauterized  either  with  carbolic 
acid,  caustic  potash,  or  the  red-hot  iron.  It  has  also  been  recommended  that 
the  entire  wound  or  scar  should  be  excised,  along  with  any  swollen  lymphatic 
glands  which  may  be  found  in  the  neighborhood.  Internal  remedies  to  pre- 
vent the  outbreak  of  the  disease  are  probably  quite  useless. 

On  the  other  hand,  Pasteur  has  recently  made  a  series  of  extremely  remark- 
able observations  which  have  led  to  a  special  method  of  prophylactic  inocula- 
tion against  rabies  in  human  beings.  If  a  bit  of  the  spinal  marrow  taken  from 
a  mad  dog  (an  emulsion  of  the  substance  of  the  cord  rubbed  up  in  salt  solu- 
tion or  bouillon)  is  introduced  beneath  the  dura  mater  of  a  rabbit  by  means 
of  trephining,  the  animal  exhibits  the  symptoms  of  rabies  after  fourteen  days' 
incubation.  If  in  the  same  way  a  second  rabbit  is  inoculated  from  the  first, 
and  so  on,  the  virulence  of  the  inoculated  material  increases  gradually  with 
every  inoculation,  while  the  period  of  incubation  grows  shorter  and  shorter, 
till  it  lasts  but  seven  days.  Beyond  this  point  the  period  of  incubation  does 
not  seem  to  diminish.  If,  on  the  other  hand,  the  same  series  of  inoculations 
is  made  on  apes,  the  virulence  of  the  poisonous  matter  does  not  increase,  but 
diminishes.  If  dogs  are  inoculated  with  material  artificially  attenuated  in 
this  manner,  the  animals  remain  in  good  health,  and  furthermore  acquire  an 
immunity  against  more  virulent  inoculations,  so  that  they  may  be  bitten  by 
mad  dogs  without  becoming  infected. 

Pasteur  has  also  published  a  still  more  simple  and  valuable  method  of 
artificial  attenuation  of  the  virus.  He  removes  small  portions  of  the  spinal 
marrow  of  rabbits  which  are  suffering  from  rabies  in  its  most  violent  form 
produced  by  the  above-detailed  method,  and  these  bits  of  marrow  he  exposes 
to  air  which  has  been  wholly  deprived  of  moisture.  In  this  way  the  poison 
contained  in  the  spinal  marrow  gradually  and  progressively  loses  its  virulence, 
until  it  finally  becomes  inert.  A  portion  of  spinal  marrow  which  by  long  dry- 
ing has  completely  lost  its  original  virulence  is  then  rubbed  up  in  sterilized 
bouillon  and  injected  into  some  animal — for  instance,  a  dog — and  then  in 
regular  succession  pieces  of  marrow  which  have  been  dried  for  shorter  and 
shorter  periods  and  so  contain  more  and  more  of  the  poison,  until  finally  the 
point  is  reached  when  it  is  possible  to  use  for  the  injection  pieces  which  are 
perfectly  fresh  and  extremely  poisonous,  without  affecting  the  animal's  health. 
That  is,  the  animal  has  attained  immunity  from  the  disease. 


150  ACUTE   GENERAL  INFECTIOUS   DISEASES 

This  method  of  Pasteur  has  now  been  employed  on  many  thousands  of 
human  beings  who  were  bitten  by  mad  dogs.  According  to  the  reports,  so 
small  a  number  of  these  inoculated  persons  (about  one  per  cent)  have  actually 
been  attacked  later  by  hydrophobia  that  we  can  no  longer  doubt  the  prophy- 
lactic value  of  Pasteur's  protective  inoculations. 

Experiences  thus  far  tend  to  show  that  there  is  no  danger  of  exciting  hydro- 
phobia by  such  "  protective  inoculation."  Ill  effects  from  the  inoculation  have 
only  been  very  rarely  observed.  There  have  been  a  few  cases  of  acute  para- 
plegic, motor,  and  sensory  paralysis,  but  they  have  always  terminated  favor- 
ably. 

At  present  prophylactic  inoculation  against  hydrophobia  can  be  practiced 
only  in  specially  equipped  institutions.  In  most  civilized  countries,  therefore, 
institutions  on  the  plan  of  the  "  Pasteur  Institute "  in  Paris  have  already 
been  established.  In  Germany,  prophylactic  treatment  against  rabies  can  be 
administered  at  any  time  in  the  Berlin  Institute  for  Infectious  Diseases  and 
in  the  Hydrophobia  Station  connected  with  the  Hygienic  Institute  at  Breslau. 
It  is  of  paramount  importance  to  commence  treatment  as  soon  as  possible 
after  the  bite,  as  immunization  requires  two  or  three  weeks'  treatment. 


CHAPTER    XXII 

GLANDERS 

(Farcy.    Malleus) 

iEtiology. — Glanders  is  a  disease  of  the  horse  and  some  animals  allied  to 
it— viz.,  the  ass  and  mule.  It  can,  however,  be  transferred  to  man.  It  is 
characterized  by  peculiar  new  growths,  either  like  nodes  ("farcy-buds"),  or 
more  rarely  diffuse.  These  are  very  prone  to  suppurate  and  break  down. 
Such  nodes,  and  the  ulcers  which  they  leave  behind  them,  occur  most  fre- 
quently in  the  mucous  membrane  of  the  nose.  In  horses  the  purulent  nasal 
discharge  is  one  of  the  earliest  and  most  important  symptoms  of  the  disease. 
Similar  nodes  are  found  in  the  larynx,  lungs,  liver,  spleen,  and  kidneys,  and 
often  also  in  the  skin.  The  cutaneous  swellings  and  deep,  crater-like  ulcers 
belong  to  that  form  of  the  disease  which  is  called  "  farcy."  The  corresponding 
lymphatic  vessels  and  glands  are  usually  much  swollen.  The  animal  has  fever, 
grows  weaker  and  weaker,  and  almost  invariably  dies  at  the  end  of  one  to 
three  weeks. 

Glanders  in  man  is  always  referable  to  infection  from  a  diseased  animal, 
although  in  certain  instances  it  is  impossible  to  demonstrate  the  source.  The 
disease  is  therefore  commonest  among  persons  who  have  much  to  do  with  horses 
— e.  g.,  hostlers,  coachmen,  farmers,  and  cavalrymen.  The  virus  is  usually 
conveyed  by  the  pus  and  nasal  secretions  of  the  diseased  animals.  A  little 
of  this  falls  upon  some  excoriation  on  the  hand  or  some  crack  in  the  skin, 
and  is  absorbed.  Man  does  not  seem  very  liable  to  the  disease;  it  is  of  rare 
occurrence. 

Loftier  and  Schutz  have  discovered  the  specific  disease-producing  agent. 
These  investigators  were  able  to  demonstrate  in  all  the  products  of  glanders 


GLANDERS  15] 

delicate  bacilli  about  the  size  of  the  bacilli  of  tuberculosis.  These  bacilli  can 
be  reared  artificially,  and,  if  inoculated  upon  horses  and  other  animals,  they 
give  rise  to  u  typical  attack  of  glanders  in  every  instance.  The  bacilli  of  glan- 
ders have  so  far  never  been  detected  in  the  blood.  It  is  also  a  very  interesting 
observation  that  they  rapidly  lose  their  virulence  in  purified  cultures  outside 
of  the  living  body.  This  is  one  more  proof  of  the  fact,  which  is  lately  coming 
more  and  more  into  prominence,  that  the  external  influences  Burrounding  the 
life  of  bacteria  greatly  modify  their  biological  peculiarities.  By  repeated  in- 
oculations of  glanders  in  tbe  horse  the  virulence  of  tbe  bacilli  rapidly  dimin- 
ishes, while,  on  tbe  other  band,  by  repeated  inoculations  in  the  weasel  the  viru- 
lence is  said  to  be  very  considerably  increased. 

Clinical  History. — Tbe  period  of  incubation  lasts  about  three  to  five  i 
and  sometimes  longer.  Tbe  first  symptoms  are  local,  if  the  infection  has 
resulted  from  a  visible  injury.  There  is  considerable  swelling  and  pain  in 
this  spot,  and  usually  considerable  lymphangitis  in  its  neighborhood.  In 
other  cases,  however,  tbe  disease  begins  with  indefinite  constitutional  symp- 
toms, such  as  fever,  headache,  and  pain  in  tbe  limbs,  so  that  there  may  be 
some  resemblance  to  beginning  typhoid  fever.  Tbe  local  and  general  dis- 
turbances increase,  and  tbe  disease  soon  attacks  other  parts  of  the  body.  In 
the  skin  we  see  small  macules  or  papules,  singly  or  in  groups,  which  soon 
change  to  pustules  like  those  of  smallpox,  or  to  larger  abscesses.  These  ab- 
scesses burst  and  discharge  offensive  pus,  leaving  behind  them  irregular,  deep 
ulcers.  Not  infrequently  the  joints  are  swollen.  The  mucous  membranes 
are  also  attacked;  chief  among  these  troubles  are  ulcers  in  the  nose.  Tbe 
nose  swells  as  if  with  erysipelas,  and  there  is  a  purulent,  foul-smelling  dis- 
charge. The  nose  rarely  escapes.  The  conjunctivas,  throat,  mucous  membrane 
of  tbe  mouth,  and  the  larynx  also  undergo  inflammation  and  ulceration.  A 
violent,  diffuse  bronchitis  develops.  Sometimes  there  is  considerable  disturb- 
ance of  the  stomach  and  intestines,  giving  rise  to  vomiting  and  diarrhea.  At 
the  same  time  the  constitutional  symptoms  become  more  and  more  severe. 
The  patient  grows  stupid  or  delirious.  In  some  few  cases  the  severe  cerebral 
symptoms  are  due  to  a  purulent  meningitis,  perhaps  through  extension  of  the 
inflammation  by  contiguity  from  the  nose.  The  fever  is  high,  and  sometimes 
it  is  quite  continuous.  More  rarely  there  are  chills  and  great  elevations  of 
temperature,  as  in  the  fever  of  pyaemia.  The  pulse  is  rapid  and  small.  The 
spleen  is  seldom  much  enlarged.    The  urine  may  contain  a  trace  of  albumen. 

In  these  severe  acute  cases  the  termination  is  almost  always  fatal.  Death 
occurs  at  the  end  of  two  to  four  weeks.  There  are  cases  with  a  more  chronic 
course,  with  tedious  persistence  of  the  troubles  in  the  skin  and  mucous  mem- 
branes, and  milder  febrile  and  constitutional  symptoms.  Such  attacks  appear 
at  first  tolerably  favorable,  but  they  may  end  fatally  with  persistent  fever  and 
increasing  physical  weakness,  or  they  may  run  on  for  months,  and  at  last  end 
in  complete  recovery. 

The  autopsy  reveals  a  condition  greatly  resembling  that  in  pyaemia.  We 
find  abscesses  in  many  parts,  particularly  tbe  muscles  and  the  lungs,  and,  next 
in  frequency  to  them,  the  spleen,  brain,  and  other  viscera.  In  the  mucous 
membrane  of  the  nasal  cavities,  the  pharynx  and  the  larynx,  are  found  nodes 
and  ulcers  such  as  occur  in  the  horse.  As  in  septicaemia,  there  are  often 
numerous  hemorrhages  into  the  serous  and  mucous  membranes.    It  has  already 


152  ACUTE  GENERAL  INFECTIOUS   DISEASES 

been  mentioned  that  the  specific  bacilli  of  glanders  are  present  in  the  abnormal 
secretions. 

Diagnosis. — Without  the  aid  of  a?tiological  factors  the  diagnosis  of  glanders 
is  often  very  difficult.  Indeed,  until  recently  there  have  been  instances  where 
even  the  autopsy  did  not  suffice  to  exclude  pysemia;  but  now  that  the  specific 
bacilli  have  been  discovered  we  can  clear  up  all  doubts.  We  cannot  here  enter 
into  a  discussion  of  the  details  of  bacteriological  examination  (inoculation  of 
guinea  pigs,  preparation  of  cultures,  agglutination,  etc.).  At  the  bedside, 
also,  getiology  is  all-important  in  diagnosis — e.  g.,  exposure  to  infection,  or 
occupation.  The  most  characteristic  symptoms  are  the  nasal  and  cutaneous. 
In  a  case  that  takes  a  chronic  course  there  is  a  possibility  of  mistaking  the 
cutaneous  ulcers  for  syphilitic  or  tuberculous  sores. 

Kalning  has  discovered  a  very  interesting  fact,  which,  for  obvious  reasons, 
has  rarely  been  applied  to  man.  A  substance  can  be  obtained  from  cultures 
of  glanders  bacilli,  the  so-called  mallein.  If  this  be  injected  in  small  amounts 
in  horses  sick  with  glanders  it  causes  high  fever,  while  the  injection  has  no 
effect  in  any  other  animal.  Mallein,  therefore,  has  the  same  significance 
in  the  diagnosis  of  glanders  as  tuberculin  has  in  the  diagnosis  of  tuber- 
culosis. 

Treatment. — We  have  already  implied  that  the  treatment  of  acute  cases  is 
almost  hopeless.  We  must  do  all  we  can  in  the  way  of  cleanliness  and  disin- 
fection to  improve  the  local  condition  of  the  skin,  the  nose,  and  the  throat. 
All  abscesses  and  nodules  must  be  opened  as  soon  as  possible  and  curetted  and 
disinfected.  Appropriate  agents  are  carbolic  acid  and  peroxid  of  hydrogen. 
Further  treatment  should  be  in  accordance  with  the  general  rules  for  the  care 
of  severe  acute  infectious  diseases.  An  inunction  treatment  with  unguentum 
cinereum  (gr.  xxx  to  xlv  [gm.  2  to  3]  daily)  has  a  \evj  favorable  effect.  Iodid 
of  potassium,  arsenic,  etc.,  have  also  been  recommended.  Chronic  glanders 
swellings  of  the  nose  are  at  times  favorably  influenced  by  Eontgen  rays,  Finsen 
light,  and  the  like. 


CHAPTER    XXIII 

MALIGNANT    PUSTULE 

(Anthrax.     Charbon.     Splenic  Fever.     Mycosis  intestinalis.     Carbunculus  contagiosus) 

.ZEtiology. — The  cause  of  malignant  pustule  is  the  infection  of  the  body 
with  a  specific  kind  of  bacilli,  the  Bacillus  OMthracis.  This  organism  was 
discovered  by  Pollender  in  1849,  and  a  few  years  later,  independently,  by 
Brauell. 

These  bacilli  are  very  minute  cylinders,  about  as  long  as  the  diameter  of  a 
red  blood  corpuscle.  They  are  found  in  enormous  numbers  in  the  blood  and 
organs  of  animals  which  die  of  anthrax.  Anilin-staining  makes  them  more 
easily  visible.  By  means  of  blood  containing  the  bacilli,  Davaine  (1803)  and 
others  have  inoculated  many  animals  with  the  disease,  including  mice,  rats, 
guinea  pigs,  cows,  sheep,  goats,  and  birds.  The  bacilli  can  also  be  isolated 
and  cultivated,  and  then  produce  infection.    This  is  proof  positive  that  they 


MALIGNANT    PUSTULE 


153 


are  the  actual  carriers  of  contagion.  The  rapid  increase  of  the  anthrax  bacilli 
in  the  blood  goes  on  by  subdivision-  In  the  artificial  cultivations,  however, 
I  lie  bacilli  grow,  as  Koch  has  shown,  into  quite  long  threads,  in  which  shortly 
appear  minute,  brilliant  egg-shaped  bodies  (cf.  Figs.  28  and  20).  The 
threads  become  disintegrated,  setting  free  the  little  shining  ovoids,  the  spores 
of  anthrax,  to  grow  into 
bacilli.  The  bacilli  can 
live  only  a  relatively  brief 
time;  but  the  spores  have 
unusual  tenacity  of  exist- 
ence. They  may  remain 
dried  up  for  years,  and 
then  be  brought  to  further 
development  if  placed  in 
favorable  conditions  of  heat 
and  moisture.  If  the 
spores  are  transferred  to 
animals,  they  develop  into  Fig.  28.— Anthrax  bacilli.  (From  Koch.)  650  diameters, 
bacilli     and    there  is   scarce-  Afrom  the  blood  of  a  guinea  pig.     B,  from  the  spleen  of 

Dacilll,   ana   tliere   IS    scarce  a  mouse  after  three  hours' culture  in  the  aqueous  humor. 

ly  room  to  doubt  that  men 

and  animals  are  quite  as  often  infected  by  spores  as  by  full-grown  bacilli. 
There  are  facts  which  render  it  not  improbable  that  the  anthrax  bacilli  exist 
in  other  places  than  the  bodies  of  men  or  animals,  and  may  there  complete 
their  circle  of  development.  Such  places  are  marshes,  the  banks  of  streams, 
and  the  like.     If  it  is  possible  for  them  to  be  carried  by  high  water  to  the 

pasture  lands,  we  have  an  explanation 
of  those  sudden  endemic  appearances 
of  anthrax  which  sometimes  occur  in 
places  previously  free  from  the  disease. 


Fig.  29. — Anthrax  bacilli ;  spore  formation  and  spore  germination.  (From  Koch.)  A,  from  the 
spleen  of  a  mouse  after  twenty-four  hours'  culture  in  the  aqueous  humor,  spores  arranged 
like  beads  in  the  filaments.  650  diameters.  B,  germination  of  the  spores.  650  diameters. 
C,  the  same,  with  a  higher  power.     1,650  diameters. 


Anthrax  in  animals  is  of  great  practical  importance  because  its  favorite 
victims  are  the  herbivorous  domestic  animals — viz.,  the  cow,  sheep,  and  horse. 
Among  these  it  is  terribly  destructive.  It  is  remarkable  that  the  carnivora 
enjoy  almost  complete  immunity.  The  disease  usually  runs  a  very  acute 
course  in  animals.  Indeed,  it  often  seems  like  apoplexy;  the  apparently 
healthy  animal  suddenly  falls,  suffers  for  a  few  minutes  from  convulsions  and 


154  ACUTE   GENERAL   INFECTIOUS   DISEASES 

dyspnoea,  and  dies.  Other  cases  have  a  somewhat  longer  and  more  intermit- 
tent course,  but  in  these  also  recovery  is  very  rare.. 

Human  beings  are  probably  infected  in  most  cases  by  direct  inoculation. 
Shepherds,  farmers,  butchers,  and  others  who  come  in  contact  with  animals 
suffering  from  anthrax,  are  liable  to  infection  through  any  little  wound  or 
scratch  upon  the  hands.  Very  often  the  disease  is  caught  from  hides,  hair, 
or  other  parts  of  dead  animals.  In  workshops  and  factories  where  wool  and 
hides  have  been  used  which  came  from  diseased  animals,  anthrax  has  repeat- 
edly occurred.  Curriers,  rope  makers,  paper  makers,  hatters,  furriers,  brush 
workers,  and  those  who  handle  horsehair  and  wool,  are  all  exposed.  Anthrax 
has  also  acquired  the  name  of  "  rag-pickers'  disease."  Another  way  of  infec- 
tion, supposed  to  happen  among  animals  as  well  as  men,  is  through  the  sting 
of  insects — e.  g.,  flies — bringing  the  poison  from  diseased  animals.  It  is  not 
likely  that  the  virus  can  be  absorbed  through  the  unbroken  skin.  It  is  certain, 
however,  that  the  intestine  may  sometimes  afford  ingress  to  the  infectious 
matter.  Koch  has  proved  this  by  putting  spores  in  the  food  of  sheep.  In- 
testinal mycosis  in  man  (vide  infra)  may  very  possibly  be  due  to  a  similar 
mode  of  infection.  Many  cases  of  poisoning  from  eating  meat  have  been 
referred  to  the  ingestion  of  the  flesh  of  animals  who  died  from  anthrax.  Some 
observations  on  pulmonary  anthrax  seem  to  favor  the.  idea  that  the  poison 
may  be  inhaled  with  dust  and  develop  primarily  in  the  lungs. 

Clinical  History. — Anthrax  in  man  has  two  distinct  forms.  These  may 
appear  in  combination.  The  first  begins  with  a  local  disorder  of  the  skin  at 
the  point  of  infection- — viz.,  the  malignant  pustule,  or  anthrax  carbuncle.  The 
second  and  rarer  form  presents  the  symptoms  of  a  severe  acute  constitutional 
infection.  An  accompanying  cutaneous  disorder  or  other  local  disease  is 
sometimes  observed. 

1.  Malignant  Pustule. — The  malignant  pustule  usually  comes  on  the  hand, 
the  arm,  or  the  throat,  and  appears  from  three  to  seven  days  after  infection. 
A  small  vesicle  forms  at  the  infected  spot,  grows  rapidly,  becomes  excoriated, 
and  usually  takes  on  a  characteristic  appearance,  being  of  a  dark-bluish  or 
black  color.  The  surrounding  parts  become  diffusely  swollen  and  red.  Sec- 
ondary vesicles  may  surround  the  original  one.  In  severe  cases  the  swelling 
becomes  more  and  more  extensive  (so-called  anthrax  erysipelas).  Inflamed 
lymph-vessels  or  veins  radiate  in  red  lines  from  the  pustule,  and  the  neigh- 
boring glands  are  also  affected.  These  appearances  are  accompanied  by  fever, 
and  more  or  less  prostration.  In  a  favorable  case  the  swelling  subsides,  the 
scab  falls  off,  and  there  is  at  last  complete  recovery.  But  in  other  cases  the 
constitutional  infection  becomes  more  and  more  prominent,  and  eclipses 
the  local  disorder.  The  fever  and  prostration  increase.  Severe  intestinal 
symptoms  appear,  or  else  stupor,  delirium,  and  other  nervous  disturbances; 
and  death  may  ensue  after  a  few  days'  illness. 

The  so-called  anthrax  oedema  (malignant  oedema,  cedeme  cliarbonneux, 
charbon  Mane)  is  a  form  of  primary  anthrax  of  the  skin  differing  from  malig- 
nant pustule.  It  is  seen  chiefly  in  the  eyelids,  lips,  and  mucous  membrane  of 
the  mouth  and  tongue,  and  also  in  other  parts  of  the  skin.  In  this  form  we 
see  a  circumscribed,  doughy,  cedematous  swelling,  in  which  small  bullae  with 
sero-sanguineous  contents  often  develop.  These  bulla?  may  become  gangre- 
nous.    On  the  neck  and  trunk  the  anthrax  oedema  may  sometimes  be  of  con- 


MALIGNANT  PUSTULE  155 

siderable  extent.  The  other  symptoms  are  similar  to  those  of  malignant 
pustule.     We  cannot  make  an  absolute  separation  of  the  two  forms. 

2.  Intestinal  Anthrax  ("Intestinal  Mycosis"). — A  quite  differenl  picture 
is  presented  by  this  second  form,  which  is  called  intestinal  anthrax  (formerly 

intestinal  mycosis)  from  the  marked  intestinal  lesions.  In  this  the  cutaneous 
disorder,  if  it  exists  at  all,  is  insignificant  compared  with  the  severe  constitu- 
tional disturbance.  It  is  only  within  a  few  years  thai  the  labors  of  Buhl, 
Wahleyer,  E.  Wagner,  Leube,  and  others  have  shown  that  attacks  of  this  kind 
have  any  connection  with  anthrax. 

In  cases  of  this  sort  the  attack  is  usually  rather  sudden,  beginning  with 
chilliness,  vomiting,  headache,  and  languor.  The  diagnosis  is  usually  very 
obscure  at  first,  unless  the  calling  of  the  patient  suggests  the  possibility  of 
anthrax.  On  careful  examination,  we  may  find  some  places  where  the  skin 
is  broken,  or  possibly  a  small  characteristic  pustule.  In  a  case  which  came 
under  our  own  observation  a  pustule  had  existed  on  tin-  hack  of  the  right 
hand  for  some  weeks  before  severe  symptoms  appeared,  but  had  not  attracted 
the  attention  of  the  patient  at  all.  In  this  case,  therefore,  the  constitutional 
infection  seems  to  have  come  from  the  local  disease.  But  in  other  cases 
cutaneous  lesions,  in  the  form  of  small  carbuncles,  may  occur  secondarily  in 
the  course  of  the  disease.  Hemorrhages  into  the  skin  and  mucous  membranes 
(especially  on  the  gums)  also  occur. 

Of  the  other  symptoms,  the  gastro-intestinal  deserve  to  be  mentioned  first. 
Vomiting  occurs  frequently,  and  also  a  moderate,  painless,  and  sometimes 
bloody  diarrhea.  There  is  usually  severe  dyspnoea,  and  a  marked  sense  of 
oppression  in  the  thorax,  but  without  objective  pulmonary  signs.  Very  soon 
there  is  collapse;  the  nose  and  extremities  grow  cool;  the  pulse  is  rapid,  but 
small ;  and  there  is  lividity.  In  a  few  instances  tetanic  or  epileptiform  convul- 
sions have  been  observed.  CEdematous  swelling  of  the  eyelids  is  sometimes 
seen.  The  temperature  is  seldom  much  elevated.  It  may  be  subnormal.  In 
a  few  days  the  prostration  becomes  complete,  and  death  ensues.  Sometimes 
these  severe  general  symptoms  are  associated  with  the  signs  of  a  circumscribed 
pneumonia  (vide  infra). 

Milder  forms  apparently  occur,  but  here  the  diagnosis  may  not  be  abso- 
lutely certain.  We  have  seen  a  few  such  cases  originating  in  a  ropewalk  where 
Eussian  hair  was  used.  The  constitutional  symptoms  were  only  moderately 
severe,  the  fever  was  mild,  and  recovery  occurred  after  two  or  three  weeks. 

3.  Pulmonary  Anthrax. — Pulmonary  anthrax  probably  arises,  as  we  have 
said,  from  the  inhalation  of  dust  containing  anthrax  spores.  The  disease 
runs  its  course  as  a  broncho-pneumonia,  usually  bilateral  and  associated  with 
high  fever,  pleurisy,  severe  dyspnoea,  cardiac  weakness,  and  great  general 
prostration.  The  anthrax  bacilli  have  been  found  in  the  sputum  and  the 
pleuritic  exudation,  and  sometimes  in  the  blood.  Most  cases  of  this  type 
terminate  fatally  in  a  few  days. 

Pathology. — In  the  fatal  cases  of  anthrax  the  intestinal  lesions  are  the 
most  characteristic.  Besides  the  signs  of  catarrhal  inflammation,  we  find 
peculiar  lesions  in  the  mucous  membrane  of  the  small  intestine,  and  some- 
times in  the  upper  portion  of  the  colon.  These  consist  of  dark,  infiltrated 
spots,  with  hemorrhages,  the  spots  being  somewhat  larger  than  a  silver  dime. 
The    microscope    reveals    numerous    collections    of    anthrax   bacilli,    situated 


156  ACUTE   GENERAL   INFECTIOUS   DISEASES 

chiefly  in  the  lumen  of  the  blood  vessels.  The  spleen  is  usually  only  moder- 
ately enlarged,  but  dark  and  congested.  There  may  be  ecchymoses  in  the 
kidneys,  the  brain,  and  tbe  serous  membranes.  Often  there  is  swelling  of  the 
lymph-glands.  In  one  case  which  we  saw,  with  slight  intestinal  lesions,  the 
mesenteric  glands  were  considerably  enlarged,  and  the  bronchial  lymph-glands 
were  perfectly  enormous.     The  bacilli  are  found  in  all  the  organs  mentioned. 

Diagnosis. — The  diagnosis  of  malignant  pustule  is  seldom  difficult,  particu- 
larly if  attention  is  directed  to  the  aBtiology.  All  doubt  is  over  if  we  find  the 
bacilli.  The  cases  of  intestinal  and  pulmonary  anthrax  may  be  more  obscure. 
The  chief  point  is  that  the  attention  be  directed  to  the  possibility  of  anthrax 
by  the  patient's  occupation,  the  severe  general  symptoms,  and  any  pustule  on 
the  skin.  For  a  positive  diagnosis  we  need,  of  course,  to  find  the  bacilli  in 
any  pustule  on  the  skin  or  in  the  blood. 

Treatment.- — 1.  Prophylactic  inoculation.  Toussaint  and  Pasteur  were  the 
first  to  show  that  the  virulence  of  anthrax  bacteria  can  be  artificially  dimin- 
ished by  certain  external  influences.  If  the  bacilli  are  kept  under  cultiva- 
tion for  several  weeks  at  an  unchanging  temperature  of  106°  to  107.5°  F. 
(42°  to  43°  C),  they  preserve  their  external  appearance  completely,  as  well 
as  their  ability  to  grow,  but  gradually  lose  their  power  of  infection.  Inocula- 
tions made  with  this  "  vaccine  virus  "  produce  at  most  an  insignificant  dis- 
turbance. Pasteur's  discovery  that  the  animals  thus  vaccinated  are  protected 
thereafter  from  infection  with  actual  anthrax  was  most  valuable.  Pasteur 
therefore  proposed  that  the  prophylactic  inoculation  of  sheep  and  other  ani- 
mals liable  to  anthrax  should  be  undertaken  on  a  large  scale,  promising  the 
farmers  that  very  great  benefit  would  result.  So  far  as  experience  has  thus 
far  gone,  the  mortality  of  anthrax  in  sheep  and  cattle  seems  actually  to  have 
been  considerably  diminished  by  the  many  protective  inoculations  which  have 
been  performed  in  France  and  Hungary. 

French  investigators  have  lately  made  known  new  methods  of  producing 
an  artificial  diminution  of  the  growth  and  virulence  of  anthrax  bacilli. 
Chauveau  has  found  that  cultures  of  anthrax  bacilli  exposed  for  several 
days  to  an  atmospheric  pressure  of  three  to  twelve  atmospheres,  or  to  com- 
pressed oxygen,  lose  a  portion  of  their  virulence;  and  that  animals  inoculated 
with  bacilli  thus  attenuated  gain  an  immunity  to  inoculations  with  the  origi- 
nal anthrax  poison.  The  statements  of  Arloing  are  very  remarkable.  He 
says  that  the  direct  play  of  sunlight,  or  even  of  a  concentrated  artificial 
light,  upon  the  cultures  exercises  a  restraining  influence  upon  the  growth  and 
poisonous  properties  of  the  bacilli,  and  that  inoculation  material  weakened  in 
this  way  may  be  emploj^ed  to  render  animals  immune.  According  to  the 
most  recent  researches,  the  serum  of  animals,  artificially  immunized,  also 
possesses  decided  protective  powers.  These  various  prophylactic  measures 
have  as  yet  been  employed  on  human  beings  only  in  isolated  instances. 

2.  The  treatment  of  malignant  pustule  is  surgical.  Cauterization  with 
caustic  potash,  nitric  acid,  or  carbolic  acid  has  been  found  ineffective  and 
even  injurious.  In  mild  cases  rest,  moist  applications  of  aluminum  subace- 
tate,  ice  bags,  and  the  like  are  sufficient.  In  severe  cases  experienced  sur- 
geons advocate  the  division  of  the  pustule,  application  of  the  thermocautery 
to  the  circumference  of  its  base,  and  the  injection  of  tincture  of  iodin,  in 
drops,  into  the  border  line  between  the  inflamed  and  the  healthy  skin. 


TRICHINOSIS 


157 


3.  The  treatment  of  intestinal  and  pulmonary  anthrax  must  be  purely 
symptomatic.  In  intestinal  anthrax  the  use  of  calomel  (gr.  ij  to  iij  [gm. 
0.1  to  0.2]  several  limes  a  day)  is  rcrosl  to  be  recommended.  Quinin  (gr.  vij 
[gm.  0.5]  four  times  a  day)  and  carbolic  acid  (gr.  xv  [gm.  Ij  a  day  in  pills 
or  subcutancousJy)  seem  also  to  have  a  favorable  influence  on  the  general 
infection. 


CHAPTER    XXIV 

TRICHINOSIS 

(Trichinatous  Disease) 


The  Natural  History  of  Trichina?. — The  Trichina  spiralis,  one  of  the  class 
of  roundworms  or  nematoda,  has  long  been  known  to  occur  occasionally  in 
the  muscles  of  men  and  certain  animals;  but  it  was 
not  until  1860  that  Zenker  showed  that  trichina?  are 
capable  of  exciting  in  man  a  dangerous  and  some- 
times fatal  disease.  Since  then  numerous  individual 
eases  and  quite  extensive  epidemics  have  been  re- 
ported; and  the  labors  of  Virchow,  Leuckart,  and 
others  have  taught  us  the  anatomy  and  mode  of 
development  of  this  peculiar  parasite. 

The  trichina  appears  in  two  shapes — as  intestinal 
trichina  and  as  muscular  trichina.  The  intestinal 
form  is  a  small  white  worm  visible  to  the  naked  eye. 
The  female  is  -J  to  £  of  an  inch  (3  to  4  mm.)  long, 
the  male  only  F1s  to  T1¥  of  an  inch  (1  to  1.5  mm.). 
They  have  well-developed  digestive  and  sexual  organs. 
The  male  is  distinguished  by  two  little  processes  at  the 
tail.  The  muscular  trichina  (vide  Fig.  30)  is  a  small 
worm,  gig  to  ijoi  an  inch  (0.7  to  1  mm.)  long.  It  is 
found  coiled  up  among  the  muscular  fibers,  inside  a 
connective-tissue  capsule  which  is  often  calcified. 

The  events  in  the  life  of  the  trichina  are  remark- 
able. If  living  muscular  trichina?  reach  the  human 
stomach  through  the  eating  of  trichinous  pork,  the 
capsules  are  dissolved,  and  the  trichina?,  thus  set  free, 
grow  in  two  or  three  days  into  sexually  perfect  intes- 
tinal trichina?.  In  the  uterus  of  the  impregnated 
female  the  eggs  develop  into  embryos,  which  are 
born  already  hatched.  The  birth  of  the  embryos  be- 
gins seven  days  after  the  ingestion  of  the  muscular 
trichina?,  and  seems  to  continue  for  some  time.  A 
single  female  is  said  to  produce  more  than  one  thou- 
sand embryos.  These  latter  begin  their  travels  soon 
after  birth,  and  reach  the  voluntary  muscles.  As  to 
the  routes  they  choose  we  are  still  somewhat  in  doubt. 
Some   authorities   state   that  the   trichinae   penetrate 


v; 


BiSwWw 


Fig.  30. — (From  Heller.) 
An  isolated  primitive  bun- 
dle with  two  free  trichinae 
in  the  sheath  of  the  sarco- 
lemma.     Much  enlarged. 


158  ACUTE   GENERAL  INFECTIOUS   DISEASES 

through  the  walls  of  the  intestine  and  the  abdominal  cavity  into  the  con- 
nective tissue.  Others  affirm  that  they  enter  the  lymphatic  vessels,  or  ex- 
ceptionally the  blood  vessels.  Eecent  experimental  investigations  (Staubli) 
certainly  argue  for  the  dissemination  by  the  blood  stream,  as  it  was  pos- 
sible to  demonstrate  numerous  embryos  of  trichinae  in  the  blood.  They 
penetrate  into  the  primitive  fibers  of  the  muscles,  and  cause  them  to  disin- 
tegrate. Finalty,  they  coil  themselves  up,  attain  the  size  of  muscular  trichinae 
in  about  fourteen  days,  and  become  encapsulated.  Each  capsule  usually  con- 
tains but  one,  although  it  may  inclose  as  many  as  four.  The  capsule  is  formed 
partly  by  an  excretion  from  the  trichina,  and  partly  from  the  reflex  hyper- 
plasia of  the  surrounding  connective  tissue.  The  process  of  development  is 
now  complete.  The  muscular  trichinae  seem,  unlike  the  intestinal  form,  to 
have  a  very  long  lease  of  life,  and  usually  endure  till  the  death  of  their  host. 
They  are  often  found  accidentally  at  autopsies.  They  are  most  abundant  in 
the  diaphragm,  the  intercostal  muscles,  the  muscles  of  the  larynx  and  throat, 
and  the  biceps. 

iEtiology  of  Trichinosis. — The  only  cause  yet  known  for  trichinosis  in  man 
is  the  ingestion  of  trichinous  raw  or  underdone  pork — e.  g.,  smoked  ham. 
Swine  are  preeminently  subject  to  trichinae.  They  probably  become  infected 
in  various  ways — e.  g.,  from  the  feces  of  human  beings  and  swine  suffering 
from  trichinosis,  or  through  the  ingestion  of  the  trichinous  flesh  of  other 
swine.  The  waste  of  slaughter  houses  is  often  fed  out  to  swine,  and  the  disease 
thus  disseminated.  Many  affirm  that  swine  are  also  infected  by  eating  rats 
infested  with  trichina?,  but  the  contrary  condition,  whereby  rats  become  tri- 
chinous from  eating  the  flesh  of  diseased  hogs,  seems  more  in  accordance  with 
the  facts. 

Clinical  History. — The  symptoms  in  man  correspond  in  general  to  the 
developmental  and  vital  processes  of  the  trichinae,  as  above  depicted.  In  indi- 
vidual cases,  however,  the  separate  stages  are  quite  often  obscured,  probably 
because  all  the  parasites  do  not  develop  simultaneously,  or  because  there  are 
relapses.  The  first  symptoms  are  gastrointestinal.  At  the  commencement 
there  is  a  feeling  of  pressure  in  the  epigastrium,  with  nausea  and  vomiting. 
Later,  diarrhea  is  prominent,  becoming  in  some  cases  so  violent  as  to  remind 
one  of  cholera.  It  is  not  impossible,  although  rare,  to  find  intestinal  trichinae 
in  the  stools.  Sometimes  there  is  constipation  instead  of  diarrhea.  In  some 
cases  the  initial  gastrointestinal  symptoms  are  but  slight.  Frequently,  even 
in  the  beginning  of  the  disease,  there  is  complaint  of  pain  and  stiffness  in  the 
muscles,  too  early  for  it  to  be  due  to  the  migration  of  the  trichinae. 

The  genuine  severe  muscular  symptoms,  due  to  the  myositis  produced  by 
the  trichinae  in  the  muscles,  do  hot  begin  till  the  second  week,  or  even  later. 
In  many  cases,  where  the  invading  parasites  seem  to  be  relatively  few  in 
number,  the  muscular  symptoms  are  slight,  or  wholly  absent.  In  the  more 
severe  cases,  however,  they  may  be  extremely  violent  and  distressing.  The 
muscles  become  swollen,  firm,  and  hard,  very  tender  on  pressure,  and  very 
painful.  The  patient  avoids  all  movements  and  contraction  of  the  muscles 
as  much  as  possible,  lying  motionless  in  bed,  with  flexed  arms  and  with  legs 
either  extended  or  likewise  flexed.  The  patellar  reflex  almost  always  disap- 
pears, and  on  testing  the  electrical  reactions  there  is  found  a  considerable 
diminution  of  muscular  excitability  to  both  the  galvanic  and  faradic  currents, 


TRICHINOSIS  1.7 1 

sometimes  associated  with  delayed  contractions,  and  abnormally  Long  dura- 
tion of  the  same  after  the  stimulus  ceases  (Eisenlohr).  The  masseters  and 
the  pharyngeal  and  Laryngeal  muscles  are  attacked,  so  thai  there  i-  difficulty 
in  mastication  and  deglutition,  and  hoarseness.  The  inVolvemenl  of  the 
ocular  muscles  causes  pain  in  the  eyes.  The  condition  of  the  diaphragm, 
intercostals,  and  abdominal  muscles  causes  serious  difficulty  in  respiration. 
There  is  distressing  dyspnoea,  and  expectoration  is  so  hampered  that  secre- 
tions accumulate  in  the  air-passages.  In  souk?  fatal  cases  of  trichinosis  death 
is  due  principally  to  this  impairment  of  respiration.  The  condition  may  be 
aggravated  by  diffuse  bronchitis  or  lobular  pneumonia. 

Third  in  the  list  of  important  symptoms  comes  oedema.  It  appears  toward 
the  end  of  the  first  week  in  the  eyelids.  Somewhat  later  it  involves  the  upper 
and  lower  extremities.  What  produces  it  is  not  quite  clear.  It  has  been  re- 
garded as  in  part  inflammatory  and  in  part  the  resull  of  occlusion  and  throm- 
bosis of  the  smaller  lymphatics.  Cutaneous  eruptions  also  develop — e.  g., 
vesicles,  wheals,  petechias,  and  pustules.  Frequently  there  is  profuse  per- 
spiration, consequent  upon  which  abundant  crops  of  miliaria  or  sudamina 
may  appear. 

In  well-marked  cases  there  may  be  quite  high  fever  and  other  severe  con- 
stitutional symptoms  in  addition  to  the  local  disturbances  already  discussed. 
The  temperature  may  for  a  time  reach  101°  to  106°  F.  (40°  to  41°  C.)  ;  but 
the  fever  is  seldom  continuous  for  any  length  of  time,  being  usually  inter- 
rupted by.  frequent  and  considerable  intermissions.  There  are  also  a  rapid 
pulse,  headache,  stupor,  and  other  symptoms  suggesting  typhus  or  typhoid 
fever.  In  fact,  the  first  case  in  which  trichinosis  was  recognized  at  the  autopsy 
(by  Zenker  of  Dresden)  had  been  regarded  before  death  as  typhoid.  The 
urine  may  be  albuminous,  and,  in  rare  instances,  nephritis  is  seen.  The 
changes  in  the  blood  are  very  interesting.  At  the  height  of  the  disease  we  find 
a  marked  leucocytosis,  and,  what  is  especially  characteristic,  a  pronounced 
increase  of  the  eosinophile  cells  in  the  blood.  In  cases  with  unfavorable 
termination  the  eosinophils  disappear  from  the  blood  shortly  before  death. 

The  duration  of  the  disease  varies  widely.  There  are  mild  cases  often 
unrecognized,  which  get  well  after  slight  symptoms  have  lasted  two  or  three 
weeks.  More  pronounced  cases  occupy  six  to  eight  weeks,  or  even  a  much 
longer  time.  Of  the  more  severe  cases  about  one  third  prove  fatal,  usually 
from  the  fourth  to  the  sixth  week.  Sometimes  death  is  caused  by  the  severity 
of  the  constitutional  disturbance,  but  usually  from  disabled  respiration.  Even 
if  the  case  ends  favorably,  recovery  is  often  very  tedious. 

Pathology. — The  autopsy  reveals  little  that  is  characteristic  excepting  the 
changes  in  the  muscles.  There  are  sometimes  the  signs  of  hemorrhagic  catar- 
rhal inflammation  of  the  small  intestine.  The  spleen  is  not  enlarged.  Very 
often  the  liver  is  decidedly  fatty.  What  should  cause  this  in  trichinosis  has 
not  yet  been  determined.  The  lungs  often  present  islets  of  lobular  pneu- 
monia, or  sometimes  even  of  gangrene.  The  trichinae  are  found  in  the  muscles, 
beginning  with  the  fifth  week.  They  can  be  recognized  by  the  naked  eye  as 
little  whitish  lines.  We  have  already  named  the  muscles  chiefly  infested. 
Under  the  microscope  we  see  the  fibers  in  which  the  trichinae  lie  transformed 
into  a  fine  granular  mass.  The  nuclei  of  the  muscular  fibrillse  are  greatly 
increased  in  number  in  the  neighborhood  of  the  coiled-up  parasite.     Finally, 


160  ACUTE   GENERAL   INFECTIOUS   DISEASES 

the  sarcolemma  collapses,  and  becomes  greatly  thickened  upon  its  external 
surface  by  a  hyperplasia  of  connective  tissue.  The  muscles  also  present  many 
other  degenerative  changes,  such  as  a  flaky  disintegration,  waxy  degeneration, 
and  the  formation  of  vacuoles.  There  is  furthermore  a  marked  increase  of 
nuclei  in  the  interstitial  tissue  of  the  muscles.  Within  the  intestines  are  some-' 
times  to  be  found,  even  after  several  weeks'  illness,  numerous  living  intes- 
tinal trichina? — a  fact  of  importance  from  a  therapeutic  point  of  view. 

Diagnosis. — The  diagnosis  of  trichinosis  is  generally  not  difficult,  since 
the  peculiar  symptoms  of  the  disease,  especially  the  extensive,  painful  inflam- 
mation of  the  muscles  and  the  oedema,  occur  in  this  way  in  only  one  other 
rare  disease,  primary  acute  polymyositis  (vide  Vol.  II).  Trichinosis  is  dis- 
tinguished from  this  partly  by  the  peculiar  astiology  (affecting  several  people, 
the  use  of  raw  pork,  etc.),  and  partly  by  the  initial  gastrointestinal  symptoms. 
Trichinosis  may  also  be  confounded  with  multiple  neuritis  and  perhaps  with 
acute  articular  rheumatism,  but  careful  observation  of  the  patient  will  usually 
make  the  diagnosis  clear.  An  absolutely  certain  diagnosis  may  be  arrived  at 
by  finding  intestinal  trichinae  in  the  dejections.  The  blood  findings,  too — 
leucocytosis,  and,  above  all,  eosinophilia,  perhaps  also  the  demonstration  of 
the  embryos — are  of  diagnostic  importance. 

Treatment. — As  trichina?  may  still  be  alive  in  pork  that  has  been  smoked, 
or  salted,  or  half-cooked  (e.  g.,  some  sausages  and  meat  balls),  the  only  possi- 
ble prophylaxis,  therefore,  as  far  as  the  individual  is  concerned,  is  to  avoid 
all  such  food.  A  real  protection  for  the  public  against  the  disease  is  also 
afforded  by  governmental  microscopic  inspection  of  meat,  as  already  estab- 
lished in  many  places. 

When  an  individual  has  become  infected  with  trichinae,  if  it  is  possible 
that  intestinal  trichina?  still  are  present,  the  treatment  must  always  begin 
with  the  exhibition  of  purgatives,  such  as  compound  infusion  of  senna,  calo- 
mel, or  castor  oil.  Since  trichina?  may  be  found  in  the  intestines  as  long  as 
eight  weeks  after  the  beginning  of  the  first  symptoms,  we  should  not  neglect 
local  action  on  the  intestinal  contents  even  in  the  later  stages  of  the  disease. 
Of  the  remedies  which  are  calculated  to  destroy  the  intestinal  trichina?,  glyc- 
erin, which  was  first  recommended  by  Fiedler,  seems  to  be  the  most  efficient. 
It  must  be  given  in  rather  large  doses,  say  a  tablespoonful  every  hour.  Other 
drugs  are  much  less  reliable,  but  we  will  name  among  them  benzine  in  the 
total  daily  dose  of  1  to  2  drachms  (gm.  4  to  8)  in  capsules,  and  picric  acid 
in  pills — the  daily  dose  being  5  to  8  gr.  (gm.  0.3  to  0.5). 

Treatment  is  unfortunately  almost  wholly  powerless  against  the  myositic 
symptoms  of  trichinosis  and  their  sequela?.  The  muscular  pains  can  be  allevi- 
ated by  narcotics,  particularly  morphin  subcutaneously,  poultices,  and  chloro- 
form oil  as  an  embrocation.1  Protracted  warm  baths  are  excellent.  Anti- 
pyrin  and  salicylic  acid  are  also  said  to  do  good  in  many  cases. 

[*  Generally  one  part  of  chloroform  to  ten  of  olive  oil.     It  is  not  officinal  in  Germany,  but  is 
weaker  than  the  linimentum  chloroformi  (U.  S.  P.). — Trans.] 


MALTA    FEVER  161 

CHAPTER    XXV 

THE     "FOURTH    DISEASE" 

[In  1900  Dukes  described  an  eruptive  disease,  said  to  resemble  both  rotheln 
and  mild  scarlet  fever  and  yet  to  afford  no  immunity  to  either.  After  an 
incubation  of  nine  to  twenty-one  days  the  body  is  covered,  in  the  course  of  a 
few  hours,  with  a  diffuse  rash  of  a  bright-red  color.  There  are  usually  no 
prodromes.  The  temperature  seldom  exceeds  101°  F.  There  is  some  glandu- 
lar enlargement.  Desquamation  may  be  slight  or  considerable.  There  are  no 
sequela3. 

The  disease  is  generally  viewed  with  skepticism,  but  at  any  rate  Dukes's 
claim  may  be  taken  as  an  illustration  of  the  general  fact  that  the  exanthems 
are  not  always  typical.] 


CHAPTER    XXVI 

MALTA    FEVER 

{Mediterranean  Fever.     Rock  Fever.      Undulant  Fever) 

[Malta  fever  is  a  disease  of  long  duration  characterized  clinically  by 
continued  fever,  profuse  perspiration,  constipation,  frequent  relapses,  rheu- 
matic or  neuralgic  pain,  swelling  of  joints,  and  orchitis;  bacteriologically,  by 
the  presence  in  the  blood  and  organs  of  the  Micrococcus  melitensis  (Bruce), 
and  anatomically  by  congestion  of  the  spleen  and  other  organs. 

It  occurs  around  the  Mediterranean,  and  probably  on  the  Red  Sea,  the 
banks  of  the  Danube,  the  southern  Atlantic  coast  of  the  United  States,  and 
the  islands  of  the  Gulf  of  Mexico.  Musser  and  Sailer  have  reported  a  case 
coming  from  the  West  Indies,  and  H.  H.  Smith  one  in  Boston,  in  a  Sicilian 
immigrant. 

It  is  due  to  infection  with  the  Micrococcus  melitensis,  above  mentioned, 
which  usually  invades  the  body  by  being  swallowed;  but  as  mosquitoes  have 
been  found  to  contain  the  organism,  they  may  possibly  transmit  it.  The 
germ  has  been  found  in  the  blood,  urine,  and  feces  of  the  patient  and  in  food, 
more  particularly  milk.  Out  of  101  blood  cultures  in  persons  suffering  from 
this  disease,  57  were  positive. 

On  post-mortem  examination  the  spleen  is  always  enlarged,  averaging 
twenty  ounces.  The  mesenteric  glands  are  swollen,  but  less  so  than  in 
typhoid. 

The  period  of  incubation  is  regarded  as  six  to  ten  days.  The  onset  may 
be  gradual  or  sudden.  There  is  generally  dyspepsia,  languor,  headache,  chilli- 
ness, and  great  weakness,  often  accompanied  with  muscular  pains.  The  fever 
is  characterized  by  extreme  irregularity  with  a  great  tendency  to  relapses. 
Its  symptoms  (says  Bruce)  are  those  commonly  met  with  in  other  fevers,  such 
as  typhoid.  Before  the  disease  had  been  differentiated,  the  fever  was  described 
as  resembling  severe  remittent  malarial  fever;  this  statement  may  give  some 
11 


162  ACUTE   GENERAL   INFECTIOUS   DISEASES 

idea  of  the  behavior  of  the  temperature.  As  Notter  says,  it  is  impossible  to 
present  any  one  ease  or  single  chart  as  characteristic  of  the  disease. 

Hughes's  description,  quoted  by  Osier,  is  as  follows :  "  Clinically  the  fever 
has  a  peculiarly  irregular  temperature  curve,  consisting  of  intermittent  waves 
or  undulations  of  pyrexia  of  a  distinctly  remittent  character.  These  pyrexial 
waves  or  undulations  last,  as  a  rule,  from  one  to  three  weeks,  with  an  apyrexial 
interval  lasting  for  two  or  more  days.  In  rare  cases  the  remissions  may  be- 
come so  marked  as  to  give  an  almost  intermittent  character  to  the  febrile 
curve,  clearly  distinguishable,  however,  from  the  paroxysms  of  paludic  in- 
fection. This  pyrexial  condition  is  usually  much  prolonged,  having  an  un- 
certain duration,  lasting  for  even  six  months  or  more.  Unlike  paludism,  its 
course  is  not  markedly  affected  by  the  administration  of  quinin.  Its  course 
is  often  irregular  and  even  erratic  in  nature." 

If  the  patient  survives  the  first  two  or  three  weeks,  he  usually  recovers. 
As  a  rule,  death  occurs,  if  at  all,  in  the  first  or  second  week,  preceded  by  con- 
tinued high  fever  with  a  tendency  to  hyperpyrexia,  delirium,  dry  tongue,  and 
diarrhea.  Very  rarely  death  occurs  at  a  later  stage  as  a  result  of  increasing 
debility.  Mild  cases  may  be  practically  well  in  twenty  or  thirty  days.  The 
average  illness  occupies  three  months,  and  a  protracted  case  may  extend  over 
three  years.  In  half  the  eases  there  are  pain  and  swelling  in  the  joints.  Neu- 
ritis and  orchitis  are  fairly  frequent.     The  spleen  is  enlarged  and  tender. 

The  mortality  is  only  two  per  cent. 

As  to  diagnosis,  we  may  obtain  the  specific  organism  by  a  blood  culture. 
There  is  also  a  specific  agglutination  reaction.  The  disease  is  not  influenced 
by  quinin,  as  is  malaria.  It  differs  from  typhoid  in  its  longer  duration,  in 
the  absence  of  rose  spots,  in  the  arthritic  and  neuralgic  symptoms,  in  consti- 
pation being  the  rule,  and  in  the  lower  mortality. 

No  specific  mode  of  treatment  has  been  as  yet  established.  Especial  atten- 
tion must  be  paid  to  the  diet  and  to  bathing.] 


CHAPTER    XXVII 

ROCKY-MOUNTAIN    SPOTTED    FEVER 

(Tick  Fever) 

[Rocky-Mountain  spotted  fever  is  an  infectious  disease  seen  in  the  high 
mountain  valleys  of  Montana,  Idaho,  Wyoming,  Utah,  Oregon,  Colorado, 
and  Nevada.  It  has  an  abrupt  onset,  with  chill,  continued  fever,  headache, 
severe  pains  in  joints  and  bones,  and  an  eruption,  at  first  hypersemic,  later 
petechial,  appearing  on  the  ankles,  wrists,  and  forehead,  and  spreading  over 
the  whole  body. 

It  occurs  in  the  spring,  and  attacks  all  ages  and  both  sexes,  but  is  most 
common  in  active  men,  because  they  are  most  exposed  to  infection.  It  is  not 
contagious.  The  disease  is  conveyed  by  the  bite  of  wood  ticks,  Dermacentor 
venustus  and  D.  modestus.  The  survivor  of  an  attack  is  therafter  immune. 
There  is  a  striking  and  constant  difference  in  mortality  in  different  localities. 


ROCKY-MOUNTAIN   SPOTTED   FEVER  163 

In  western  Montana  the  average  death  rate  is  sixty-five  to  about  ninety  per 
cent,  while  in  [daho  it  rarely  rises  above  five  per  cent. 

Exactly  how  the  bite  of  the  tick  imparts  the  infection  Is  not  settled.  It  is 
pretty  certain  that  the  disease  is  not  a  pirojilasmosis.  Ricketts  has  found  in 
both  kinds  of  tick  a  bacillus  which  gives  an  agglutination  reaction  with  im- 
mune serum,  but  this  bacillus  is  present  not  only  in  virulent  ticks  but  also 
in  those  incapable  of  transmitting  the  disease. 

The  period  of  incubation  is  three  to  ten  days,  during  which  there  is  in- 
creasing malaise,  with  pain  in  the  bones  and  muscles.  Usually  there  is  a 
severe  chill  at  the  onset.  The  bowels  are  constipated.  There  is  jaundice. 
Bleeding  from  the  nose,  mouth,  stomach,  and  bowels  may  occur.  The  pulse 
is  characteristically  rapid.  Pneumonia  may  develop.  The  spleen  is  large  and 
tender.    Coma  usually  precedes  death. 

The  rash  appears  on  the  second  to  the  seventh  day  after  the  onset.  It  is 
first  seen  on  the  wrists  and  ankles,  spreading  toward  the  trunk.  It  also  ap- 
pears on  the  forehead  and  breast,  but  is  especially  marked  on  the  back.  In 
severe  cases  there  may  be  superficial  gangrene. 

Death,  if  it  takes  place,  usually  comes  between  the  sixth  and  the  twelfth 
days.  After  two  weeks  recovery  is  likely.  Convalescence  is  slow  and  begins 
about  the  fourth  week. 

As  to  treatment,  attempts  to  obtain  specific  sera  and  vaccines  are  being 
made  (Eicketts),  but  are  not  yet  perfected.  Meanwhile  therapy  is  symp- 
tomatic. Free  purgation  is  usually  recommended,  and  water  should  be  urged 
upon  the  patient.] 


II.    DISEASES  OF  THE  RESPIRATORY  ORGANS 


SECTION   I 

Diseases  of  the  Nose  1 

CHAPTER    I 

CORYZA 

(Snuffles.  Rhinitis.  Cold  in  the  Head) 

iEtiology. — The  well-known  symptoms  of  coryza  depend  upon  a  catarrhal 
inflammation  of  the  nasal  mucous  membrane.  Although  this  catarrh  is  cer- 
tainly due  to  infectious  influences,  still  we  cannot  deny  that  it  is  one  of  those 
diseases  in  which  taking  cold  is  a  contributory  cause.  Daily  experience  teaches 
us  how  often  coryza  follows  an  evident  exposure  to  cold,  such  as  wetting  the 
feet.  But  the  nasal  hyperemia  and  hypersecretion  and  sneezing,  reflexly 
induced  by  the  chill,  soon  pass  away.  In  order  to  produce  a  real  coryza  with 
continued  sickness,  a  subsequent  infection  is  necessary.  For  this,  however, 
opportunity  is  afforded  by  the  changes  in  the  mucosa  brought  about  by  the 
chill.  The  sensitiveness  of  the  nasal  mucosa  to  reflex  or  direct  excitation 
differs  widely  in  different  persons,  and  on  this  depends  the  varying  suscep- 
tibility of  the  individual  to  coryza.  The  indubitable  infectiousness  of  many 
coryzas  is  mainly  proved  by  the  contagiousness  of  the  disease.  Handkerchiefs, 
kissing,  or  even  mere  social  intercourse,  may  suffice  to  transmit  rhinitis. 
Frequently  the  infectious  catarrh  starts  in  the  nasal  pharynx  and  thence 
invades  the  nasal  mucosa.  The  first  sensations  are  of  burning  and  irritation 
in  the  throat. 

Coryza  may  also  arise  from  the  action  of  chemical  irritants  or  mechanical 
irritants,  such  as  dust,  on  the  nasal  mucous  membrane.  The  iodin  coryza, 
which  occurs  from  the  internal  use  of  iodin,  is  noteworthy.  In  this  form 
iodin  can  easily  be  detected  in  the  nasal  secretion.  The  idiosyncrasy  of  many 
people  to  ipecacuanha  is  also  well  known,  the  very  smell  of  it  setting  up  a 
coryza,  and  sometimes  considerable  asthmatic  disturbances.  A  severe  coryza  is 
the  chief  symptom,  too,  in  hay  fever  (vide  infra),  which  is  probably  due  to 

1  Special  treatises  on  the  pathology  and  therapeutics  of  nasal  diseases  are  to  be  found  in  the 
following  works:  M.  Schmidt,  "Die  Krankheiten  der  oberen  Luf twege, "  Third  Edition,  1903: 
K.  Zarniko,  "Die  Krankheiten  der  Nase,  ihrer  Nebenhohlen  und  des  Nasenrachenraumes, " 
Second  Edition,  1905;  Griinwald,  "Atlas  und  Grundriss  der  Krankheiten  der  Mundhohle,  des 
Rachens  und  der  Nase,"  1902.  O.  Chiari,  "Krankheiten  der  oberen  Luftwege. "  M.  Hajek, 
"Pathol,  u.  Therapie  d.  entziindl.    Erkrankungen  der  Nebenhohlen  der  Nase, "  1903,  and  others. 

164 


CORYZA  105 

the  action  of  the  pollen  of  certain  grasses  on  the  respiratory  mucous  mem- 
brane.    Finally,  we  must   bear   in   mind   thai   coryza   may   often   be  onl 

symptom  of  some  oilier  disease,  sueli  as  measles,  syphilis,  or  glanders,  and 
that  severe  purulent  inflammation  of  the  nasal  mucous  membrane  may  be 
excited  by  the  presence  of  the  secretion  from  a  gonorrhea]  or  blennorrhea! 
conjunctivitis. 

Symptoms. — The  symptoms  of  coryza  are  in  most  of  the  milder  case-  of 
a  local  nature  only.  The  secretion  is  troublesome;  at  first  it  is  scanty  and 
mucous,  but  later  it  becomes  more  abundant  and  watery;  and  sometimes  it  is 
purulent.  The  nasal  passages  are  not  infrequently  closed  from  the  swelling 
of  the  mucous  membrane.  The  patient  necessarily  has  to  breathe  through 
the  mouth,  which  explains  the  well-known  nasal  speech.  This  closure  of  the 
nares  may  give  rise  to  dangerous  attacks  of  dyspnoea  in  children,  especially 
in  infants,  who  have  to  breathe  through  the  nose  when  sucking  at  the  breast. 
The  sense  of  smell  is  always  diminished.  The  local  sensations  of  pain  and 
burning  are  due  chiefly  to  a  mild  inflammation  of  the  skin  of  the  nostrils  and 
upper  lip  set  up  by  the  irritation  of  the  secretion.  The  irritated  condition 
of  the  inflamed  mucous  membrane  occasions  a  feeling  of  tickling  and  itching 
in  the  nose,  and  frequently  by  a  reflex  action  violent  sneezing.  The  symptoms 
are  more  severe  if  the  cavities  adjacent  to  the  nose  are  attacked  by  catarrh, 
and  if  in  them  accumulations  of  secretion  occur.  Marked  pain  in  the  forehead 
occurs  in  catarrh  of  the  frontal  sinuses.  The  sinuses  of  the  ethmoid  and 
sphenoid  bones,  and  the  antrum  of  Highmore,  may  also  be  implicated.  Much 
more  frequently  a  severe  coryza  sets  up  inflammation  in  adjacent  mucous 
membranes.  Thus  we  find,  following  coryza,  conjunctivitis,  affection  of  the 
ear,  sore  throat,  or  laryngitis.  In  persistent  coryza  eczema  is  not  infrequently 
excited  on  the  skin  of  the  upper  lip,  and  mention  has  already  been  made  of 
the  fact  that  coryza  may  sometimes  act  as  the  exciting  cause  of  erysipelas. 

In  severe  coryza  we  may  sometimes  have  quite  a  marked  general  disturb- 
ance, and  often  slight  elevations  of  temperature.  The  "  feverish  cold "  of 
children,  for  instance,  is  well  known.  Brief  mention  may  be  made,  also,  of 
a  peculiar  form  of  coryza.  It  consists  in  sudden  attacks  of  a  very  profuse 
discharge  of  a  watery  secretion  from  the  nose.  Such  attacks  are  probably 
due  to  nervous  influences.     Therapeutic  measures  are  of  little  avail. 

Treatment. — Special  treatment  is  usually  unnecessary,  for  most  cases 
recover  of  themselves  in  a  few  days.  It  seems  doubtful  whether  the  internal 
use  of  quinin  in  fresh  coryza  is  of  service,  as  is  claimed.  With  abundant 
secretion,  especially  in  fresh  cases,  Hager's  "coryza  remedy"  (as  an  inhala- 
tion) is  worthy  of  trial;  this  consists  of  ten  parts  each  of  alcohol  and  car- 
bolic acid,  and  five  parts  of  ammonia  water.  Painting  the  nasal  mucous  mem- 
brane with  a  solution  of  cocain  (two  to  five  per  cent)  is  also  greatly  praised 
[but  it  may  lead  to  the  formation  of  the  cocain  habit].  A  remedy  that 
apparently  is  often  effective  is  "  f orman  "  (forman  cotton,  forman  pastils). 
In  the  presence  of  warm  water,  this  drug  splits  up  into  formalclehyd,  men- 
thol, and  hydrochloric  acid.  It  should  be  inhaled  through  the  nose.  When 
the  secretion  forms  abundant  dry  scabs,  an  attempt  should  be  made  to  wash 
them  out  by  injections  of  warm  fluids,  such  as  warm  milk.  The  upper  lip 
and  the  nostrils  should  be  smeared  with  vaselin  or  simple  ointment  to  pro- 
tect the  skin  from  the  action  of  the  secretion.     Only  in  the  rare  cases  of  a 


166  DISEASES   OF   THE   RESPIRATORY   ORGANS 

severe  purulent  catarrh  is  energetic  local  treatment  of  the  nasal  mucous 
membrane  necessary.  Here  we  may  use  douches  or  sprays  of  astringents 
like  tannin  or  alum,  or  let  the  patient  snuff  them  up,  or  we  may  apply  caustics 
like  nitrate  of  silver.  In  children  who  cannot  blow  the  nose,  it  is  advisable 
to  cleanse  the  nose  frequently  with  a  small  sponge  and  a  one-per-cent  solution 
of  boric  acid. 

HAY   FEVER  (HAY  ASTHMA) 

The  so-called  hay  fever  {catarrh  wtivus)  is  of  frequent  occurrence  in 
England  and  North  America,  although  rarer  in  Germany.  It  usually  af- 
fects men  in  middle  life,  less  often  women.  Some  individuals  are  peculiarly 
liable  to  the  disease.  For  them  an  attack  may  be  produced  merely  by  walking 
across  a  meadow  or  near  a  grain  field  at  that  season  when  the  grasses  are  in 
bloom — i.  e.,  about  May  to  July.  As  already  intimated,  it  is  supposed  that 
the  grains  of  pollen  excite  the  disease,  being  diffused  in  the  air  and  thus  drawn 
into  the  nostrils.  At  any  rate,  they  have  repeatedly  been  found  in  the  nasal 
secretion  and  also  in  the  tears  of  affected  persons.  The  symptoms  consist  in 
a  very  severe  coryza,  with  burning  of  the  nose  and  violent  sneezing.  The 
erectile  tissue  of  the  nose  is  probably  acutely  swollen.  Usually  these  symp- 
toms are  accompanied  by  a  well-marked  conjunctivitis  with  oedema  of  the 
eyelids.  In  severer  cases  there  is,  furthermore,  a  catarrh  of  the  larynx  and 
bronchi.  There  is  frequently  a  tendency  to  violent  attacks  of  asthma 
("hay  asthma"),  especially  at  night  (see  the  chapter  on  bronchial  asthma). 
The  treatment  consists  first  in  avoiding  the  cause  by  change  of  residence,  as 
by  going  to  the  seashore.  For  the  nasal  catarrh,  douches  are  most  to  be  rec- 
ommended, such  as  a  solution  of  1  part  of  quinin  to  500  to  1,000  parts  of 
water,  or  a  solution  of  carbolic  acid,  etc.  Some  authors  praise  massage  of 
the  nasal  mucosa  and  the  topical  use  of  cocain  and  suprarenin  solutions.  Of 
the  internal  remedies,  sodium  or  potassium  iodid  should  be  tried  in  pro- 
nounced asthmatic  conditions.  A  peculiar  method  of  treatment  has  been  pro- 
posed by  Dunbar.  He  produces  an  alleged  antitoxic  serum  by  the  action  of 
pollen  grains  on  animals,  and  asserts  that  the  penciling  of  this  serum  on  the 
nasal  mucosa  or  the  use  of  a  snuff  impregnated  with  it  (pollantin)  very  mate- 
rially lessens  the  suffering  of  hay-fever  patients.  The  practical  results  of  this 
method  are  not  entirely  harmonious. 


CHAPTER    II 

CHRONIC    RHINITIS 

(Rhinitis  chronica  hypertrophica  et  atrophica  ozmna) 

1.  Chronic  Hypertrophic  Rhinitis. — It  is  in  many  cases  impossible  to 
determine  the  causes  of  hypertrophic  rhinitis.  Sometimes  the  condition 
seems  to  develop  as  a  sequel  to  frequently  repeated  nasal  catarrh,  although  in 
this  case  the  relation  is  often  reversed — it  being  the  chronic  rhinitis  which 


CHRONIC   RHINITIS  107 

occasions  a  predisposition  to  the  frequent  acute  exacerbations  of  the  catarrh. 
Certain  diatheses  (anaemia,  scrofula)  appeal-  to  influence  the  development  of 
the  disease.  This  is  also  true  of  occupations  which  expose  the  individual  to 
dust  or  smoke,  and  sometimes  true  of  malformation  of  the  nose  (for  instance, 
deviation  of  the  septum)  and  perhaps  also  of  hereditary  predisposition. 

The  anatomical  changes  consist  of  a  slow  hut  progressive;  swelling  and 
hypertrophy  of  the  mucous  membrane.  This  seems  spongy,  and  of  a  red  or 
reddish-gray  color.  The  greatest  change  is  almost  always  found  over  the 
inferior  turbinated  bone,  and  next  to  that  over  the  middle  turbinated.  In 
advanced  cases  the  mucous  membrane  presents  rough,  uneven  swellings, 
and  even  polypi.  These  changes  are  often  visible  upon  inspection  of  the 
nostrils  anteriorly,  but  they  may  escape  discovery  until  a  rhinoscopic  examina- 
tion of  the  posterior  choanse  is  made. 

The  disturbance  occasioned  by  chronic  hypertrophic  rhinitis  may  be  very 
considerable.  Eespiration  through  the  nose  is  obstructed,  the  voice  becomes 
nasal,  the  senses  of  smell  and  taste  are  impaired.  The  nasal  secretion  is  for 
the  most  part  increased,  but  it  may  be  diminished.  Often  there  is  a  tendency 
to  nosebleed.     Many  patients  complain  also  of  headache. 

The  frequent  involvement  of  neighboring  organs  is  important.  This 
applies  particularly  to  the  ear.  Deafness  is  caused  both  by  the  obstruction 
of  the  openings  of  the  Eustachian  tubes,  and  not  infrequently  also  by  exten- 
sion of  the  catarrh  to  the  lining  membrane  of  the  tubes  and  the  middle  ear. 
Very  frequently  the  disease  is  associated  with  chronic  nasopharyngitis  or 
pharyngitis.  The  visible  portion  of  the  nose  is  not  infrequently  affected,  as 
shown  by  redness  and  swelling  of  its  tip. 

A  fact  of  especial  interest  is  that  such  a  diseased  state  of  the  nasal  mucous 
membrane  may  give  rise  to  reflex  neuroses  (Voltolini,  Hack,  and  others). 
Although,  in  our  opinion,  many  of  the  specialists  of  the  nose  go  too  far  in 
this  direction,  there  is  no  room  for  doubt  that  attacks  of  migraine,  vertigo, 
certain  varieties  of  headache,  and,  above  all,  many  forms  of  bronchial  asthma, 
may  bear  a  close  relation  to  diseases  of  the  nose.  We  shall  revert  to  this  point 
later  on.     (See  especially  the  chapter  on  bronchial  asthma.) 

The  treatment  of  chronic  hypertrophic  rhinitis,  in  order  to  be  successful, 
demands  complete  destruction  and  removal  of  the  hypertrophic  portions  by 
means  of  the  galvano-cautery.  For  particulars,  we  must  refer  to  the  direc- 
tions of  specialists.  Only  in  milder  cases  does  benefit  follow  penciling  with 
cocain,  nasal  douches,  and  the  insufflation  of  a  powder  composed  of  gr.  -§-  to 
If  =  0.05  to  0.1  gm.  nitrate  of  silver  to  oijss.  =  gm.  10.0  of  common  starch 
or  the  like. 

2.  Simple  Chronic  Atrophic  and  Fetid  Atrophic  Rhinitis.  Ozaena  Simplex. — 
The  disease  consists  in  a  slow,  progressive  atrophy  not  only  of  the  mucous 
membrane  with  its  vessels  and  glands,  but  finally  also  of  the  bones,  and  this 
atrophy  is  not  preceded  by  hypertrophy.  Thus  the  nasal  cavities  become 
abnormally  large.  The  turbinated  bones  grow  smaller  and  smaller,  so  that 
finally  they  are  represented  merely  by  narrow  ridges.  Furthermore,  the 
scanty  purulent  secretion  has  a  tendency  to  dry  up  and  form  adherent  green- 
ish-yellow scabs  and  crusts,  which  undergo  a  peculiar  putrefactive  decompo- 
sition and  give  rise  to  an  unbearable  stench.  We  do  not  yet  know  what  special 
form  of  bacterium  causes  this  putrefactive  decomposition  of  the  secretion. 


168  DISEASES   OF  THE   RESPIRATORY   ORGANS 

When  this  very  characteristic  and  extremely  repulsive  stench  occurs  in  the 
nose;  we  usually  give  the  affection  the  brief  name  of  ozsena  (  o£«v,  to  stink), 
but  in  the  other  and  practically  less  important  cases  we  speak  of  a  simple 
atrophic  rhinitis.     The  latter  may  sometimes  change  into  true  ozsena. 

Ozama  generally  develops  in  childhood.  It  usually  begins  insidiously,  but 
in  other  cases  apparently  is  a  sequel  of  some  acute  disease,  such  as  measles, 
etc.  Anaemia  and  scrofula  deservedly  rank  as  important  predisposing  causes. 
Storck's  view  that  ozaena  is  usually  connected  with  syphilis  in  the  parents  is 
not  sufficiently  supported.  It  is  worthy  of  note  that  patients  with  ozsena  often 
have  from  birth  a  nose  with  a  flat,  broad  bridge,  which  is  perhaps  a  family 
trait,  favoring  the  development  of  the  disease. 

The  subjective  symptoms  are  often  not  marked.  This  is  partly  explained 
by  the  fact  that  the  patient  has  usually  completely  lost  his  sense  of  smell, 
but  for  that  very  reason  the  discomfort  of  his  friends  may  be  the  greater.  The 
feeling  of  dryness  in  the  nose  may  prove  annoying  and  there  are  often  com- 
plaints of  headache  and  of  pressure  in  the  eyes.  Inasmuch  as  the  naso- 
pharynx and  the  posterior  pharyngeal  wall  are  almost  always  implicated  in 
the  process,  the  patient  often  suffers  from  hacking  and  a  tendency  to  cough 
and  vomit.  Such  portions  of  the  secretion  as  are  swallowed  sometimes  give 
rise  to  a  considerable  chronic  disturbance  of  the  stomach.  Upon  physical 
examination  we  are  first  struck  by  the  unusual  breadth  of  the  nostrils.  With 
the  rhinoscope  the  extent  of  the  atrophy  is  still  better  seen.  The  mucous 
membrane  is  pale  or  slightly  red,  and  covered  with  dry  scabs.  Sometimes 
superficial  ulcers  are  formed.  Usually,  as  we  have  said,  the  superior  portion 
of  the  pharyngeal  mucous  membrane  shares  in  the  disease.  The  posterior 
wall  of  the  pharynx  is  seen  to  be  atrophied,  smooth  as  if  it  were  varnished, 
and  often  covered  with  crusts.  The  process  may  involve  the  soft  palate,  "and 
even  the  larynx,  and  not  infrequently  the  disease  is  associated  with  inflamma- 
tion of  the  middle  ear. 

It  should  be  added  that  the  true  ozaena  must  not  be  confounded  with 
other  processes  which  likewise  give  rise  to  a  foul  smell  from  the  nose.  Tuber- 
culous disease  of  the  nasal  mucous  membrane  and  nasal  bones  is  not  rare, 
particularly  in  "  scrofulous  "  children  (Demme)  ;  nor  should  we  forget  the 
syphilitic  affections  of  tbe  nose,  tertiary  and  hereditary  syphilis. 

Treatment. — An  alleviation  of  ozsena  can  be  accomplished  only  by  the  aid 
of  local  applications  as  prescribed  by  specialists.  Even  then  the  treatment 
is  a  prolonged  one,  and  demands  much  patience  on  the  part  of  both  patient 
and  physician.  A  complete  cure  of  atrophic  rhinitis  is  impossible.  Besides 
local  applications,  we  must  also  bear  in  mind  the  necessity  of  constitutional 
treatment. 

The  object  of  local  treatment  is  to  remove  the  secretion  in  order  to  get  rid 
of  the  bad  odor.  Nasal  douches,  with  disinfectant  solutions,  such  as  per- 
manganate of  potassium  (1  to  3,000),  or  phenol,  or  boric  acid,  etc.,  are  here 
most  used.  The  solution  is  carefully  injected  into  the  nose  (best,  by  means 
of  a  small  rubber  ball  having  a  short  rubber  tip — so  called  "  Heller's  nasal 
syringe"),  or  the  fluid  is  allowed  to  run  gently  into  one  nostril  from  an  irri- 
gator while  the  patient  keeps  his  bead  bent  forward;  it  then  runs  through 
the  nasopharynx  and  out  through  the  other  nostril.  The  patient  soon  learns 
to  retain  the  fluid  in  the  pharynx  and  eject  it  from  the  mouth.     All  nasal 


NOSEBLEED  1 69 

douches  must  at  first  be  used  with  care  and  under  the  eye  of  the  physician. 
The  fluid  should  be  injected  at  the  lowest  pressure  possible,  so  that  none  of 
it  may  enter  the  adjacent  cavities  or  the  Eustachian  tube.  Furthermore,  all 
solutions  used  as  a  douche  must  be  lukewarm — 90°  to  95°  P.  (25°  to  28°  C). 
Besides  the  regular  use  of  douches,  the  insufflation  of  powders,  such  as  boric 
acid,  aceto-tartrate  of  aluminum,  aristol,  zinc  sozoiodid,  etc.,  is  sometimes 
employed.  The  insertion  of  tampons  of  dry  absorbent  cotton  is  to  be  recom- 
mended; under  their  use  the  secretion  dries  less  easily  and  the  odor  is  dimin- 
ished. These  tampons  should  be  changed  daily.  It  is  advantageous  to 
medicate  the  tampons  with  a  one-per-cent  solution  of  creolin  or  with  Peru- 
vian balsam  or  some  similar  drug.  Tincture  of  iodin  is  also  recommended. 
Of  late  many  attempts  have  been  made  to  treat  chronic  nasal  catarrh  by  the 
galvano-cautery.  With  regard  to  the  details  of  this  as  well  as  of  other  methods, 
we  must  refer  to  special  treatises  on  the  subject. 


CHAPTEE    III 

NOSEBLEED 

(Epistaxis) 

Although  in  many  cases  nosebleed  is  only  a  symptom,  still  we  are  justified 
in  a  short  description  of  it,  partly  because  frequently  repeated  nosebleeds  often 
first  call  our  attention  to  some  other  existing  disease,  and  partly  because  the 
treatment  is  of  practical  importance. 

Many  persons  are  subject  to  habitual  nosebleed,  which  comes  on  either 
from  slight  causes,  from  violently  blowing  the  nose,  from  physical  exertion, 
from  overheating,  or  even  without  any  special  cause.  This  habitual  nosebleed 
is  sometimes,  but  by  no  means  always,  the  sign  of  a  general  hemorrhagic  di- 
athesis, which  is  hereditary  in  many  instances.  (See  the  chapter  on  hemo- 
philia.) In  other  cases  the  nosebleed  is  the  result  of  some  chronic  disease.. 
It  occurs  especially  in  leukaemia,  in  disease  of  the  heart,  in  contracted  kidney, 
and  as  a  symptom  of  the  so-called  hemorrhagic  diseases,  such  as  scurvy,  pur- 
pura hemorrhagica,  etc.  Finally,  diseases  of  the  nose  itself  may  give  rise  to 
hemorrhage.  The  periodic  occurrence  of  nosebleed  in  young  girls  as  a  form 
of  so-called  "  vicarious  menstruation  "  has  often  been  described,  but  we  must 
always  be  very  guarded  in  arriving  at  this  assumption.  Nosebleed  sometimes 
occurs  at  the  beginning  of  many  infectious  diseases,  especially  typhoid  and 
scarlet  fevers,  etc.,  and  in  septic  affections.  We  may  add  that  the  point  of 
hemorrhage  is  very  frequently  at  the  anterior  lower  end  of  the  cartilaginous 
septum  (Kiesselbach). 

In  many  cases  nosebleed  is  a  very  transitory  symptom,  wholly  without  dan- 
ger, and  in  one  sense  it  may  even  be  advantageous.  Headache,  or  a  feeling 
of  fullness  in  the  head,  is  often  improved  after  an  epistaxis.  Nosebleed  is 
dangerous,  however,  when  it  takes  place  in  those  who  are  already  weak  and 
anaemic,  or  when  it  is  so  persistent  and  abundant  as  to  cause  a  marked  general 
anaemia.  The  latter  is  recognized  by  the  pallor  of  the  face,  by  the  appearance 
of  general  weakness,  by  vertigo,  tinnitus,  and  a  weakened  pulse.    In  such  cases 


170  DISEASES   OF  THE  RESPIRATORY   ORGANS 

the  physician's  interference  is  always  necessary.  In  every  case  of  nosebleed 
it  is  important  to  examine  the  posterior  wall  of  the  pharynx  in  order  to  see 
whether  the  blood  is  not  flowing  backward  from  the  posterior  nares.  The 
hemorrhage  is  often  thought  to  stop  when  no  more  blood  comes  from  the  nos- 
trils, and  yet  the  blood  keeps  flowing  posteriorly. 

In  every  severe  nosebleed  rest  is  the  chief  thing  to  be  enjoined,  and  the 
patient  must  be  told  to  avoid  unnecessarily  blowing,  wiping,  or  drying  the 
nose.  By  quietly  and  persistently  closing  the  nostrils  with  a  handkerchief  a 
thrombus  is  often  formed  without  any  further  medication,  and  the  bleeding 
stops.  The  application  of  cold  water  (iced  water),  in  which  a  little  vinegar 
may  be  put,  is  a  good  thing.  An  effective  hemostatic  is  adrenalin  (applied  in 
l-to-1,000  solution).  If  the  bleeding  does  not  stop,  we  may  next  try  a  tampon 
of  common  absorbent  cotton  or  styptic  cotton,  or,  still  better,  of  strips  of 
iodoform  gauze  in  the  nostril  from  which  the  blood  comes.  Penghawar  Djam- 
bi,  a  plant  fiber,  appears  to  be  a  very  good  hemostatic.  If  this  does  not  suc- 
ceed, the  posterior  nares  must  be  plugged  by  means  of  a  "  Bellocq's  cannula." 
In  case  of  emergency  we  may  use  an  elastic  catheter,  which  is  passed  through 
the  inferior  meatus  into  the  pharynx  and  out  by  the  mouth.  The  tampon  is 
fastened  to  the  catheter  and  brought  up  into  the  posterior  nares  by  drawing 
the  catheter  back  through  the  nose.  Internal  remedies  to  check  the  flow  of 
blood  (ergotin,  hydrastis,  etc.)  are  very  uncertain  in  their  action. 


SECTION    II 
Diseases  of  the  Larynx 

CHAPTER    I 

ACUTE  LARYNGEAL  CATARRH 

(Acute  Laryngitis) 

etiology. — Taking  cold  plays  a  prominent  part  in  the  popular  setiology 
of  acute  laryngeal  catarrh.  Its  influence  cannot  be  wholly  denied,  for  it  is 
entirely  in  accord  with  our  experiences  otherwise  that  a  mucosa  which  has 
been  injured  by  chilling  is  rendered  thereby  more  receptive  for  infection.  The 
disposition  to  laryngitis  differs  very  much  in  different  people,  so  that  some 
take  a  catarrh  much  more  easily  and  more  frequently  than  others.  Besides 
cold,  direct  irritants  which  attack  the  laryngeal  mucous  membrane  often  set 
up  a  laryngitis ;  among  these  are  in  particular  the  inhalation  of  smoke  and  of 
noxious  gases  and  vapors.  Many  laryngeal  catarrhs,  too,  arise  from  excessive 
speaking,  shouting,  or  singing,  particularly  if  other  injurious  influences  act 
on  the  larynx  at  the  same  time.  Finally,  laryngitis  may  appear  as  a  compli- 
cation or  as  a  secondary  affection,  in  other  diseases,  especially  in  measles,  less 
frequently  in  typhoid,  scarlet  fever,  and  erysipelas.  Catarrh  of  the  larynx  is 
very  often  combined  with  catarrh  of  the  nose,  the  pharynx,  and  the  larger 
bronchi. 


ACUTE  LARYNGEAL  CATARRH  171 

Symptomatology. — Although  the  symptoms  of  laryngitis  usually  make  the 
diagnosis  easy  and  certain,  yet  an  accurate  understanding  of  the  exteni  and 
intensity  of  the  catarrh  can  be  obtained  only  by  a  laryngoscopic  examination,1 
which  therefore  should  be  employed  in  every  severe  case.  The  laryngeal  mirror 
shows  a  decided  reddening  and  swelling  of  the  mucous  membrane,  varying  with 
the  intensity  of  the  catarrh,  and  most  marked  on  the  true  and  false  vocal  cords 
and  between  the  arytenoid  cartilages.  We  often  see  small  collections  of  mucus 
here  and  there  on  the  membrane.  In  individual  cases  different  parts  of  the 
larynx  are  especially  affected.  In  intense  inflammations  superficial  erosions  are 
often  met  with,  especially  on  the  vocal  cords.  In  other  cases  the  mucous  mem- 
brane shows  a  grayish-white  coloring  in  some  places,  apparently  due  to  a  thick- 
ening of  the  epithelium.  Small  hemorrhages  in  the  mucous  membrane  are  also 
occasionally  seen.  Very  often  we  see  on  phonation  an  incomplete  closure  of 
the  glottis,  so  that  a  little  oval  space  is  left  between  the  vocal  cords.  This 
slight  "  catarrhal  paresis  of  the  vocal  cords  "  is  probably  of  muscular  origin, 
and  depends  chiefly  upon  an  affection  of  the  thyro-arytamoid  muscles. 

Of  the  other  symptoms  of  laryngeal  catarrh,  hoarseness  is  particularly  to 
be  mentioned,  for  in  many  cases  the  diagnosis  of  laryngitis  may  be  made  from 
this  alone.  It  is  either  due  directly  to  the  anatomical  changes  of  the  cords, 
or  to  the  paresis  just  mentioned.  The  degree  of  hoarseness  is  of  course  very 
different  in  different  cases,  and  varies  from  a  simple  "  roughening  "  or  "  dead- 
ening "  of  the  voice  to  a  complete  loss  of  voice  (aphonia). 

The  cough  in  laryngitis  may  be  very  severe,  and  is  often  recognizable  by 
its  harsh,  hoarse  ring  as  a  "  laryngeal  cough."  It  is  usually  dry  at  first,  and 
later  on  it  is  associated  with  a  scanty  mucopurulent  expectoration,  which  is 
sometimes  tinged  with  blood. 

Pain  in  the  larynx  is  generally  only  moderate.  The  subjective  symptoms 
consist  chiefly  of  a  disagreeable  feeling  of  itching,  burning,  and  dryness  in  the 
throat.  After  prolonged  speaking,  however,  the  pain  in  the  larynx  may  some- 
times be  quite  severe.  External  pressure  on  the  larynx  is  often  somewhat  pain- 
ful. Difficulty  in  swallowing,  when  it  occurs,  is  due  usually  to  an  accompa- 
nying pharyngitis,  but  it  may  also  be  dependent  upon  an  affection  of  the 
epiglottis  and  the  arytamoid  cartilages. 

The  general  health  is  affected  in  very  different  degrees.  Many  patients  feel 
quite  well  except  for  the  hoarseness,  while  others  are  affected  with  considerable 
debility,  mild  headache,  and  even  at  times  slight  febrile  disturbances.  Of  late 
years  we  have  frequently  seen  cases  of  primary  acute  laryngitis,  with  great 
hoarseness  and  marked  catarrhal  inflammation  of  the  upper  part  of  the  larynx, 
especially  of  the  vocal  cords.  These  cases  begin  with  high  fever  (over  104°  F. 
[40°  C] )  and  quite  severe  general  symptoms,  and  make  a  complete  recovery 
in  a  week  or  two.  They  apparently  have  an  infectious  origin,  and  are  perhaps 
connected  with  influenza. 

Dyspnoea  is  not  present  in  the  common  laryngitis  of  adults,  even  if  there  is 

1  More  extensive  observations  on  laryngoscopy  and  on  many  details  of  the  pathology  of  laryn- 
geal diseases,  which  have  been  carefully  investigated  by  specialists  and  which  cannot  be  men- 
tioned here,  are  to  be  found  in  the  following  works:  Schrotter,  "  Vorlesungen  iiber  die  Krankheiten 
des  Kehlkopfes. "  P.  Heymann,  "Handbuch  d.  Laryngologie  u.  Rhinologie. "  O.  Chiari, 
"Krankheiten  des  Kehlkopfes  u.  der  Luftrohre."  Griinwald,  "Grundriss  d.  Kehlkopfkrank- 
heiten  u.  Atlas  d.  Laryngoscopie,"  etc.     See  also  the  literature  given  on  p.  164. 


172  DISEASES  OF  THE   RESPIRATORY  ORGANS 

decided  swelling  of  the  false  vocal  cords  or  of  the  ary-epiglottic  folds.  There 
is,  however,  a  severe  form  of  acute  laryngitis,  the  so-called  laryngitis  hypo- 
glottica  acuta  gravis  (chorditis  vocalis  inferior),  affecting  not  only  children, 
but  adults,  in  which  well-marked  symptoms  of  suffocation  may  be  present.  In 
this  form  there  is  an  acute,  very  well-marked  swelling  of  the  mucous,  mem- 
brane in  the  inferior,  subchordal,  laryngeal  space,  which  leads  to  a  stenosis. 
The  rare  cases  of  phlegmonous  inflammation  of  the  larynx  may  also  cause  con- 
siderable stenosis  and  dyspnoea. 

In  children,  however,  on  account  of  the  greater  narrowness  of  the  child's 
larynx,  symptoms  of  stenosis  are  not  rare  even  in  the  milder  forms  of  laryn- 
gitis, and  therefore  they  have  led  to  the  establishment  of  a  special  disease,  the 
so-called  false  croup. 

False  Croup. — The  false  croup  (laryngitis  stridula)  of  children  usually 
follows  a  slight  coryza.  A  harsh,  hollow,  ringing  cough  comes  on,  almost 
alwaj^s  suddenly  and  usually  at  night,  by  which  the  child  is  awakened  out  of 
sleep.  The  paroxysms  of  coughing  are  broken  by  long-drawn,  noisy  inspira- 
tions. The  child  is  anxious  and  restless,  the  respiration  is  labored.  The  acces- 
sory muscles  of  respiration  are  brought  into  action,  but  the  deep  inspiratory 
retraction  of  the  lower  intercostal  spaces  and  the  epigastrium  shows  how  im- 
perfectly the  air  enters  the  lungs.  The  pulse  is  small  and  rapid.  The  attack 
lasts  several  hours,  when  the  cough  gradually  becomes  looser  and  the  breathing 
easier.  Finally,  the  child  falls  asleep  and  usually  wakes  the  next  morning  quite 
lively  and  playful,  a  slight  cough  being  the  only  relic  of  the  terrifying  events 
of  the  night  before.  The  next  night  the  same  severe  attack  may  be  repeated, 
and  perhaps  for  two  or  three  nights  more.  After  that  there  remains,  as  a  rule, 
nothing  but  a  slight  catarrh,  which  completely  disappears  in  a  week  or  two. 
The  anatomical  cause  of  false  croup  is  acute  laryngitis  with  marked  swelling 
of  the  mucous  membrane  on  and  below  the  vocal  cords.  In  the  narrow  space 
of  the  child's  larynx  this  speedily  causes  marked  stenosis,  and  the  individual 
attacks  are  probably  excited  by  the  accumulation  and  drying  of  the  secretion 
during  the  night.  There  is  never  any  true  croupous-diphtheritic  change  to 
be  seen  either  in  the  pharynx  or  the  larynx.  It  is  remarkable  that  many  chil- 
dren, and  sometimes  several  children  of  the  same  family,  have  a  specially 
marked  predisposition  to  false  croup.  The  statement,  therefore,  that  a  child 
has  had  the  croup  several  times  almost  always  means  that  it  has  had  this  form 
of  false  croup  just  described. 

Acute  laryngitis  lasts  only  a  few  days  in  mild  cases,  and  a  week  or  more  in 
severe  cases.  With  improper  care  and  unreasonable  conduct  on  the  patient's 
part  an  acute  catarrh  may  run  into  the  chronic  form.  We  hardly  ever  see 
a  fatal  result  in  adults,  even  in  the  severe  form,  and  in  children  false  croup 
very  rarely  has  an  unfavorable  termination  unless  the  child  is  extremely  weak 
or  rachitic. 

Treatment. — The  treatment  of  acute  laryngitis  requires  that  especial  atten- 
tion be  paid  to  the  removal  of  all  injurious  influences.  In  every  severe  laryn- 
gitis the  patient  should  stay  in  his  room,  and  children  are  better  off  in  bed. 
The  patient  should  talk  as  little  as  possible.  In  all  severe  cases  smoking,  too,  is 
to  be  forbidden.  It  is  a  good  plan  to  furnish  plenty  of  warm  drink.  Hot  milk, 
mixed  with  Seltzer  or  Ems  water,  is  readily  taken  by  most  patients.  If  there 
is  a  steam  atomizer  at  our  disposal,  we  may  let  the  patient  inhale  simple 


CHRONIC   LARYNGITIS  173 

steam,  or  a  one-  or  two-per-cent  solution  of  common  salt.     Inhalations  of 

astringents  are  usually  unnecessary.  The  patient  may  also  breathe  steam 
without  any  special  apparatus.  When  there  is  marked  irritation  from  cough- 
ing we  may  give  a  little  morphin.  With  more  marked  Local  symptom-,  espe- 
cially if  there  is  much  pain  on  swallowing,  from  swelling  of  the  epiglottis  and 
the  mucous  membrane  over  the  arytenoid  cartilages,  the  patient  may  suck 
pieces  of  ice  slowly.  In  severe  cases  of  acute  laryngitis,  with  evident  symp- 
toms of  stenosis,  ice  must  he  energetically  used  as  an  internal  and  an  external 
application.  Sometimes,  too,  a  few  leeches  applied  in  the  region  of  the  larynx 
afford  distinct  relief.  Among  external  applications  a  mustard  plaster  over 
the  front  of  the  neck  is  to  be  recommended  when  there  are  marked  local  .symp- 
toms.    Cold,  wet  compresses  about  the  neck  are  also  of  advantage  in  all  cases. 

In  the  false  croup  of  children  we  should  use,  as  a  rule,  the  same  treatment 
as  has  just  been  described.  The  child  should  take  plenty  of  warm  drink,  in- 
hale warm  steam  or  salt  solution,  and  a  mustard  paste  or  hot  poultices  should 
be  applied  to  the  neck.  An  ice  bag  on  the  neck  is  sometimes  useful.  We 
should  be  rather  cautious  with  regard  to  the  favorite  treatment  with  emetics, 
such  as  ipecac  and  sulphate  of  copper,  although  it  cannot  be  denied  that  they 
sometimes  work  very  well  in  severe  dyspnoea! 

These  means  are  entirely  sufficient  for  the  treatment  of  acute  laryngitis. 
It  is  only  exceptionally  that  we  find  ourselves  led  to  employ  in  acute  laryngeal 
catarrh  an  energetic  local  treatment  of  the  laryngeal  mucous  membrane,  like 
painting  with  a  l-to-15  solution  of  nitrate  of  silver. 

We  must  bear  in  mind  that  a  rational  hardening  process  is  of  distinct 
prophylactic  value  in  persons,  especially  in  children,  with  a  recognized  tend- 
ency to  laryngitis,  sore  throat,  etc.  The  best  method  is  to  bathe  the  neck  and 
chest  with  cold  water  regularly  morning  and  night. 

[A  mild  emetic  can  do  no  possible  harm  in  false  croup,  and  very  often  cuts 
the  attack  short.  The  application  of  a  sponge,  moistened  with  water  as  hot 
as  the  child  will  bear,  to  the  region  of  the  larynx  deserves  mention.] 


CHAPTEE    II 

CHRONIC    LARYNGITIS 

(Chronic  Laryngeal  Catarrh) 

iEtiology. — Chronic  laryngitis  develops  from  an  acute  catarrh,  or  comes 
on  gradually  from  the  action  of  injurious  influences  on  the  larynx  (see  the 
preceding  chapter).  Chronic  laryngitis,  therefore,  is  in  many  cases  due  to 
the  occupation,  and  is  seen  especially  in  singers,  public  speakers,  criers,  inn- 
keepers, workmen  exposed  to  dust,  etc.  It  is  very  frequent  in  drunkards,  and 
in  such  cases  it  is  almost  always  associated  with  a  chronic  pharyngitis.  It  is 
probably  not  true  that,  as  frequently  stated,  too  long  a  uvula  may  set  up  laryn- 
gitis by  irritation  of  the  entrance  to  the  larynx. 

Symptomatology. — A  laryngoscopic  examination  is  very  desirable  in  acute 
laryngeal  catarrh,  but  it  is  the  physician's  absolute  duty  to  make  one  in 
chronic  laryngitis,  for  only  too  frequently  a  persistent  hoarseness  is  referred 


174  DISEASES   OF  THE   RESPIRATORY  ORGANS 

to  a  "  simple  "  catarrh  when  the  laryngoscope  gives  quite  another  cause  for  it, 
such  as  paralysis  of  the  vocal  cords  or  new  growths.  Furthermore,  we  must 
always  remember  that  a  chronic  laryngitis  may  be  a  complication  of  tuber- 
culosis, syphilis,  or  chronic  nephritis.  We  should  never  omit  a  careful  exami- 
nation of  the  rest  of  the  body  as  well  as  the  larynx. 

The  laryngoscopic  appearance  in  chronic  catarrh  may  be  so  like  that  in  an 
acute  catarrh  that  we  cannot  distinguish  between  them  without  the  history 
obtained  from  the  patient.  The  redness  of  the.  mucous  membrane,  however,  is 
usually  less  intense,  and  the  vocal  cords  have  more  of  a  dirty  grayish-red 
appearance.  In  most  cases  there  is  also  considerable  swelling  of  the  mucous 
membrane  as  well  as  redness.  Much  more  rarely  we  find  atrophic  conditions, 
resembling  those  of  ozama  and  sometimes  associated  with  it.  Quite  frequently 
in  persistent  catarrhs  a  thickening  of  particular  parts  of  the  mucous  membrane 
is  developed,  especially  of  the  folds  between  the  arytenoid  cartilages.  This 
swelling  is  of  practical  importance,  because  it  furnishes  a  mechanical  hin- 
drance to  the  closure  of  the  arytenoid  cartilages,  and  in  that  way  contributes 
to  the  development  of  the  hoarseness.  We  also  find  marked  thickening  of  the 
false  vocal  cords  (especially  in  public  speakers  and  preachers)  and  of  the  true 
vocal  cords.  Virchow  described,  under  the  name  of  pachydermia  laryngis.  a 
condition  of  the  larynx  seen  especially  in  drinkers  and  characterized  by  a 
thickening  of  the  epithelium  over  the  whole  laryngeal  mucous  membrane. 
Tiirck  has  described  a  peculiar  form  of  chronic  laryngitis,  in  which  rough 
prominences  are  formed  in  the  middle  of  the  true  vocal  cords,  under  the  name 
of  cliorditis  tuberosa.  We  not  infrequently  find  in  chronic  catarrh  superficial 
erosions,  especially  on  the  vocal  cords.  We  never  see  actual  ulceration  in  sim- 
ple laryngitis.  We  also  very  often  see  a  disturbance  of  motion  of  one  or  both 
vocal  cords,  especially  incomplete  closure,  due  sometimes  to  muscular  paresis 
and  sometimes  to  mechanical  conditions. 

The  other  symptoms  of  chronic  laryngitis  are  hoarseness,  cough,  and  ab- 
normal sensations  in  the  larynx.  The  hoarseness  is  of  every  degree,  from  mere 
roughness,  frequent  "  cracking "  of  the  voice,  to  almost  complete  aphonia. 
The  cough  is  ringing,  hoarse,  deep,  and  rough.  The  expectoration  is  scanty, 
usually  simply  mucous,  but  sometimes  a  little  bloody.  The  subjective  sensa- 
tions in  the  larynx  are  a  feeling  of  burning  and  itching,  and  of  dryness  and 
tickling.     They  usually  increase  after  any  protracted  use  of  the  voice. 

We  must  also  mention  as  a  peculiar  and  very  rare  but  practically  important 
form  of  chronic  laryngitis  the  cliorditis  vocalis  inferior  hypertrophica  (Ger- 
hardt),  or  laryngitis  hypoglottica  chronica  hypertrophica  (Ziemssen).  In 
this  form  there  is  a  very  gradual  hypertrophy,  and  finally  a  contraction  of  the 
mucous  and  especially  the  submucous  connective  tissue  in  the  inferior  laryngeal 
space.  More  rarely  the  same  changes  are  seen  in  the  upper  part  of  the  larynx. 
The  special  symptom  of  the  disease,  besides  a  chronic  hoarseness,  is  the  ap- 
pearance of  a  gradually  increasing  stenosis  of  the  larynx.  The  respiration 
is  always  labored,  the  inspiration  noisy  and  protracted.  In  many  cases  there 
are  at  times  such  attacks  of  suffocation  that  life  can  be  prolonged  only  by 
tracheotomy.  The  diagnosis  requires  the  aid  of  the  laryngoscope.  We  see 
beneath  the  glottis  a  little  fissure  surrounded  by  the  thick  and  swollen  mucous 
membrane  of  the  laryngeal  walls. 

The  nature  of  this  affection  is  not  yet  fully  explained.     It  often  seems  to 


LARYNGEAL  PERICHONDRITIS  175 

be  a  simple  chronic  hypertrophic  inflammation,  bul  in  othei  case£  Schrotter 
considers  it  the  same  bacillary  disease  of  the  mucous  membranes,  which  is 
known  as  rhinoscleroma  when  il  occurs  in  the  nose. 

Treatment. — The  treatment  of  chronic  laryngeal  catarrh  is  alwa 
tedious  and  laborious  task,  the  success  of  which  depends  in  greal  measure 
upon  the  good  will  and  energy  of  the  patient.  In  the  first  place,  then,  we 
should  endeavor  to  remove  as  far  as  possible  those  injurious  influences  which 
have  excited  and  kept  up  the  catarrh.  Jt  is  often  easier  to  give  good  advice 
here  than  to  follow  it.  Nevertheless,  it  is  the  duty  of  the  physician  to  impress 
upon  the  patient  the  urgent  necessity  of  taking  care  of  the  larynx,  and  to 
forbid  as  far  as  possible  all  protracted  speaking,  singing,  staying  in  smoke 
or  dust,  smoking,  and  the  use  of  alcohol. 

Local  treatment  takes  the  second  place.  Among  the  most  useful  means  to 
employ  are  sprays  of  astringent  solutions,  such  as  a  one-per-cent  solution  of 
either  tannin  or  alum.  If  there  is  much  secretion  of  mucus,  turpentine  inhala- 
tions are  advisable.  When  there  is  great  irritability  of  the  larynx,  the  patient 
may  also  inhale  vaporized  narcotics,  a  mixture  of  fifty  parts  of  cherry-laurel 
water  with  a  thousand  parts  of  water,  or  a  four-per-cent  solution  of  bromid 
of  potassium.  The  inhalations  should  be  used  two  or  three  times  a  day,  and 
last  about  five  minutes  each  time.  Direct  applications  to  the  larynx  are  much 
more  effective  than  inhalations,  but  these  can  be  employed  only  by  the  aid  of  a 
laryngeal  mirror.  Of  these  we  use,  first  of  all,  nitrate,  of  silver,  at  first  in  a 
weak  solution  (1  to  50)  ;  later  in  a  more  concentrated  form  (1  to  10,  or 
even  1  to  5).  These  applications  are  made  every  two  or  three  days.  Besides 
nitrate  of  silver,  the  larynx  may  also  be  painted  with  pure  tincture  of  iodin, 
or  with  iodin  and  glycerin  (iodin,  4  parts,  iodid  of  potassium,  6  parts,  and 
glycerin,  500  parts),  or  with  concentrated  solutions  of  alum  or  tannin.  (See 
formulas  in  the  Appendix.)  The  importance  of  local  treatment  must  not  be 
overestimated.  At  all  events,  too  prolonged  irritation  of  the  laryngeal  mucous 
membrane  should  be  avoided. 

Water  cures  are  also  often  prescribed  in  chronic  catarrh  of  the  larynx. 
These  are  of  advantage  from  the  avoidance  of  astiological  factors,  and  from 
the  good  air.  Empirically,  we  prescribe,  especially  for  "  full-blooded  "  j3a- 
tients,  the  cold  sulphur  springs,  such  as  Nenndorf,  Eilsen,  or  Weilbach,  or 
the  sulphate-of-sodium  waters,  such  as  Carlsbad  and  Marienbad,  while  we  send 
those  of  delicate  constitutions  to  Ems,  Salzbrunn,  Salzungen,  Beichenhall,  etc. 

The  treatment  of  laryngitis  hypertrophica,  when  it  leads  to  stenosis,  must 
be  mechanical.  Schrotter,  in  particular,  has  devised  several  methods  of  dilating 
the  stenosis  gradually  by  the  introduction  of  bougies  and  harder  dilators.  The 
details  of  this  treatment  are  to  be  found  in  the  newer  special  works. 


CHAPTEE    III 

LARYNGEAL    PERICHONDRITIS 

^Etiology  and  Pathological  Anatomy. — The  inflammation  of  the  perichon- 
drium of  the  laryngeal  cartilages  is  in  very  rare  cases  apparently  a  primary 
disease.     It  is  much  more  frequently  secondary  to  other  laryngeal  affections, 


176  DISEASES   OF   THE   RESPIRATORY   ORGANS 

especially  tuberculosis  and  syphilis  of  the  larynx.  Furthermore,  it  develops 
secondarily  in  severe  acute  diseases,  most  frequently  in  typhoid  fever,  more 
rarely  in  smallpox,  diphtheria,  etc.  Superficial  ulcerative  processes  in  the  mu- 
cous membrane  often  precede  the  perichondritis  in  these  cases,  and  the  par- 
ticipation of  the  perichondrium  in  the  inflammation  arises  from  their  gradual 
deepening.  Anatomically,  we  have  to  do,  as  a  rule,  with  a  purulent  inflam- 
mation, which  usually  leads  to  the  formation  of  circumscribed  abscesses.  Most 
laryngeal  abscesses  have  their  origin  in  the  perichondrium.1  The  perichon- 
drium is  in  part  destroyed  by  the  abscess  and  in  part  elevated  from  the  car- 
tilage. The  cartilage  then  becomes  necrotic,  breaks  in  pieces,  and  is  expelled 
in  small  particles  or  in  masses. 

Perichondritis  occurs  most  frequently  in  the  cricoid  and  arytenoid  carti- 
lages, much  more  rarely  on  the  internal  or  external  surface  of  the  thyroid 
cartilage.  Hence  we  distinguish  an  internal  and  an  external  perichondritis. 
A  perichondritis  of  the  epiglottis  has  also  been  repeatedly  observed. 

Symptomatology. — In  the  rare  cases  of  primary  perichondritis,  marked 
laryngeal  symptoms  are  speedily  developed  in  a  person  previously  healthy. 
These  symptoms  are  pain  and  tenderness  on  pressure  over  the  larynx,  hoarse- 
ness, and  cough;  and  to  them  are  usually  soon  added  the  signs  of  a  dangerous 
stenosis  of  the  larynx.  In  secondary  cases,  which  occur  almost  always  in 
patients  who  are  already  seriously  ill,  the  symptoms  of  stenosis  are  often  the 
first  to  point  to  a  severe  disease  of  the  larynx.  On  laryngoscopic  examination, 
besides  the  general  redness  and  swelling  in  particular  places,  we  can  sometimes 
recognize  a  circumscribed  prominence  of  the  mucous  membrane  caused  by  the 
abscess.  If  the  abscess  be  already  broken  we  can  see  the  abscess  cavity  and 
sometimes  the  cartilage  lying  free  within  it.  In  most  cases  we  find  a  consid- 
erable collateral  oedema  of  the  surrounding  mucous  membrane,  which  oedema 
frequently  has  a  greater  share  in  the  production  of  stenosis  than  has  the 
primary  affection  itself.  The  dreaded  oedema  of  the  glottis  (oedema  of  the 
ary-epiglottic  ligament)  in  typhoid,  tuberculosis  of  the  larynx,  etc.,  is  usually 
due  to  perichondritis  of  the  cricoid  or  arytaenoid  cartilages.  Finally,  we  can 
see  with  the  laryngoscope,  especially  in  perichondritis  arytaenoidea,  a  consid- 
erable disturbance  of  motion  of  the  affected  arytaenoid  cartilage,  and  also  of 
the  vocal  cords. 

Laryngeal  perichondritis  terminates  fatally  in  a  great  number  of  cases  from 
the  development  of  stenosis.  In  thyroid  perichondritis  the  pus  may  sometimes 
gravitate,  causing  a  severe  purulent  inflammation  of  the  mediastinum.  In 
other  cases  the  most  threatening  symptoms  may  be  averted  for  a  time,  but  the 
primary  disease,  such  as  tuberculosis,  finally  comes  to  an  unfavorable  termi- 
nation. In  the  rare  cases  in  which  recovery  occurs  after  primary  perichon- 
dritis or  after  the  termination  of  the  primary  disease,  such  as  typhoid,  this 
recovery  is  often  incomplete,  since  a  chronic  stenosis  of  the  larynx  remains 
from  the  ensuing  cicatricial  contractions. 

Diagnosis. — The  diagnosis  is  usually  obscure  during  the  first  period  of 
severe  symptoms  of  stenosis,  since  it  is  difficult  to  make  a  laryngoscopic  ex- 
amination, and  it  is  also  not  always  easy  to  determine  the  condition.     We 

i  True  submucous  abscesses,  the  so-called  phlegmonous  laryngitis,  occur  only  in  very  rare 
cases. 


(EDEMA   QI    THE   GLOT]  I-  177 

are  usually  justified,  however,  in  making  the  diagi 

which  we  have  mentioned,  in  which  we  know  bj  experience  that  a  perichon- 
dritis quite  frequently  occurs,  the  danger  of  suffocation  ai  -  addition 
to  the  other  laryngeal  symptoms.  Ii  i-  of  practical  importance  to  recognize 
stenosis  of  the  larynx  with  certainty,  for  it  demande  -  therapeutic 
interference. 

Treatment. — In  the  beginning  of  the  affection  we  may  try  to  reduce  the 
inflammation  by  the  internal  and  external  application  of  ice  or  by 
The  pain  may  be  alleviated  by  injections  of  morphin  or  painting  with  cocain. 
If  stenosis  of  the  larynx  occurs,  surgical  interference  is  usually  qi     --       .  for 
only  in  very  rare  cases  do  we  see  the  abscess  open  of  itself  with  a  snbsideni 
the  dangerous  symptoms.  In  the  majority  of  cases  the  patient  can  b    -  xom 

suffocation  only  by  the  timely  performance  of  tracheotomy  or  laryngotomy. 
The  laryngeal  abscess  has  been  repeatedly  opened  internally  by  laryng  _  -  - 
with  favorable  results.  If  a  chronic  stenosis  of  the  larynx  remains  after  a 
favorable  termination  of  the  disease,  either  the  patient  must  wear  a  tracheal 
cannula  all  his  life,  or  the  attempt  may  be  made  to  dilate  the  stenosis  gradually 
by  the  methods  referred  to  in  the  preceding  chapter. 


CHAPTER    IT 
(EDEMA    OF    THE    GLOTTIS 

The  practical  importance  of  the  subject  demands  a  brief  special  description 
of  oedema  of  the  glottis,  by  which  we  mean  oedema  of  the  entrance  of  the  lar- 
ynx, especially  of  the  ary-epiglottic  ligaments.  We  have  already  learned  to 
recognize  laryngeal  perichondritis  as  one  of  its  most  frequent  causes.  In  less 
deeply  seated  inflammations  in  the  larynx  and  its  neighborhood,  however, 
cedema  of  the  glottis  may  sometimes  develop  as  a  dangerous  complication, 
especially  in  cases  of  laryngitis  occurring  in  the  course  of  severe  acute  disea  -  - 
such  as  typhoid,  smallpox,  or  erysipelas,  or  in  inflammations  of  the  larynx 
arising  from  severe  mechanical  or  chemical  irritation,  as  from  hot  steam  or 
corrosive  substances,  or  from  wounds  of  the  larynx,  or,  finally,  from  foreign 
bodies  in  the  larynx.  The  collateral  cedema  in  angina  Ludovici,  in  intense 
inflammations  of  the  parotid  gland,  or  the  tonsils,  etc.,  may  in  rare  cases 
extend  to  the  ary-epiglottic  ligaments.  Finally,  cedema  of  the  glottis 
occurs  in  rare  cases  as  a  complication  of  general  cedema  of  the  body,  as 
a  result  of  Bright's  disease,  disease  of  the  heart,  emphysema  of  the  lungs, 
etc.  (Edema  of  the  glottis,  without  extensive  oedema  elsewhere,  has  been 
repeatedly  observed  to  come  on  quite  suddenly,  especially  in  acute  and  chronic- 
nephritis. 

The  chief  symptom  of  cedema  of  the  glottis  is  dyspnoea,  which  comes  on  as 
a  result  of  the  stenosis  of  the  entrance  of  the  larynx,  and  is  sometimes  ex- 
treme. At  first  this  is  chiefly  on  inspiration,  but  it  soon  comes  on  with 
expiration  also.  Respiration,  especially  inspiration,  is  accompanied  by  a  loud 
laryngeal  stridor.  As  a  result  of  the  incomplete  entrance  of  the  air,  the 
efforts  at  inspiration  cause  depression  of  the  root  of  the  neck,  the  epigastrium, 
12 


178  DISEASES  OF  THE  RESPIRATORY  ORGANS 

and  the  sides  of  the  thorax.  We  see  with  the  laryngoscope,  if  the  examination 
be  successful,  an  cedematous  swelling  of  the  ary-epiglottic  ligaments,  and  often 
a  swelling  of  the  epiglottis  and  the  false  vocal  cords.  Sometimes  we  succeed 
in  feeling  the  swollen  parts  with  the  finger. 

If  the  dyspnoea  reaches  a  degree  which  threatens  life,  an  operation  is  the 
only  thing  which  can  afford  relief.  Laryngologists  attempt  to  reduce  the 
swelling  by  long  incisions  in  the  cedematous  parts.  If  this  does  not  succeed, 
tracheotomy  must  be  performed.  If  the  immediate  danger  to  life  is  thus 
averted,  further  treatment  should  be  directed  to  the  disease  which  has  given 
rise  to.  the  cedema. 


CHAPTEE   V 

TUBERCULOSIS    OF    THE    LARYNX 

(Laryngeal  Phthisis.     Consumption  of  the  Larynx) 

etiology. — Since  tuberculosis  of  the  larynx  is  in  most  cases  combined 
with  tuberculosis  of  other  organs,  especially  of  the  lungs,  we  must  refer  to  the 
description  of  tuberculosis  of  the  lungs  for  the  general  Eetiology  and  pathology 
of  the  disease.  A  particular  description  of  the  special  appearances  in  lar- 
yngeal tuberculosis  is,  however,  justifiable,  because  tuberculosis  may  at  times 
begin  in  the  larynx  and  may  remain  isolated  there,  at  least  for  a  time;  and, 
furthermore,  in  many  cases  of  laryngeal  tuberculosis,  which  are  evidently  com- 
bined with  pulmonary  tuberculosis,  the  laryngeal  symptoms  are  predominant 
in  the  clinical  picture  of  the  disease.  Many  physicians  have,  wrongly  as  we 
think,  disputed  the  fact  that  tuberculosis  can  begin  in  the  larynx.  Clinical 
experience  not  infrequently  teaches  us  that  men,  who  have  been  apparently 
in  good  health,  are  attacked  with  hoarseness,  the  disease  being  at  first  thought 
to  be  a  common  laryngitis,  but  at  last,  by  its  course,  proving  to  be  tubercu- 
losis. In  spite  of  the  most  careful  examination,  there  are  not  to  be  found  at 
first  the  slightest  physical  signs  of  disease  in  the  lungs,  and  not  till  later  do 
the  manifest  signs  of  a  pulmonary  tuberculosis  succeed  the  symptoms  of  a 
laryngeal  affection.  In  such  cases  it  seems  to  us  an  affectation  to  claim  that 
there  is  a  primary  pulmonary  tuberculosis  which  could  not  be  made  out  at 
first.  Everything  is  much  more  in  favor  of  the  opinion  that  tubercle  bacilli 
may  sometimes,  if  not  frequently,  first  fix  upon  the  larynx,  excite  the  first 
symptoms  of  tuberculosis  there,  and  then  attack  the  lungs. 

In  the  great  majority  of  cases  of  laryngeal  tuberculosis  the  symptoms  are 
developed,  of  course,  secondarily  in  the  course  of  chronic  pulmonary  phthisis. 
We  shall  see  that  in  most  cases  the  disease  of  the  larynx  is  to  be  considered 
as  the  result  of  an  infection  of  the  mucous  membrane  of  the  larynx  by  the 
tuberculous  sputum  which  passes  over  it.  More  rarely  the  infectious  material 
seems  to  reach  the  larynx  by  way  of  the  lymph  or  blood  vessels.  In  favor 
of  this  theory  we  may  mention  that  men  of  great  experience  (Schrotter 
and  others)  have  stated  that,  when  the  laryngeal  trouble  was  particularly 
marked  on  one  side,  that  side  was  very  often  affected  which  corresponded 
to   the   affected   lung.      In    about   one    fourth    of    all   cases    of   pulmonary 


TUBERCULOSIS   OF   THE   LARYNX  179 

tuberculosis  this  complication  occurs,  if  we  include  all  the  mild  laryngeal 
cases.  Marked  and  extensive  tuberculosis  of  the  larynx  is  much  rarer, 
however. 

Pathological  Anatomy. — Tuberculosis  of  the  laryngeal  mucous  membrane 
begins,  like  tuberculosis  of  other  mucous  membranes,  with  the  formation  of 
small  subepithelial  nodules,  which  soon  become  cheesy,  break  down,  and  form 
small  ulcers.  In  the  further  course  of  the  disease  there  is  wit  often  a  more 
extensive  tubercular  infiltration,  which  gives  rise  on  the  one  hand  to  irregular 
thickening  of  the  mucous  membrane,  and  on  the  other  to  deep  ulceration.  Tin- 
tubercular  infiltration  is  most  frequently  situated  in  the  interarytasnoid  space, 
on  the  false  or  true  cords  (at  first  on  one  side),  and  on  the  epiglottis.  The 
tuberculous  ulceration  usually  develops  later  in  one  of  these  places.  The  ulcer- 
ation may  extend  from  the  epiglottis  to  the  neighboring  parts  of  the  tongue. 
In  severe  cases  we  often  find  a  marked  collateral  cedema  in  the  surrounding 
parts  accompanying  the  inflammation,  and  sometimes  the  tubercular  peri- 
chondritis which  has  already  been  described. 

The  rest  of  the  laryngeal  mucous  membrane  (especially  the  vocal  cords) 
not  involved  in  the  specific  tubercular  process  is  usually  the  seat  of  a  simple 
catarrh. 

Clinical  Symptoms. — In  the  beginning  of  tuberculosis  of  the  larynx  the 
laryngoscope  usually  shows  nothing  but  the  appearances  of  a  simple  ca- 
tarrh, since  the  primary  miliary  nodules  of  tuberculosis  are  usually  hard 
to  make  out.  If  the  catarrhal  symptoms  be  only  on  one  side,  we  should 
always  suspect  tuberculosis.  In  the  later  stages,  however,  most  of  the  special 
details  of  the  destructive  tubercular  process,  described  above  (ulcers,  in- 
filtration, etc.),  can  be  very  satisfactorily  made  out  with  the  laryngoscope. 
The  infiltration  and  ulcers  are  either  chiefly  on  one  or  on  both  vocal 
cords  or  on  the  posterior  wall  of  the  larynx,  or  mainly  in  the  neigh- 
borhood of  one  arytaenoid  cartilage,  or  the  whole  epiglottis  is  irregularly 
ulcerated  on  its  edge.  Single  tubercular  nodules 
are  often  plainly  to  be  seen.  In  severe  cases 
almost  the  whole  upper  portion  of  the  larynx 
appears  like  an  ulcerated  surface  covered  with 
mucus  and  pus.  In  laryngeal  tuberculosis, 
however,  the  soft  palate  usually  looks  very  pale 
and  anasmic.  The  redness  and  swelling  of  the 
affected  parts  are  more  distinct  in  the  living 
subject  than  in  the  cadaver;  but  the  autopsy 
often  shows  a  far  greater  extension  of  the  tu-  Fig.  31.— Beginning  laryngeal  tu- 
bercular disease  than  we  can  determine  by  the  berculosis  (from  Sahli)  . 
laryngoscope. 

The  other  clinical  symptoms  of  tuberculosis  of  the  larynx  vary  very  much 
with  the  extent  and  intensity  of  the  process.  Sometimes  they  consist  merely 
in  moderate  roughness  and  hoarseness  of  the  voice,  but  in  other  cases  they 
increase  to  the  most  painful  condition  which  is  ever  seen  in  any  variety  of 
tuberculosis.  This  is  especially  apt  to  be  the  case  if  the  ulceration  involves 
the  epiglottis  and  the  arytenoid  cartilages.  Swallowing  is  then  extremely 
painful,  so  that  the  nutrition  is  very  often  impaired,  and  painful  attacks  of 
coughing  frequently  occur.    A  practiced  ear  can  often  distinguish  at  once  the 


180  DISEASES   OF  THE   RESPIRATORY   ORGANS 

hoarse  sound  of  a  "  laryngeal  cough  "  from  the  ordinary  pulmonary  cough. 
If  severe  ulcerations  attack  the  vocal  cords-,  and  their  free  mobility  is  affected 
to  a  marked  degree,  the  hoarseness  increases,  and  finally  reaches  a  complete 
aphonia.  Death  finally  occurs  from  general  inanition,  or,  exceptionally,  from 
oedema  of  the  glottis. 

Diagnosis. — The  diagnosis  of  tuberculosis  of  the  larynx  is  not  difficult  if 
pulmonary  phthisis  is  already  known  to  be  present.  When  attention  has  been 
called  to  it  from  the  onset  of  hoarseness  or  from  some  disturbance  in  swallow- 
ing, we  recognize  the  character  and  seat  of  the  changes  by  the  aid  of  the 
laryngoscope.  The  diagnosis,  however,  may  present  much  difficulty  in  cases 
where  we  are  not  sure  that  an  affection  of  the  lungs  coexists.  As  has  been 
said,  the  symptoms  at  first  are  not  unlike  those  of  a  simple  catarrh,  and  the 
suspicion  of  the  existence  of  tuberculosis  is  first  aroused  from  the  stubborn- 
ness of  the  disease,  the  condition  of  the  patient,  the  knowledge  of  some  in- 
herited taint,  the  onset  of  fever,  and  the  remarkable  ansemia  and  emaciation. 
With  the  changes  in  the  larynx  which  have  been  described,  without  evidence 
of  pulmonary  tuberculosis,  the  distinction  between  tuberculosis  and  syphilis 
may  be  very  difficult.  In  syphilis  of  the  larynx,  however,  we  find  that  coexist- 
ing changes  in  the  pharynx  are  much  commoner  than  in  tuberculosis,  and  the 
cicatricial  formation  which  is  usually  visible  furnishes,  besides,  a  very  charac- 
teristic evidence  of  syphilis.  The  diagnosis  of  tuberculosis  of  the  larynx,  how- 
ever, is  made  perfectly  certain  in  all  doubtful  cases  by  the  discovery  of  tubercle 
bacilli  in  the  patient's  expectoration  or  in  the  secretion  from  the  ulcer,  which 
often  can  be  easily  obtained  by  the  aid  of  a  fine  laryngeal  brush.  In  regard 
to  the  laryngoscopic  appearances,  we  may  also  say  that  a  thickening  and 
infiltration  of  the  epiglottis  with  a  partial  ulceration  of  the  same  is  an  appear- 
ance  which  is  almost  exclusively  confined  to  tuberculosis.  The  same  is  true 
with  regard  to  a  marked  projecting  infiltration  of  the  interarytsenoid  region. 
In  doubtful  cases  it  may  aid  the  diagnosis  to  inject  tuberculin,  or,  on  the  other 
hand,  to  watch  the  results  of  antisyphilitic  treatment. 

Treatment. — For  the  constitutional  treatment  of  tuberculosis  of  the  larynx 
the  reader  is  referred  to  the  description  of  pulmonary  tuberculosis.  We  shall 
here  discuss  merely  the  local  tieatment.  This  is  in  the  milder  forms  the  same 
as  for  simple  laryngeal  catarrh.  There  is  no  doubt  that  even  genuine  tuber- 
culous ulceration  of  the  larynx  may  be  healed.  Nevertheless,  permanent  cures 
of  this  sort  are  exceptional.  Of  course  very  much  depends  upon  the  coexisting 
state  of  the  lungs.  For  local  treatment  insufflations  of  iodoform  and  iodol  were 
for  a  time  strongly  recommended,  but  they  are  now  for  the  most  part  aban- 
doned. Cauterizing  the  tuberculous  ulcers  with  nitrate  of  silver  does  more 
harm  than  good.  We  sometimes  see  better  results  from  blowing  powdered 
boric  acid  on  the  ulcers  or  from  a  twenty-per-cent  solution  of  menthol  in  oil. 
At  present  lactic  acid  is  most  recommended — cauterizing  the  ulcers  with  a 
solution  of  increasing  strength  (twenty  to  eighty  per  cent),  at  first  daily,  and 
later,  after  the  ulcers  have  been  cleaned  off,  less  frequently.  Preliminary 
cocainization  of  the  parts  to  be  cauterized  is  always  necessary.  Ulcers  pre- 
senting exuberant  granulations  should  be  scraped  with  specially  constructed 
spoons  and  curettes. 

If  we  were  to  give  a  general  estimate  of  the  local  treatment  of  laryngeal 
tuberculosis  we  should  have  to  admit  that  its  success  has  not  been  great.     We 


TUBERCULOSIS   OF   THE    LARYNX  181 

do  not  deny  that  skill  and  perseverance  may  be  of  much  service,  bul  only  too 
often  do  we  become  discouraged  by  the  failure  of  the  mosl  careful  local  treat- 
ment, and  in  many  cases  cauterization  of  the  larynx  is  only  a  useless  di 
to  the  patient. 

Witli  incipient  disease  there  may  he  considerable  improvemenl  and  even 
recovery  without  any  local  treatment  if  the  larynx  be  spared  any  exertion  and 
given  complete  rest  and  if,  at  the  same  time,  careful  general  treatmenl  be 
instituted.  The  most  we  need  to  use  is  the  atomizer  or  nebulizer  with  simple 
salt  solution,  alkaline  waters,  etc.  We  have  also  found  inhalations  of  a  weak 
carbolic  solution,  and  especially  of  vapor  of  Peruvian  balsam  (bals.  Peruviani, 
oijss.  [gm.  10]  ;  spiritus  vini,  3j  T1\xv  [gm.  5],  20  drops  in  hot  water,  to 
be  inhaled  through  a  funnel  three  times  daily)  of  service.  In  advanced  cases, 
where  pronounced  pulmonary  tuberculosis  coexists,  we  must  content  ourselves 
with  a  purely  palliative  treatment.  The  constant  use  of  cracked  ice,  and  espe- 
cially a  lavish  employment  of  narcotics,  are  of  most  service  in  relieving  the  pain 
and  the  difficulty  in  swallowing.  Subcutaneous  injections  of  morphin  a  quar- 
ter of  an  hour  before  a  meal  often  afford  great  relief.  We  have  seen  ver}r  good 
results  from  cocain.  If  we  paint  the  ulcerated  mucous  membrane  at  the 
entrance  of  the  larynx  with  a  ten-  or  twenty-per-cent  solution  of  cocain,  in  a 
few  minutes  such  an  anaesthesia  of  the  affected  parts  ensues  that  swallowing 
may  take  place  without  any  pain.     The  following  formula  may  be  used : 

I>   Cocainas  muriatis    gr.  xv-xxx,  gm.  1.0-2.0 ; 

Alcohol '.f oss.,  2.0  c.c. ; 

Aquae  destillatae 5ij,  8.0  c.c. 

M. 

Unfortunately  the  action  of  cocain  is  very  transitory,  so  that  the  painting 
must  be  frequently  repeated.  Insufflations  of  orthoform  or  of  morphin  in 
powdered  form  (gr.  -J  [gm.  0.01],  morphin  with  gr.  iijss.  [gm.  0.2],  pulv. 
gummosus  1)  are  worthy  of  trial.  With  a  severe  laryngeal  cough  and  irritation 
relief  may  also  be  obtained  by  inhalations  of  a  two-  to  three-per-cent  solution 
of  bromid  of  potassium  or  a  three-  to  ten-per-cent  solution  of  bitter-almond 
water. 

If  a  pronounced  stenosis  of  the  larynx  develop,  tracheotomy  is  indicated. 
Many  recent  observations  seem  to  show  that  tracheotomy  may  also  be  of  service 
in  marked  laryngeal  tuberculosis.  When  the  laryngeal  respiration  is  shut  off 
the  tubercular  lesions  seem  to  improve  faster. 

In  cases  of  pronounced  but  comparatively  limited  laryngeal  tuberculosis, 
without  much  implication  of  the  lungs,  the  attempt  has  been  made,  after  a 
preliminary  laryngotomy,  to  remove  the  diseased  parts  as  completely  as 
possible  by  surgical  means.  We  still  lack  extended  practical  experience 
in  this  matter,  but  further  trials  of  the  operation  seem  to  me  to  be  very 
desirable. 

1  P.  G.  Gumacacia  15  parts,  licorice  root  10,  sugar  5. 


182  DISEASES   OF  THE   RESPIRATORY   ORGANS 

CHAPTEE   VI 

PARALYSES  OF  THE  LARYNGEAL  MUSCLES 

PARALYSES    IN    THE    DISTRIBUTION    OF    THE    SUPERIOR 
LARYNGEAL    NERVE 

The  superior  laryngeal  nerve,  arising  from  the  vagus,  is  the  sensory 
nerve  for  the  mucous  membrane  of  the  upper  portion  of  the  larynx  down  to 
the  glottis,  and  also  for  the  mucous  membrane  of  the  epiglottis  and  its  neigh- 
borhood. Besides  this,  it  also  supplies  motor  fibers  to  the  cricothyroid  mus- 
cle, probably  from  the  accessory  nerve.  Clinical  experience  renders  it  prob- 
able that  the  superior  laryngeal  nerve  also  supplies  the  depressors  of  the 
epiglottis,  the  thyro-epiglottideus,  and  the  arytaeno-epiglottidei  muscles,  and 
perhaps  also  the  arytaenoideus  muscle.  The  last  three  muscles  mentioned, 
however,  perhaps  derive  some  motor  fibers  from  the  recurrent  nerve  also  (the 
inferior  laryngeal  nerve). 

Paralysis  of  the  cricothyroid  muscles  and  of  the  depressors  of  the  epi- 
glottis is  seen  most  frequently  after  recovery  from  diphtheria.  It  is  usually 
a  part  of  a  more  extensive  paralysis,  and,  in  addition,  is  sometimes  associated 
with  anaesthesia  of  those  portions  of  the  mucous  membrane  which,  as  we  have 
seen,  derive  their  sensory  fibers  from  the  superior  laryngeal  nerve  (von 
Ziemssen).  Choking  is  therefore  easy  and  there  is  danger  of  inhalation 
pneumonia. 

Paralysis  of  the  thyro-epiglottideus  and  the  arytamo-epiglottidei  muscles 
is  recognized  by  the  immobility  and  the  erect  position  of  the  epiglottis,  which 
is  directed  toward  the  back  of  the  tongue. 

Paralysis  of  the  cricothyroid  muscles  makes  the  voice  rough,  and  espe- 
cially renders  the  production  of  high  tones  impossible,  since  for  this  purpose 
we  need  the  action  of  this  muscle  as  a  tensor  of  the  vocal  cords  by  approxi- 
mating the  cricoid  and  thyroid  cartilages.  The  detection  of  this  paralysis  by 
the  laryngoscope  is  extremely  difficult.  Its  chief  signs  are  a  concavity  of  the 
edges  of  the  vocal  cords,  a  lack  of  visible  vibration  in  them,  and  perhaps, 
in  unilateral  paralysis,  a  higher  position  of  the  vocal  cord  on  the  sound  side. 

For  paralysis  of  the  arytaenoideus  muscle,  vide  infra. 

PARALYSES    IN    THE    DISTRIBUTION     OF    THE    INFERIOR 
LARYNGEAL   OR    RECURRENT    NERVE 

The  recurrent  nerve  supplies  with  sensory  fibers  the  mucous  membrane 
of  the  inferior  cavity  of  the  larynx  below  the  glottis,  and  it  is  the  motor 
nerve  for  all  the  laryngeal  muscles  except  the  cricothyroid,  and  except  pos- 
sibly the  depressors  of  the  epiglottis  {vide  supra).  The  muscles  innervated 
by  it  are  arranged  according  to  their  function  in  the  three  following 
groups : 

a.  The  openers  of  the  glottis — the  posterior  crico-arytaenoid  muscles. 

b.  The  closers  of  the  glottis — the  lateral  crico-arytasnoids  and  the  arytae- 
noideus  (transverse  and  oblique). 


PARALYSES  OF  THE  LARYNGEAL  MUSCLES  L83 

c.  The  tensors  of  the  vocal  cords — the  thyro-arytamoids,  which  aci  usually 

as  closers  of  the  glottis,  hut  which  very  often  produce  the  line  differences  in 
tension  in  the  vocal  cords  which  are  necessary  in  singing  and  in  modulations 
of  speech.  They  accordingly  have  the  same  task  a.-  the  coarser-working  crico- 
thyroid muscles,  which  are  innervated  by  the  superior  laryngeal  nerve. 

The  motor  libers  for  all  these  muscles  have  their  special  origin  in  the 
accessory  nerve,  from  which  they  pass  into  the  trunk  of  the  vagus,  and  from 
this  into  the  laryngeal  nerves. 

Most  of  the  paralyses  of  the  recurrent  nerve  are  of  peripheral  origin. 
Except  in  the  pure  muscular  pareses  (vide  supra),  which  arise  not  infre- 
quently in  the  course  of  other  laryngeal  affections,  peripheral  paralyses  of  the 
vocal  cords  occur  with  the  greatest  relative  frequency  from  an  abnormal  pres- 
sure on  the  trunk  of  the  recurrent  nerve,  especially  in  aneurism  of  the  arch 
of  the  aorta,  which  may  cause  a  left-sided  paralysis.  Tumors  of  the  bronchial 
glands,  cancer  of  the  oesophagus,  thyroid  or  mediastinal  tumors,  and,  in  rare 
cases,  even  large  pericardial  effusions,  may  also  cause  a  paralysis  of  the 
recurrent  on  one  side.  Paralyses  on  the  right  side  are  seen  quite  frequently 
in  contractions  at  the  apex  of  the  right  lung  and  in  rare  cases  of  aneurism 
of  the  subclavian  artery.  The  paralyses  of  the  laryngeal  muscles,  which  are 
sometimes  met  with  after  recovery  from  diphtheria  (q.  v.),  also  belong  to  the 
peripheral  paralyses  of  the  recurrent  nerve,  and  their  cause  is  to  be  found 
in  a  degeneration  of  the  branches  of  the  affected  nerves.  In  other  cases  the 
paralysis  of  the  recurrent  nerve  is  due  to  an  affection  of  its  fibers  in  the  vagus 
or  even  in  the  accessorius.  Excluding  certain  injuries  from  operations,  these 
affections  are  usually  due  to  new  growths  which  cause  a  paralysis  of  con- 
duction. Paralyses  of  the  recurrent  nerve  also  arise  from  affections  of  the 
nucleus  of  the  accessory  nerve  in  diseases  of  the  medulla,  in  the  different 
forms  of  acute  bulbar  paralysis,  in  chronic  bulbar  paralysis,  in  multiple  scle- 
rosis, etc.  The  frequent  hysterical  paralyses  affecting  the  closers  of  the  glottis 
and  the  tensors  of  the  vocal  cords  are  to  be  regarded  as  central  disturbances  of 
innervation  (see  the  chapter  on  hysteria). 

1.  Complete  Paralysis  of  the  Recurrent  Nerve.— Paralysis  of  all  the  laryn- 
geal muscles  supplied  by  the  recurrent  nerve  occurs  quite  frequently  in  the 
pressure  paralysis  of  the  trunk  of  the  recurrent, 
or  of  its  fibers  in  the  vagus.  With  the  laryngo- 
scope (see  Fig.  32)  we  find  the  vocal  cord  on 
the  paralyzed  side  in  a  middle  position,  often 
falsely  called  a  "  cadaveric  position,"  and  com- 
pletely motionless  on  respiration,  and  also  on 
phonation.  The  arytenoid  cartilage  on  the 
paralyzed,  side  is  often  turned  inward.  On 
phonation   as    strongly    as    possible,    the    vocal     Fig.  32.— (From  Ziemssen.)    Po- 

COrd     On     the     sound     side     passes     beyond     the  sition  on  inspiration  in  paralysis 

n.        ..  ,..  .  ,  ,.,  i  of  the  left  vocal  cord,  or  paraly- 

median  line,  the  arytenoid  cartilage  also  crosses  sis  of  conduction  in  the  recur- 

the  line,   and   consequently  the  glottis   is   put          rent  nerve. 

into  an  oblique  position.     The  other  symptoms 

are  sometimes  so  slight  that  without  a  laryngoscopic  examination  we  do  not 

even  think  of  a  paralysis.     The  voice,  however,  is  usually  not  pure;  it  often 

breaks  into  a  falsetto,  and  the  patient  is  easily  tired  by  speaking.     With 


184 


DISEASES   OF  THE   RESPIRATORY   ORGANS 


complete  bilateral  paralysis  of  the  recurrent  nerve,  which  is  very  rare,  we 
find  both  vocal  cords  motionless  in  a  middle  position.  Complete  aphonia 
exists,  and  it  is  impossible  to  cough,  since  in  coughing  we  have  to  make  at 
first  a  complete  closure  of  the  glottis.  There  is  no  dyspnoea,  however,  if  the 
patient  keeps  quiet. 

It  is  an  interesting  fact,  first  reported  by  Eosenbach,  that  in  incomplete 
recurrent  paralysis  almost  invariably  the  abductors  of  the  vocal  cords  (the 
openers  of  the  glottis)  are  alone  paralyzed,  whence  the  cords  remain  in 
adduction.  Only  with  the  further  advance  of  the  disease  does  complete 
recurrent  paralysis  occur;  then  the  adductors  also  become  paralyzed,  and  the 
vocal  cords  become  completely  motionless,  and  assume  the  middle,  so-called 
cadaveric  position. 

2.  Paralysis  of  the  Dilators  of  the  Glottis,  the  Posterior  Crico-arytsenoid 
Muscles. — Bilateral  paralysis  of  these  muscles  is  quite  a  rare  phenomenon, 
but  clinically  it  is  of  the  utmost  importance,  since  it  results  in  a  condition  of 
most  marked  inspiratory  dyspnoea.  Neuritic  changes,  central  diseases  (tabes, 
multiple  sclerosis,  etc.),  cancer  of  the  oesophagus,  etc.,  may  lead  to  paralysis 
of  the  posterior  muscles.  In  many  cases  the  cause  is  obscure.  The  sequela? 
of  the  paralysis  usually  develop  slowly  and  gradually.  The  affection  may  last 
for  years.  The  greatest  impairment  of  breathing  probably  occurs  when  the 
vocal  cords  are  fixed  in  adduction  by  the  contracture  of  the  antagonistic  closers 
of  the  glottis.  The  dyspnoea  may  increase,  especially  from  external  causes,  to 
severe  attacks  of  suffocation,  and  tracheotomy  is  frequently  necessary.  The 
respiration  is  affected  in  such  a  way  that  inspiration  only  is  difficult,  pro- 
tracted, and  noisy,  while  expiration  is  free  and  unhindered.  This  depends  on 
a  valvelike  action  of  the  vocal  cords.  They  are  drawn  together  by  the  dilata- 
tion of  the  thorax  on  inspiration,  while  the  current  of  air  in  expiration  easily 
pushes  them  aside.  Phonation  is  usually  entirely  undisturbed.  With  the  la- 
ryngoscope (see  Fig.  33)  we  find  the  glottis  changed  to  a  small  slit,  which 
grows  narrower  instead  of  wider  on  inspiration.  The  prognosis  is  usually 
unfavorable.  Only  in  the  hysterical  can  these  apparently  severe  conditions 
appear  and  disappear  again  in  a  short  time. 

In  unilateral  paralysis  of  the  posterior  crico-arytsenoid  muscle  there  is,  as 
a  rule,  no  marked  dyspnoea.  The  voice  is  somewhat  hoarse,  and  with  the 
laryngoscope  we  can  see  that  the  paralyzed  vocal  cord  does  not  deviate  outward 
on  inspiration. 


Fig.  33. — (From  Ziemssen.)  Complete  bilat- 
eral paralysis  of  the  posticus  at  the  moment 
of  inspiration. 


Fig.  34. — (From  Ziemssen.)  Paralysis  of  both 
internal  thyro-arytamoid  muscles  in  the 
course  of  an  acute  laryngitis. 


3.  Paralysis    of    the    Thyro-arytaenoid    Muscles. — The    paralysis    or   pare- 
sis of  these  muscles,  which  run  into  the  vocal  cords,  and  which  are  their 


PARALYSES  OF  THE  LARYNGEAL  MUSCLES  185 

chief  tensors,  is  one  of  the  most  frequent  of  the  paralyses  of  the  Laryngeal 
muscles.  It  occurs  especially  in  acute  and  chronic  catarrh  of  the  laryngeal 
mucous  membrane,  and  is  often  the  chief  cause  of  the  accompanying  hoai 

ness.  It  also  frequently  develops  as  the  result  of  an  habitual  strain  of  the 
voice  in  singers  and  public  speakers,  and  it  is  one  of  the  commonest  causes  of 
hysterical  aphonia. 

Paralysis  of  the  thyro-arytaenoid  muscles  may  be  bilateral  or  unilateral. 
It  is  frequently  associated  with  a  paresis  of  the  other  closers  of  the  glottis,  the 
arytaenoidei  and  the  cricothyroid  muscles.  With  the  laryngoscope  (see  Fig. 
34),  in  the  ordinary  bilateral  paresis  of  the  thyro-arytaenoid  muscles,  we  see 
that  on  phonation  the  glottis  does  not  close  completely,  but  that  an  oval  space 
is  left  between  the  vocal  cords. 

In  unilateral  paralysis  the  affected  cord  shows  a  concavity  of  its  edge. 
The  voice  is  always  more  or  less  hoarse  and  weak,  and  the  speech  is  strained. 

In  many  cases,  after  a  cure  of  the  original  catarrh,  a  complete  recovery 
from  the  paralysis  may  follow  by  taking  good  care  of  the  voice.  Hysterical 
paralyses  are  diagnosticated  by  their  sudden  disappearance  and  reappearance, 
usually  after  some  psychical  disturbance.  They  are  quite  common  in  children 
of  the  age  of  ten  to  fourteen  years,  especially  in  girls.  (See  chapter  on 
Hysteria. ) 

4.  Paralysis  of  the  Arytsenoideus  Muscle. — Paralysis  of  this  muscle  is 
rarely  an  isolated  phenomenon.  It  is  sometimes  seen  in  laryngeal  catarrh  or 
in  hysterical  aphonia.  The  voice  is  quite  hoarse,  and  with  the  laryngoscope 
(see  Fig.  35)  we  find  on  phonation  that  the  whole  anterior  part  of  the  vocal 


Fig.  35. — (From  Ziemssen.)     Paralysis  of  the       Fig.  36. — (From  Ziemssen.)     Bilateral  paraly- 
arytsenoideus  in  acute  laryngitis.  sis  of  the  thyro-arytsenoids  combined  with 

paresis  of  the  arytaenoideus. 

cords  closes  well,  but  that  the  cartilaginous  glottis  remains  open  as  a  triangu- 
lar gap  on  account  of  the  imperfect  motion  of  the  arytamoid  cartilages 
toward  each  other.  When  the  thyro-arytaenoids  are  paralyzed  with  the  arytae- 
noideus, the  glottis  shows  on  phonation  a  narrow  hour-glass  opening  (see 
Fig.  36).  Both  the  anterior  and  the  posterior  portions  of  the  glottis  fail  to 
close,  while  the  vocal  processes  take  their  usual  median  position  on  phonation 
from  the  normal  turning  of  the  arytaenoid  cartilages  inward  by  the  action 
of  the  lateral  crico-arytaenoid  muscles. 

5.  Paralysis  of  the  Lateral  Crico-arytasnoid  Muscles. — As  an  uncomplicated 
condition,  paralysis  of  these  muscles  has  never  been  observed  with  certainty. 
Some  cases  of  a  complete  and  simultaneous'  paralysis  of  all  the  closers  of  the 
glottis  have  been  described,  however,  in  which  the  vocal  cords  are  immovable 
laterally  and  the  glottis  remains  abnormally  wide  open. 


186  DISEASES   OF  THE   RESPIRATORY   ORGANS 

TREATMENT 

We  may  expect  success  from  the  treatment  of  paralysis  of  the  vocal  cords 
only  when  the  primary  disease  is  capable  of  cure.  If  catarrhal  or  other  dis- 
eases of  the  larynx  coexist,  we  must  first  treat  these  by  the  methods  already 
mentioned.  Paralysis  from  the  compression  of  tumors,  etc.,  may  be  relieved 
in  rare  cases  by  extirpation,  or  by  partial  resolution  of  the  tumors  when  of 
strumous  origin.  In  catarrhal,  diphtheritic,  and  the  so-called  "  rheumatic  " 
pareses — that  is,  those  which  occur  without  any  assignable  cause — and  also  in 
all  hysterical  aphonias,  electricity  often  works  very  well.  Von  Ziemssen  has 
made  electrodes  for  the  endolaryngeal  stimulation  of  single  muscles,  but 
external  galvanization  is  usually  sufficient  in  practice.  In  hysterical  aphonia 
the  chief  task  is  to  accustom  the  patient  again  to  the  necessary  and  proper 
voluntary  innervation.  We  usually  accomplish  our  purpose  most  rapidly  by 
commanding  the  patient  to  cough  and  then  say  "  Ah,"  while  we  faradize  or 
galvanize  the  neck.  It  is  often  of  advantage  to  reverse  the  current.  If  the 
patient  succeeds  in  saying  "  Ah  "  once,  the  voice  usually  returns  very  quickly. 
Internally  we  may  try  subcutaneous  injections  of  strychnin  in  doses  of  gr. 
^o  to  gr.  i-  daily  (gm.  0.003  to  0.01). 


CHAPTEE    VII 

SPASM    OF    THE    GLOTTIS 

"  (Laryngismus  Stridulus.     Millar's  Asthma.     Thymic  Asthma) 

JEtiology. — Spasm  of  the  glottis  is  a  disease  which  occurs  almost  exclu- 
sively in  children  under  three  years  of  age,  and  consists  of  attacks  of  spas- 
modic closure  of  the  glottis,  and  consequently  of  most  severe  dyspnoea.  Boys 
are  more  frequently  attacked  by  this  disease  than  girls,  but  the  cause  of  this 
is  wholly  unknown.  The  old  name  of  thymic  asthma  arose  from  the  idea 
that  the  attacks  were  due  to  an  increase  in  the  size  of  the  thymus  gland,  but 
this  opinion  is  wholly  unfounded.  The  relation  between  spasm  of  the  glottis 
and  rachitis  is  remarkable,  but  it  is  unexplained.  Nearly  two  thirds  of  all 
the  children  who  suffer  from  spasm  of  the  glottis  are  rachitic,  but  the  opinion 
which  was  once  held  that  spasm  of  the  glottis  has  a  special  relation  to  the 
rachitic  craniotabes  is  not  clearly  proved.  The  fact  that  it  is  often  combined 
with  eclampsia,  in  that  the  attacks  of  spasm  of  the  glottis  are  aggravated  by 
eclamptic  attacks,  and  that  the  two  alternate  with  each  other,  is  an  argument 
in  favor  of  a  central  origin  for  the  disease.  In  the  cases  which  come  on,  as 
they  often  do,  at  the  time  of  dentition,  we  think  it  possible  to  assume  a  reflex 
origin  for  the  spasm,  just  as  we  may  in  those  cases  which  seem  to  follow  a 
laryngitis  due  to  taking  cold. 

Symptomatology. — The  single  attacks  usually  come  on  suddenly  by  day 
or  by  night,  either  without  any  cause  or  from  some  external  influence,  such 
as  crying,  swallowing  fluid,  or  some  psychical  disturbance.  They  usually 
begin  with  a  deep  inspiration,  followed  by  complete  cessation  of  respiration. 
The  child  becomes  pale,  cyanotic,  looks  anxiously  about,  rolls  his  eyes,  and 


NEW  GROWTHS   IN   THE   LARYNX  187 

makes  strained  and  labored  efforts  a1  respiration.  En  severe  cases  there  is  a 
temporary  loss  of  consciousness,  and  tonic  and  clonic  spasms  in  the  mus< 
of  the  extremities  and  the  trunk,  as  has  been  mentioned.  The  attack  lasts 
from  sonic  seconds  up  to  two  minutes.  In  very  severe  cases  the  attack  may 
be  immediately  fatal.  As  a  rule,  however,  the  spasm  passes  off,  deep,  noisy 
inspirations  follow,  and  in  a  short  time  the  child  is  completely  well.  The 
severity  of  the  attacks  varies,  moreover,  in  different  cases,  and  it  varies  very 
markedly,  too,  in  the  same  child.  Sometimes  we  have  only  one  attack  or  a 
small  number  of  them,  while  in  other  children  they  may  come  on  ten  or 
twenty  times  a  day,  and  even  oftener,  and  may  last  with  varying  intensity 
for  months.  If  the  child  reaches  his  third  year  the  disease  almost  alu 
disappears,  but  quite  a  large  number  of  the  children  who  suffer  from  spasm, 
of  the  glottis  die  before  that  age,  either  in  the  attack  itself  or  from  other 
affections. 

Genuine  spasm  of  the  glottis  hardly  ever  occurs  in  adults,  but  similar 
attacks,  which,  of  course,  have  quite  a  different  significance,  are  sometimes 
observed  in  hysteria. 

Treatment. — The  treatment  must  be  especially  directed  to  the  child's 
general  condition.  The  child  is  usually  pale  and  emaciated,  and  if  we  suc- 
ceed in  improving  its  nutrition  with  iron  and  cod-liver  oil,  the  attacks  become 
less  frequent,  and  milder,  and  finally  may  wholly  disappear.  If  rachitis  exists, 
we  should  first  of  all  try  phosphorus  (1  part  in  10,000  of  cod-liver  oil).  The 
child  should  also  be  kept  in  moderately  warm  air  and  guarded  from  any  ex- 
posure to  cold.  Internal  remedies  to  prevent  the  recurrence  of  the  attacks 
are  very  uncertain  in  their  action.  We  may  employ  1  or  2  gr.  (gm.  0.05  to 
0.10)  of  chloral  hydrate  in  solution  every  hour  or  so;  bromid  of  potassium, 
10  to  30  gr.  daily  (gm.  0.5  to  2.0)  ;  extract  of  belladonna,  etc. 

In  the  attack  itself  the  child  must  be  raised  up.  The  face  should  be 
sprinkled  with  water,  or,  if  the  attack  be  of  long  duration,  a  cool  shower  bath 
should  be  given.  Friction  should  be  applied  to  the  skin,  aided  by  mustard, 
or  a  mustard  plaster  applied  to  the  chest  and  calves.  If  the  attacks  are  very 
frequent  and  intense,  we  must  use  narcotics,  either  inhalations  of  chloroform 
or  subcutaneous  injections  of  morphin,  with  care,  in  doses,  for  a  child,  of 
eV  to  TV  of  a  gr.  (gm.  0.001  to  0.005). 


CHAPTER   VIII 

NEW    GROWTHS    IN    THE    LARYNX 

Since  new  growths  in  the  larynx  are  of  interest  mainly  to  specialists  and 
surgeons,  we  will  here  glance  but  briefly  at  them.  We  must  remember  espe- 
cially, however,  that  they  can  be  recognized  only  by  the  aid  of  the  laryngo- 
scope. It  unfortunately  often  happens  that  a  patient  is  treated  for  a  long 
time  without  success  for  a  "  chronic  laryngeal  catarrh,"  when  the  laryngo- 
scope finally  shows  that  a  new  growth  is  the  cause  of  the  hoarseness.  It  is  of 
especial  importance,  however,  to  make  a  diagnosis  as  early  as  possible,  par- 
ticularly in  carcinoma,  since  the  earlier  the  operation  is  done  the  better  is 
the  chance  for  success  (vide  infra). 


188 


DISEASES  OF   THE   RESPIRATORY   ORGANS 


A.     BENIGNANT   GROWTHS   IN   THE   LARYNX 

1.  Papilloma. — Papilloma  is  one  of  the  commonest  new  growths  in  the 
larynx.  It  forms  glandular,  cauliflower-like  excrescences,  which  are  usually 
situated  on  the  anterior  part  of  the  vocal  cords,  rarely  on  the  false  cords. 
The  base  of  the  swelling  is  broad  or  pediculated.  The  growths  are  often 
multiple.  We  do  not  know  the  special  cause  of  their  origin.  It  is  worthy  of 
note  that  papilloma,  like  other  benignant  growths  in  the  larynx,  is  seen  much 
more  frequently  in  men  than  in  women. 

2.  Fibroma. — Fibroma  in  the  larynx  is  comparatively  common.  The 
pediculated  tumors  known  as  "  laryngeal  polypi "  are  usually  fibromata. 
They  are  generally  situated  on  the  vocal  cords  and  form  whitish  or  reddish- 


Fig.  37.  Fig.  38. 

Figs.  37  and  38. — (From  Ziemssen.)     Pediculated  fibromata. 

brown  swellings,  from  the  size  of  a  pea  to  that  of  a  cherry,  vascular  and 
dense  or  soft  (see  Figs.  37  and  38).  There  is  no  evidence  that  persons 
who  use  their  voices  very  much  are  especially  liable  to  the  formation  of 
fibromata. 

3.  Cysts  and  Polypi. — Cysts  and  "  mucous  polypi  "  rarely  occur.  They  are 
probably  due  to  the  retention  of  the  secretion  in  a  mucous  gland  from  the 
stoppage  of  its  orifice.  We  find  them  in  the  ventricles  of  Morgagni,  on  the 
epiglottis,  etc.  In  a  very  few  cases  we  also  sec  in  the  larynx  lipomata, 
myxomata,  separated  portions  of  thyroid-gland  tissue  which  have  begun  to 
grow,   enchondromata,   etc. 

The  symptoms  which  are  excited  by  benignant  tumors  in  the  larynx  de- 
pend partly  upon  the  situation  and  partly  upon  the  size  of  the  new  growth. 
Small  polypi  may  exist  wholly  without  symptoms,  and  they  are  found  only  by 
chance  on  laryngoscopic  investigation.  Usually,  however,  the  presence  of 
disturbances  of  phonation  (hoarseness,  a  marked  change  in  pitch,  secondary 
tones),  persistent  cough,  or  respiratory  disturbances  when  the  tumor  is  a 
large  one,  are  the  symptoms  which  give  occasion  for  an  examination.  Abnor- 
mal sensations  in  the  larynx  are  by  no  means  the  rule,  and  pain  is  wholly 
absent. 


B.    MALIGNANT   GROWTHS.     CARCINOMA   OF  THE   LARYNX 

Sarcomata,  arising  from  the  true  or  false  vocal  cords,  are  very  rare.  The 
only  malignant  new  growth  of  the  larynx  of  great  practical  importance  is 
carcinoma. 

Carcinomata    develop    usually    in    old    people,    either    primarily    in    the 


NEW   GROWTHS   IN   THE   LARYNX  IS'.) 

Larynx  or  secondarily  from  affection  of  the  neighboring  organs.  In  the  lir-t 
case  the  vocal  cords  or  the  ventricles  of  Morgagni  are  the  points  mosl 
frequently  attacked.  An  extension  of  the  disease  to  the  larynx  is  seen 
especially  in  cancer  of  the  tongue  or  pharynx,  rarely  in  cancer  of  the 
oesophagus. 

The  symptoms  of  cancer  of  the  larynx  develop  slowly.  Hoarseness,  dys- 
phagia, pains  in  the  larynx  often  shooting  up  into  one  ear  or  the  temporal 
region,  the  appearance  of  respiratory  symptoms,  and  finally,  but  only  in  the 
later  stages,  as  a  rule,  the  signs  of  general  weakness  and  emaciation  which  are 
seen  in  almost  all  forms  of  carcinoma,  form  the  picture  of  the  disease.  En- 
largement of  the  cervical  lymph-glands  is  sometimes  an  early  symptom,  but  it 
may  he  wholly  lacking.  The  diagnosis  is  possible  only  by  the  aid  of  the 
laryngoscope.  Besides  this,  a  digital  examination  may  at  times  be  of  diag- 
nostic value  by  the  detection  of  the  characteristic  hardness  about  the  entrance 
or  in  the  neighborhood  of  the  larynx.  A  general  description  of  the  laryngo- 
scopy appearances  cannot  be  given  on  account  of  the  diverse  character  of  the 
cases.  We  see  the  uneven,  injected  new  growth,  covered  with  mucus  and  often 
ulcerated,  and  besides  this  at  times  the  secondary  appearances  of  catarrh, 
a  developing  perichondritis,  etc.  In  many  instances  the  diagnosis  is  quite 
easy,  but  in  other  cases  protracted  observation  is  required.  It  may  be  diffi- 
cult, however,  at  times,  to  distinguish  it  from  tuberculosis  or  from  syphilis. 
We  may  be  aided  in  such  cases  by  a  search  for  tubercle  bacilli,  by  tuberculin 
injections,  or  by  the  results  of  antisyphilitic  treatment.  All  the  other  organs 
of  the  patient  therefore  must  always  be  carefully  examined.  In  doubtful 
cases  it  is  proper  to  remove  a  bit  of  the  endolaryngeal  growth  and  examine 
it  histologically. 

TREATMENT 

Surgical  treatment  is  the  only  one  for  all  laryngeal  new  growths.  We 
must  refer  to  the  special  works  for  the  details.  Laryngologists  have  devised 
numerous  instruments  for  the  removal  of  benignant  polypi,  by  which,  under 
the  guidance  of  the  laryngoscope,  the  new  growth  is  cut,  snared,  crushed,  or 
torn  off.  The  performance  of  the  operation  is  made  much  easier  by  inducing 
local  anaesthesia  of  the  laryngeal  mucous  membrane  by  painting  with  cocain. 
Nevertheless,  we  firmly  believe  that  in  all  severe  cases  the  "  endolaryngeal " 
operations  should  be  superseded  by  laryngotomy.  Carcinoma  of  the  larynx 
can  be  cured  only  through  removal  of  the  tumor  by  laryngotomy  (splitting  of 
the  larynx)  or  by  total  extirpation  of  the  larynx.  Laryngotomy  is  compara- 
tively free  from  clanger,  while  total  extirpation  has  met  with  permanent  suc- 
cess as  yet  in  but  few  instances.  If  surgical  interference  is  no  longer  prac- 
ticable, we  can  endeavor  merely  to  mitigate  the  suffering  of  the  patient  by 
means  of  morphin,  cocain,  and  other  narcotics. 


190  DISEASES   OF  THE   RESPIRATORY  ORGANS 

SECTION  III 
Diseases  of  the  Trachea  and  the  Bronchi 

CHAPTEK   I 

ACUTE  CATARRH  OF  THE  TRACHEA  AND  THE  BRONCHI 

(Tracheitis  and  Acute  Catarrhal  Bronchitis) 

./Etiology. — Acute  catarrh  of  the  larger  air-passages,  of  the  trachea,  and 
larger  bronchi,  is  a  frequent  disease,  and  it  may  often  arise  from  taking  cold. 
It  is  conceivable  that  the  inhalation  of  cold,  damp  air  sometimes  directly 
affects  the  mucous  membrane  of  the  upper  air-passages.  Bronchial  catarrh 
is  very  often  associated  with  a  coincident  catarrh  of  the  larynx,  and  more 
rarely  of  the  pharynx.  In  the  ordinary  mild  forms  the  catarrh  is  usually  con- 
fined to  the  trachea  and  the  first  large  branches  of  the  bronchi,  while  the  finer 
bronchi  remain  healthy. 

More  intense  inflammation  of  the  bronchial  mucous  membrane  is  the  re- 
sult of  active  mechanical  or  chemical  irritation.  A  severe  bronchitis  develops 
after  the  inhalation  of  noxious  gases,  nitrous  and  sulphurous  oxids,  chlorin, 
bromin,  etc.,  as  is  often  observed  in  operatives.  The  inhalation  of  smoke  and 
dust,  especially  vegetable  dust,  works  in  the  same  injurious  fashion,  and  the 
followers  of  many  trades  and  employments,  such  as  millers,  wool  workers,  col- 
liers, etc.,  are  especially  subject  to  disease  from  this  cause.  In  this  form  of 
bronchitis  the  catarrh  often  extends  to  the  finer  bronchi. 

The  bronchitis  which  develops  in  the  course  of  other  acute  and  chronic 
disease  is  still  commoner  than  the  primary  forms  already  mentioned.  It  is 
often  due  to  infectious  causes,  such  as  certain  infectious  diseases,  especially 
measles,  whooping  cough,  and  influenza.  In  these  diseases  bronchitis  is  one 
of  the  most  constant  local  affections,  and  is  probably  dependent  immediately 
upon  the  primary  infection.  Bronchitis,  however,  develops  secondarily  in 
most  of  the  other  acute  infectious  diseases,  and  is  due  largely  to  the  inhala- 
tion of  noxious  substances  from  the  upper  part  of  the  air-passages.  This  is 
the  explanation  of  the  bronchitis  in  diphtheritic  processes  in  the  pharynx 
and  larynx,  in  so  far  as  it  does  not  depend  upon  a  direct  extension  of  the 
disease,  and  also  of  the  bronchitis  in  smallpox,  etc.  Bronchitis  may  also  be 
met  with  in  all  other  forms  of  severe  disease,  because  retention  of  secretion, 
putrefactive  processes,  inflammation,  thrush,  etc.,  occur  in  the  cavity  of  the 
mouth  and  pharynx,  and  from  them  chemical  or  organic  irritants  may  easily 
be  inhaled  into  the  bronchi.  The  imperfect  expectoration  in  all  severe  dis- 
eases is  a  still  more  harmful  factor  than  this  inhalation.  The  secretion  re- 
mains in  the  bronchi,  processes  of  decomposition  arise  in  the  stagnating 
mucus,  bacteria  collect  and  lead  to  a  bronchitis,  and  finally  to  the  lobular 
pneumonia  which  is  so  often  found  (vide  infra).  The  lessened  power  of 
resisting  injurious  influences,  produced  in  the  mucous  membrane  by  severe 
bodily  disease,  also  facilitates  the  development  of  catarrhal  inflammation.    In 


ACUTE   CATARRH   OF  THE   TRACHEA   AND  THE   BRONCHI       191 

all  disease!  in  which  deglutition  is  affected  (as  in  paralysis  of  the  epiglottis 
or  of  the  pharyngeal  muscles),  and  in  all  diseases  attended  by  frequent  vomit- 
ing or  choking  (cancer  of  the  oesophagus,  etc.),  secondary  bronchitis  with  its 
sequelae  may  ensue  from  the  inhalation  of  small  particles  of  easily  decompos- 
able food. 

We  do  not  know  how  far  we  may  claim  that  infectious  agents  act  as  a 
cause  of  primary  bronchitis,  yet  it  is  not  improhahle  that  many  cases  have 
such  an  aetiology.  It  is  especially  likely  that  many  cases  of  bronchitis  due  to 
"catching  cold"  really  have  something  infectious  about  them,  and  that  the 
preceding  exposure  to  cold  has  merely  lowered  the  natural  powers  of  resist- 
ance, and  thus  permitted,  or  at  any  rate  promoted,  infection.  This  infection 
is  probably  not  due  to  any  special  specific  bacteria  but  to  the  ordinary  germs 
of  inflammation  (staphylococci,  etc.). 

Finally,  we  must  mention  that  acute  bronchitis  is  sometimes  merely  an 
exacerbation  of  a  previous  chronic  bronchitis.  We  will  return  later  to  this 
important  and  not  uncommon  process. 

The  predisposition  to  acute  bronchitis  varies  in  different  persons.  We  do 
not  know  definitely  on  what  ground  such  an  increased  predisposition  to  bron- 
chial disease  rests,  nor  why  we  meet  with  it  sometimes  in  the  weak  and 
anaemic,  and  at  other  times  in  so-called  "  full-blooded  "  persons.  Bronchitis  is 
more  frequent  in  children  and  old  people  than  in  those  in  middle  life.  Most 
of  the  cases  occur  in  the  spring  and  autumn. 

Symptoms. — Pain  in  the  chest  may  be  present  in  some  cases  of  simple 
catarrhal  bronchitis,  but  usually  only  in  a  moderate  degree.  In  severe 
tracheitis  patients  often  have  a  painful  feeling  of  soreness  in  the  neck  and 
behind  the  upper  part  of  the  sternum,  and  this  is  increased  on  coughing. 
The  mucous  membrane  of  the  bronchi,  apparently,  has  no  nerve  fibers  which 
are  sensitive  to  pain,  and  the  pains  in  the  chest  which  are  often  present  in 
bronchitis  are,  as  a  rule,  muscular  pains  in  the  intercostal  muscles,  or  the 
insertion  of  the  diaphragm,  due  to  the  severe  paroxysms  of  coughing. 

Cough  is  one  of  the  most  constant  symptoms  of  bronchitis,  and  by  it  usu- 
ally the  attention  of  the  patient  or  of  the  physician  is  first  called  to  the  exist- 
ing thoracic  affection.  The  cough  may,  of  course,  be  due  to  a  laryngitis,  if 
that  is  also  present.  There  is  no  doubt,  however,  that  a  cough  may  be  ex- 
cited in  a  reflex  manner  from  the  mucous  membrane  of  the  trachea  and  of 
the  larger  as  well  as  of  the  finer  bronchi.  Experiments  have  shown  that  the 
point  of  bifurcation  of  the  tracbea  is  especially  irritable,  and  many  severe 
paroxysms  of  coughing  may  be  due  to  an  irritation  of  this  very  spot  from 
the  accumulation  of  secretion.  The  intensity  of  the  cough,  moreover,  is  very 
different  in  individual  cases,  which  is  due  in  part  to  the  degree  and  extent  of 
the  bronchitis  and  in  part  to  the  individual  irritability  of  the  person  affected. 

The  expectoration  consists  of  the  secretion  and  exudation  from  the  in- 
flamed mucous  membrane.  Its  abundance  and  consistence  vary  considerably 
in  the  different  cases.  We  distinguish  a  catarrh  with  an  abundant  secretion 
from  the  so-called  "  dry  catarrh.''  In  the  latter  only  a  little  viscid  sputum 
is  expectorated,  but  in  the  former  the  expectoration  is  more  abundant  and 
mucopurulent,  or  seromucous,  a  thin  fluid  separating  into  layers  on  stand- 
ing (vide  infra).  Very  often  in  the  beginning  of  the  disease  the  expectora- 
tion is  scanty  and  viscid — the  sputum  crudum  of  the  old  physicians ;  and  later 


192  DISEASES   OF  THE   RESPIRATORY  ORGANS 

it  becomes  more  abundant,  more  fluid,  and  more  purulent — the  sputum  coc- 
tum.  In  catarrh  of  the  finer  bronchi  the  expectoration  may  contain  little 
tough  mucous  or  mucopurulent  casts  of  the  bronchi.  It  may  be  stated  in 
general  that  the  characteristic  of  simple  bronchitic  sputum  is  the  mucous 
admixture  in  contrast  to  the  purulent  or  seropurulent  sputum  from  phthisical 
cavities,  etc.  We  may  readily  recognize  the  mucous  contents  of  the  sputum 
by  the  tenacity  with  which  it  clings  to  the  bottom  of  the  sputum  cup  when  the 
cup  is  tipped.  A  simple  catarrhal  expectoration  shows  nothing  peculiar  under 
the  microscope.  The  pus  corpuscles  are  often  swollen,  and  show  more  or  less 
marked  fatty  degeneration.  A  slight  admixture  of  blood  may  occasionally  be 
present  in  severe  bronchitis,  but  it  usually  has  no  special  significance,  being 
at  times  merely  the  result  of  severe  fits  of  coughing.  A  more  marked  and 
persistent  admixture  of  blood  is  seen  in  the  catarrhal  sputum  of  some  cases 
of  intense  bronchitis  in  drunkards,  so  that  we  may  even  speak  of  a  "  hemor- 
rhagic bronchitis." 

Dyspnoea  is  usually  entirely  absent  in  simple  mild  bronchitis,  but  marked 
shortness  of  breath  may  be  noticed  in  extensive  catarrh  of  the  finer  bronchi. 

Physical  Examination. — We  may  obtain  direct  evidence  of  the  condition 
of  the  tracheal  mucous  membrane,  with  due  practice,  by  the  laryngoscope.  We 
see  a  reddening  of  the  membrane,  and  sometimes  an  abnormal  abundance  of 
secretion  on  it,  if  there  is  a  tracheitis.  Other  methods  of  physical  examination 
are  at  our  service  for  judging  of  the  changes  in  the  bronchi. 

Inspection  of  the  thorax  shows  nothing  abnormal  in  the  milder  forms  of 
bronchitis.  The  respiration  is  somewhat  accelerated  and  the  expiration  pro- 
longed in  severe  bronchitis,  especially  if  the  finer  bronchi  are  affected.  Per- 
cussion in  uncomplicated  bronchitis  shows  nothing  abnormal  in  the  pulmonary 
resonance.  In  extensive  catarrh  of  the  finer  bronchi  an  acute  dilatation  of  the 
lung  is  apt  to  occur,  with  a  descent  of  the  lower  margin  of  the  lung.  Auscul- 
tation, too,  shows  nothing  unusual  in  many  cases  of  mild  catarrh  limited  to 
the  trachea  and  large  bronchi,  but  in  the  cases  in  which  the  smaller  bronchi 
are  the  seat  of  the  catarrh  and  there  is  a  marked  accumulation  of  secretion 
in  them,  we  hear,  besides  the  vesicular  respiration,  the  so-called  rhonchi  which 
almost  wholly  hide  it.  In  dry  bronchitis  we  speak  of  humming  or  buzzing 
sounds  (sonorous  rhonchi)  or  shrill,  whistling  sounds  (sibilant  rhonchi^/ ac- 
cording to  their  pitch.  These  sounds  are  probably  due  to  stenosis,  and  are 
caused  by  the  passage  of  the  air  through  narrow  portions  of  the  bronchi.  The 
narrowing  occurs  in  part  from  the  swelling  of  the  mucous  membrane,  in  part 
from  the  accumulation  of  secretion.  The  masses  of  secretion  themselves,  if 
they  are  set  in  vibration  at  the  same  time,  may  jwssibly  take  part  in  the  pro- 
duction of  the  humming  noises.  If  the  amount  of  secretion  collected  in  the 
bronchi  is  more  abundant  and  of  a  more  fluid  consistence,  it  gives  rise  to 
"  moist  rales "  on  the  passage  of  the  air.  These  are  distinguished  as 
"  coarse,"  "  medium,"  or  "  fine  moist  rales,"  according  as  they  occur  in  the 
larger  or  smaller  bronchi. 

Other  symptoms  of  disease  are  often  present  besides  those  already  men- 
tioned as  being  due  directly  to  the  bronchitis.  The  general  health  is  usually 
disturbed  in  a  severe  bronchial  catarrh.  The  patient  does  not  feel  well,  and 
has  less  appetite  than  usual.  A  moderate  amount  of  fever  is  often  present, 
especially  toward  evening.    An  increase  of  temperature  above  102°  or  103°  F. 


ACUTE  CATARRH  OF  THE  TRACHEA  AND  THE  BRONCHI   193 

(39°  C.)  is  rarely  seen  except  in  children.  The  patienl  sometimes  complains 
of  headache,  which  is  increased  by  severe  coughing.  There  can  be  ;i  question 
of  complications  only  when  the  inflammation  extends  to  other  parts  of  the 
respiratory  mucous  membrane.  Mild  bronchitis  is  often  associated  with  coryza 
and  laryngitis,  while  severe  bronchitis  may  lead  to  catarrhal  pneumonia  (vide 
infra). 

Forms  of  Bronchitis. — The  separate  forms  of  bronchitis  are  distinguished 
chiefly  by  the  degree  of  extension  of  the  catarrh. 

1.  The  Milder  Forms  of  Acute  Bronchitis. — In  most  cases  of  simple 
primary  bronchitis,  as  well  as  in  many  milder  attacks  of  secondary  bronchitis, 
the  catarrh  is  limited  to  the  mucous  membrane  of  the  larger  bronchi.  Ex- 
posure to  cold  and  other  injurious  influences  are  frequent  causes  of  the  pri- 
mary form.  The  symptoms  are  moderate.  The  cough,  however,  ma}r  be  quite 
troublesome.  Often  fever  is  absent  or  but  slight.  Upon  auscultation,  par- 
ticularly over  the  lower  lobes,  but  sometimes  over  the  entire  lungs,  are  heard 
numerous  rather  coarse  wheezing  or  rattling  sounds,  usually  with  some  sym- 
metry of  distribution;  but  in  many  cases,  as  we  have  said,  there  may  be  noth- 
ing abnormal  heard,  so  that  the  diagnosis  will  have  to  rest  merely  upon  the 
subjective  discomfort  in  the  chest,  the  cough,  and  the  expectoration.  With 
proper  care,  simple  primary  bronchitis  runs  its  course  in  a  few  days,  or  at 
the  most  in  a  few  weeks,  and  ends  in  complete  recovery.  If  the  patient  exposes 
himself  recklessly,  or  the  serological  factors  continue  to  be  active,  the  disease 
may,  however,  grow  worse,  prove  to  be  very  tedious,  and  finally  develop  into 
chronic  bronchitis. 

2.  The  Severer  Febrile  Forms  of  Acute  Bronchitis. — Sometimes 
acute  bronchitis  assumes  a  severer  form,  whether  because  the  influences  which 
give  rise  to  it  are  unusually  violent,  or  because  it  is  due  to  some  special  and 
perhaps  infectious  cause.  In  such  cases  the  symptoms  are  more  marked,  the 
bronchial  rales  more  abundant,  the  general  condition  of  the  patient  worse. 
Not  infrequently  there  is  fever  for  several  days,  or  even  for  one  or  two  weeks, 
the  type  being  irregularly  remittent,  but  the  temperature  is  usually  102°  or 
103°  F.  (39°  to  39.5°  C),  although  it  may  go  higher.  The  expectoration  is 
usually  mucopurulent,  but  it  often  contains  much  pus ;  in  other  cases  it  may 
be  sero-mucopurulent.  The  amount  is  then  greater,  and  it  forms  distinct 
layers  on  standing  in  a  beaker  glass.  The  author  has  not  infrequently  noticed 
that  there  is  more  liability  in  the  severer  forms  of  acute  bronchitis  to  have 
the  disease  mainly  limited  to  one  lobe,  or  at  least  to  one  lung,  but  we  may 
have  a  severe  diffuse  bronchitis  on  both  sides. 

The  aetiology  of  acute  febrile  bronchitis  has  been  but  little  studied.  Bac- 
teriological examination  of  the  sputum  usually  gives  no  definite  results,  since 
we  always  find  many  microorganisms.  Many  acute  cases  may  be  caused  by 
the  ordinary  pus  cocci.  At  the  time  of  a  pneumonia  epidemic  we  have  repeat- 
edly seen  cases  of  acute  bronchitis  with  high  fever  and  herpes,  but  without  any 
signs  of  pneumonic  infiltration.  These  were  probably  due  to  pneumococcus 
infection.     In  other  cases  there  is  perhaps  an  influenza  infection. 

We  would  add  in  particular  that  many  acute  febrile  cases  of  bronchitis 
prove  on  closer  investigation  (more  careful  questioning)  to  be  acute  exacer- 
bations of  a  mild  chronic  bronchitis — "  acute  recurrent  bronchitis."  The 
chronic  disease  of  the  bronchial  mucous  membrane  apparently  affords  a  favor- 
13 


194  DISEASES   OF   THE   RESPIRATORY   ORGANS 

able  opportunity  for  new  infection.  In  other  instances  it  is  merely  an  acute 
exacerbation  of  the  old  chronic  process.  Such  an  acute  bronchitis  may,  of 
course,  occur  repeatedly  in  the  same  patient. 

3.  Catakkh  of  the  Finer  Bronchi — Capillary  Bronchitis. — A  sim- 
ple primary  bronchial  catarrh  rarely  extends  to  the  finest  bronchi  in  adults. 
The  secondary  bronchitis,  however,  which  develops  in  other  severe  diseases 
(vide  supra)  often  extends  into  the  ultimate  divisions  of  the  bronchi,  and 
finally  leads  to  the  formation  of  nodules  of  lobular  pneumonia — "  catarrhal 
pneumonia"  (vide  infra).  We  recognize  the  implication  of  the  finer  bronchi 
by  hearing  the  high,  shrill,  whistling  rhonchi  (sibilant  rhonchi),  or  the 
abundant  fine,  moist  rales.  Bespiratory  symptoms  may  be  quite  marked  in 
extensive  catarrh  of  the  finer  bronchi.  Bespiration  is  evidently  accelerated, 
the  inspiration  is  of  the  costal  type  and  requires  the  aid  of  the  accessor}'- 
respiratory  muscles  of  the  neck  (the  sternomastoids  and  scaleni),  and  expi- 
ration is  usually  prolonged.  There  is  often  quite  a  severe  cough.  The  ex- 
pectoration is  mucopurulent  and  usually  not  very  abundant. 

Capillary  bronchitis  in  children  is  of  great  practical  importance.  Bron- 
chitis in  young  children  always  has,  as  experience  tells  us,  a  tendency  to 
attack  the  smaller  bronchi.  Extensive  bronchitis  is  seen  especially  in  weak 
children  who  are  rachitic  or  predisposed  to  tuberculosis.  Children  have  a 
great  tendency  to  be  attacked  with  bronchitis  at  the  time  of  the  first  den- 
tition. 

The  parents'  attention  is  usually  called  to  the  disease  by  the  appearance  of 
a  cough,  which  is  excited  especially  by  the  child's  crying.  Small  children 
never  expectorate,  for  they  swallow  the  secretion  which  is  coughed  up  inlo  the 
pharynx.  The  rapidity  of  respiration  is  very  striking,  it  being  increased  to 
sixty  or  eighty,  or  even  more,  in  a  minute.  The  respiration  is  also  labored, 
but  it  is  usually  superficial,  and  in  severe  cases  irregular.  There  is  generally 
a  distinct  respiratory  play  of  the  alse  nasi.  We  often  see  a  retraction  of  the 
lower  lateral  portions  of  the  thorax  on  inspiration  as  a  result  of  the  imper- 
fect entrance  of  air  into  the  smaller  bronchi.  The  expiration  is  frequently 
noisy  and  groaning  in  children.  We  hear  extensive  fine,  moist  rales  over  the 
lungs.  In  severe  cases  the  child  becomes  restless,  anxious,  perhaps  markedly 
pale  and  cyanotic,  and  finally  apathetic  and  stupid.  In  such  cases,  however, 
we  have  no  longer  to. deal  with  simple  bronchitis,  but  catarrhal  pneumonia 
has  already  developed.  The  disease  almost  always  runs  its  course  with  fever, 
the  temperature  rising  to  104°  F.  (40°  C.)  and  over.  The  pulse  is  increased 
to  120  or  140  or  more  per  minute.  The  duration  of  the  disease  is  seldom  less 
than  two  or  three  weeks,  and  it  may  last  much  longer.  Death  may  ensue,  espe- 
cially in  ill-nourished  children,  partly  as  a  result  of  general  weakness,  and 
also  directly  from  the  imperfect  respiration.  In  such  cases  we  find  at  the 
autopsy  not  only  diffuse  bronchitis,  but  also  almost  always  lobular  pneumonia. 
In  many  cases  a  gradual  recovery  finally  takes  place  in  spite  of  the  most 
severe  symptoms. 

The  secondary  bronchitis  in  children  complicating  measles,  whooping 
cough,  diphtheria,  etc.,  has  the  same  tendency  to  involve  the  finer  bronchi 
and  to  lead  to  lobular  pneumonia. 

In  conclusion,  we  must  mention  that  acute  bronchitis  in  old  persons  is 
also  apt  to  attack  the  finer  bronchi,  and  it  may  be  dangerous  partly  from  the 


ACUTE  CATARRH   OF  THE  TRACHEA  AND  THE   BRONCH]        195 

general  exhaustion,  partly  from  the  occurrence  of  respiratory  symptoms  and 

cardiac  weakness,  as  in  Lobular  pneumonia. 

Diagnosis. — The  diagnosis  of  bronchitis  presents  no  special  difficulty.  It 
is  obtained  directly  by  the  discovery  of  rhonchi  on  auscultation.  ](  these 
fail,  we  conclude  that  there  is  a  mild  catarrh  of  the  larger  bronchi  from  the 
presence  of  cough  and  expectoration,  if  no  cause  for  the  cough  is  to  be  found 
in  an  affection  of  the  larynx.  The  question  is  more  difficult,  but  it  um-t 
always  be  considered,  whether  a  given  bronchitis  is  a  common  primary  catarrh 
or  secondary  to  some  other  affection.  This  question  naturally  can  be  decided 
only  by  a  very  careful  examination  of  the  body.  We  must  always  remember, 
furthermore,  that  severe  pulmonary  affections  may  be  at  first  quite  latent 
and  show  obectively  merely  the  signs  of  simple  bronchitis,  while  later  pneu- 
monia, a  tubercular  affection,  or  something  similar,  develops.  A  bronchitis 
which  is  unilateral,  or  in  which  the  signs  are  to  be  found  in  circumscribed 
localities,  must  therefore  be  regarded  as  suspicious.  It  has  long  been  known 
that  bronchitis  in  the  apices  of  the  lungs,  the  "  apex-catarrh,"  is  often  the 
first  objective  change  to  be  met  with  in  pulmonary  phthisis.  "We  can  only 
conjecture,  and  not  pronounce  with  certainty  on  objective  evidence,  whether 
nodules  of  lobular  pneumonia  are  present  or  not  in  diffuse  bronchitis  affecting 
the  finer  bronchi. 

From  what  has  been  said,  it  is  clear  that  we  should  be  cautious  in  our 
prognosis  regarding  cases  of  severe  bronchitis,  especially  in  children  and  old 
people.  The  prognosis  in  the  milder  forms  of  bronchitis  is,  of  course,  always 
very  favorable. 

Treatment. — The  prophylaxis  of  primary  bronchial  catarrh  consists  in  the 
removal  of  all  the  injurious  influences  mentioned  which,  as  experience  shows, 
may  give  rise  to  bronchitis.  Careful  hardening  of  the  skin  to  the  effects  of  a 
change  in  temperature  is  of  service  in  persons,  particularly  children,  who  have 
a  special  tendency  to  bronchitis,  as  we  have  already  said  in  regard  to  the 
prophylaxis  of  laryngitis.  It  is  very  important  to  remember,  in  this  connec- 
tion, that  we  can  also  be  successful  in  our  prophylactic  measures  against  sec- 
ondary bronchitis.  Keeping  the  mouth  and  pharynx  clean,  urging  deep 
inspirations,  and  aiding  expectoration  by  the  timely  use  of  tepid  baths  and 
shower  baths,  may  often  prevent  bronchitis  or  keep  it  within  bounds,  when  it 
would  surely  develop  if  the  patient  .were  neglected. 

Simple  hygienic  measures  suffice  in  the  treatment  of  mild  cases  of  acute 
bronchitis.  The  patient  should  be  kept  warm,  should  remain  in  his  room, 
or,  if  there  be  any  fever,  in  becL  Diaphoretic  remedies  have  long  been  praised 
as  especially  potent  in  the  treatment  of  acute  bronchial  catarrh.  The  patient, 
therefore,  should  drink  hot  tea,  pectoral  tea  1  ("  Brustthee  "),  or  elder  tea,  etc., 
or  hot  milk  mixed  with  Seltzer,  a  remedy  whose  efficacy  is  frequently  praised 
by  the  patient.  The  tougher  the  sputum  and  the  more  difficult  expectoration, 
the  more  abundantly  should  we  give  warm  drinks  (Ems  water,  pectoral  tea, 
etc.).  Local  treatment  of  the  mucous  membrane  by  inhalations  is  usually 
illusory,  for  only  the  smallest  part  of  the  inhaled  fluid  reaches  the  bronchi. 
We  may,  however,  prescribe  inhalations  of  warm  steam,  or  a  one-  or  two- 

1  A  favorite  German  household  remedy,  consisting  of  an  infusion  of  eight  parts  of  althaea, 
three  parts  of  licorice,  one  part  of  orris  root,  four  parts  of  coltsfoot,  and  two  parts  each  of  mullein 
and  aniseed. — Trans. 


196  DISEASES   OF   THE   RESPIRATORY   ORGANS 

per-cent  solution  of  common  salt,  especially  with  a  dry  cough  and  a  secretion 
which  is  hard  to  loosen. 

Otherwise  we  must  employ  symptomatic  treatment.  A  mustard  plaster  or 
a  cold,  wet  compress  about  the  chest  does  good  service  with  severe  subjective 
thoracic  symptoms.  In  severe  cases  a  few  dry  cups  may  be  very  useful  in 
adults,  but  local  abstractions  of  blood  are  never  necessary  in  simple  bron- 
chitis. If  there  is  troublesome  cough,  so  as  to  disturb  the  rest  at  night,  we 
may  prescribe  small  doses  of  morphin,  5  to  8  grains  of  Dover's  powder 
(gm.  0.3  to  0.5),  15  to  20  drops  of  cherry-laurel  water,  codein,  etc.  When 
expectoration  is  difficult,  we  may  use  the  so-called  expectorants — ipecac, 
chlorid  of  ammonium,  apomorphin,  senega,  etc. 

We  have  already  repeatedly  mentioned  the  use  of  tepid  baths  and  shower 
baths,  indicated  in  severe  diffuse  bronchitis  developing  secondarily  in  the 
course  of  other  acute  diseases. 

Warm  or  tepid  baths  with  somewhat  cooler  shower  baths,  two  or  three  times 
a  day,  are  also  to  be  used  as  a  most  powerful  remedy  in  severe  cases  of  capillary 
bronchitis  in  children.  The  baths  assist  expectoration  and  guard  against  the 
possibility  of  the  development  of  lobular  pneumonia.  Wet  packs  applied  to 
the  thorax  or  over  the  whole  body  are  serviceable.  The  child  should  be  wrapped 
to  the  neck  in  a  sheet  which  has  been  previously  dipped  in  water  at  a  tem- 
perature varying  with  the  degree  of  the  fever  from  68°  to  77°  F.  (20°  to 
25°  C.)  and  well  wrung  out.  It  is  best  to  leave  the  arms  free.  A  dry  woolen 
blanket  may  be  wrapped  around  the  moist  sheet.  This  procedure  must  often 
be  repeated  three  or  four  times  a  day.  As  to  other  remedies,  we  use  the 
same  as  in  adults.  With  weak  children  our  care  must  be  to  keep  up  the 
strength  by  giving  the  most  nourishing  food  possible  and  small  amounts  of 
wine.  An  emetic  is  sometimes  indicated  in  cases  with  an  abundant  accumu- 
lation of  mucus  in  the  bronchi,  and  is  of  good  service.  As  experience  has 
shown,  we  should  use  opiates  for  small  children  only  with  the  greatest  caution. 
Senega  and  benzoin  may  be  employed  as  expectorants. 

In  the  bronchitis  of  old  people  our  chief  aim  should  be  to  keep  up  and 
improve  the  patient's  strength.  We  prescribe  liquor  ammonii  anisatus,  infu- 
sion of  senega,  etc.,  to  aid  expectoration,  which  is  usually  difficult,  since  the 
cough  is  feeble.  We  must  keep  close  watch  on  the  condition  of  the  heart 
(digitalis).  Tepid  baths  may  be  of  advantage,  but  they  must  be  used  with 
care. 


CHAPTEE    II 

CHRONIC    BRONCHITIS 

(Chronic  Bronchial  Catarrh) 

.ZEtiology. — Chronic  bronchial  catarrh  may  develop  gradually  from  exter- 
nal causes,  or  in  rare  cases  it  may  follow  acute  bronchitis.  The  same  noxious 
influences  which  excite  acute  bronchitis  may,  by  the  frequent  repetition  of 
their  action,  result  in  chronic  bronchitis.  The  constant  inhalation  of  dust  is 
one  of  the  commonest  causes  of  primary  chronic  bronchitis  (see  the  chapter  on 
Diseases  from  the  Inhalation  of  Dust).    In  many  cases  it  is  therefore  a  definite 


CHRONIC   BRONCHITIS  197 

occupation  disease,  ami  is  seen  in  millers,  bakers,  wool  workers,  stonecutters, 
colliers,  etc. 

In  a  large  number  of  cases  severe  chronic  bronchial  catarrh  is  not  an  inde- 

pendent  disease,  but  occurs  as  a  complication  or  ;i  resull  of  other  diseased 
conditions.  The  combination  of  chronic  bronchitis  with  emphysema  of  the 
lungs  (vide  infra)  is  the  most  common.  A  large  number  of  case-  also  are 
the  result  of  some  form  of  heart  disease,  such  as  valvular  disease  or  myo- 
carditis, or  of  disease  of  the  vessels,  leading  to  stasis  in  the  |>ulnionary  circu- 
lation, and  finally  to  a  chronic  catarrh  of  the  bronchi.  Chronic  bronchial 
catarrh  in  renal  diseases  also  depends  in  part  upon  circulatory  disturbances, 
and  in  part  on  the  toxic  action  of  urinary  constituents  which  have  not  heen 
normally  excreted.  Finally,  we  find  a  more  or  less  extensive  chronic  catarrh 
of  the  bronchi  in  other  chronic  affections  of  the  lungs  and  pleura,  as  in  tuber- 
culosis or  pleurisy. 

Chronic  bronchitis  is  seen  especially  in  adults  and  old  people,  and  more 
frequently  in  men,  on  account  of  their  exposure  in  the  various  trades,  than  in 
women,  but  children  may  also  have  pronounced  cases  of  chronic  diffuse  bron- 
chitis. Such  cases  may  often  he  referred  to  a  previous  acute  disease  of  the 
respiratory  organs,  especially  whooping  cough,  less  often  measles,  etc.  Such 
cases  in  childhood  often  continue  into  later  life,  and  on  careful  inquiry  we 
may  trace  many  of  the  severe  cases  of  chronic  bronchitis  in  adults  hack  to 
childhood. 

Pathological  Anatomy. — Chronic  bronchitis  is  characterized  anatomically 
by  a  persistent  and  chiefly  venous  hyperemia  and  swelling  of  the  bronchial 
mucous  membrane  with  increased  secretion  of  mucus  and  morbid  exudation 
of  serum  and  pus  corpuscles.  There  is  often  a  hyperplasia  of  the  mucous 
membrane  with  puffiness  of  the  surface.  In  old  cases,  however,  we  finally  meet 
with  an  atrophy  of  all  the  layers  of  the  mucous  membrane.  One  of  the  most 
frequent  results  of  chronic  bronchitis  is  a  cylindrical  dilatation  of  the  middle 
and  lesser  bronchi — bronchiectasis — especially  in  the  lower  lobes.  This  arises 
gradually  from  the  loss  of  elasticity  of  the  diseased  bronchial  walls,  and  their 
diminished  resistant  powers,  as  well  as  from  the  pressure  of  the  stagnating 
secretions. 

Symptoms  and  Course  of  the  Disease. — The  symptoms  which  are  due  to 
chronic  bronchitis  are  dyspnoea,  cough,  and  expectoration.  To  these  should  be 
added  the  results  of  a  physical  examination,  in  making  a  diagnosis. 

The  cough  is  of  very  different  severity  in  different  cases.  Usually  it  is 
worse  early  in  the  morning,  in  the  evening,  and  at  night,  than  in  the  daytime. 
The  amount  of  expectoration  is  also  subject  to  great  variations.  In  many 
cases  there  is  a  dry  cough  (catarrhe  sec,  vide  infra),  in  which  only  small 
amounts  of  tough,  viscid  sputum  are  expectorated.  In  other  cases  the  expec- 
toration is  more  abundant  and  mucopurulent,  sometimes  rather  seropurulent, 
and  occasionally  thin  and  separating  into  layers  on  standing.  In  catarrh  of 
the  finer  bronchi  the  mucopurulent  sputum  at  times  indicates  its  origin  by 
partly  formed  casts.  We  may  also  note  the  formation  of  so-called  spirals  (vide 
infra,  bronchial  asthma).  Microscopically,  the  expectoration  has  no  special 
characteristic  appearances,  but  contains  only  the  usual  elements  of  sputum — 
pus  corpuscles  mixed  with  pavement  epithelium,  ciliated  epithelium,  often 
many  bacteria,  sometimes  needles  of  fat  acids,  and  rarely  a  few  pointed  octa- 


198  DISEASES  OF  THE  RESPIRATORY  ORGANS 

hedral  crystals,  the  so-called  asthma,  crystals  {vide  infra).  Small  amounts  of 
blood  may  be  seen  in  severe  chronic  bronchitis,  especially  in  the  catarrh  of 
passive  congestion,  bronchitis  with  very  severe  attacks  of  coughing,  etc.,  but 
they  do  not  have  any  bad  significance. 

Dyspnoea  of  moderate  or  even  severe  degree  may  be  due  solely  to  an  exten- 
sive catarrh  of  the  finer  bronchi  with  narrowing  of  their  lumen.  In  many 
cases  in  which  there  is  bronchitis  the  dyspnoea  is  due  chiefly  to  some  coexisting 
abnormal  condition  of  the  heart,  the  lungs,  or  the  aorta. 

Physical  Examination. — The  percussion  in  bronchitis  shows  no  special 
change.  At  most  the  resonance  may  be  somewhat  tympanitic  from  the  relaxa- 
tion of  the  lung  tissue,  especially  in  the  lower  and.  posterior  portions  of  the 
lungs,  or  with  an  abundant  retention  of  secretion  in  the  bronchi,  it  may  he  a 
little  diminished.  The  inspiratory  descent  of  the  lower  edge  of  the  lung  is 
lessened  when  the  entrance  of  air  is  much  impeded  by  the  contracted  or 
plugged  bronchi.  Auscultation  may  give  either  rhonchi,  whistling,  hissing, 
humming,  etc.,  or  moist  rales,  according  to  the  extent  of  the  catarrh  and  the 
amount  and  consistence  of  the  secretion.  The  sounds  are  usually  to  be  heard 
over  the  whole  lung,  or  especially  over  the  lower  lobes,  because  here  the  catarrh 
is  usually  most  marked,  and  retention  of  secretion  is  most  apt  to  occur.  The 
respiratory  murmur  in  some  places  may  be  quite  obscured  by  the  rales.  Other- 
wise it  is  vesicular,  sometimes  exaggerated,  sometimes  rough  and  indefinite. 
Expiration  is  usually  prolonged,  because  the  exit  of  air  from  the  alveoli  is 
much  hindered  by  the  narrowed  bronchioles.  The  respiratory  murmur  may 
be  much  diminished,  or  even  entirely  suppressed  in  places  where  the  bronchi 
are  stopped  by  secretion,  which  happens  most  frequently  in  the  lower  lobes. 

Forms  of  Chronic  Bronchial  Catarrh. — Except  in  mild  cases,  we  usually  dis- 
tinguish several  different  forms  of  chronic  bronchial  catarrh,  which  may  run 
into  one  another. 

1.  Dry  Chronic  Catarrh. — The  dry  chronic  catarrh  (catarrhe  sec  of 
Laennec)  is  the  form  in  which  the  mucous  membrane  has  only  a  slight  secre- 
tion. The  cough  is  usually  very  troublesome  and  labored,  but  the  patient 
raises  merely  a  little  tough  sputum,  or  none  at  all.  On  auscultation  we  hear 
sibilant  rhonchi,  but  no  moist  rales.  This  form  of  catarrh  is  usually  associated 
with  pulmonary  emphysema,  and  asthmatic  attacks  are  also  frequent.  The 
disease  is  stubborn,  and  usually  lasts  for  years. 

2.  Bronchial  Blennorrhea. — In  that  form  of  chronic  bronchitis  termed 
bronchial  blennorrhea  there  is  a  very  copious  seropurulent  exudation  on  the 
surface  of  the  mucous  membrane.  The  cough  is  therefore  associated  with  a 
very  abundant  and  quite  thin  expectoration,  the  amount  of  which  in  the 
twenty-four  hours  may  exceed  a  half  pint  (quarter  of  a  liter).  The  expectora- 
tion runs  together  in  the  sputum-cup  and  usually  separates  on  standing,  the 
more  purulent  portion  sinking  to  the  bottom,  and  the  seromucous  portion, 
which  is  usually  frothy  on  the  surface,  remaining  at  the  top.  Numerous  moist 
rales  are  heard  in  the  lungs,  especially  in  the  lower  portions.  These  diminish 
if  large  amounts  of  sputum  are  coughed  up.  Anatomically,  the  bronchi  are 
almost  always  found  dilated  in  this  form  of  chronic  bronchitis. 

3.  Serous  Bronchorrhea. — The  so-called  serous  bronchorrhea  (catarrhe 
pituiteux  of  Laennec)  is  quite  rare  but  very  interesting.  It  is  characterized 
by  the  expectoration  of  a  very  large  amount  of  frothy,  almost  purely  serous, 


CHRONIC   BRONCHITIS  199 

or  seromucous,  thin  sputum  containing  only  a  slight  admixture  of  pus.    The 

cough  usually  comes  on  in  very  violent  paroxysms  which  last  from  half  an 
hour  to  an  hour  or  more.  The  respiratory  symptoms  are  quite  severe,  espe- 
cially during  these  attacks,  and  have  given  rise  to  the  old  and  useful  term 
"  asthma  humidum."  The  expectoration  collected  in  twenty-four  hours  may 
amount  to  one  or  two  quarts  (liters).  Examination  of  the  lungs  usually  re- 
veals very  ahundant  and  extensive  moist  rales.  The  resonance  on  percussion 
is  normal  or  a  little  diminished,  from  the  accumulation  of  secretion. 

The  special  cause  of  this  peculiar  disease  is  quite  obscure.  There  are  mild 
afebrile  and  also  very  severe  forms  of  this  type  of  chronic  bronchitis.  We  have 
seen  several  chronic  cases,  which  were  attended  with  persistent  fever,  and  which 
led  to  great  emaciation  and  weakness.  In  one  case  which  came  to  autopsy 
there  was  found  a  marked  tuberculosis  of  the  retrobronchial  lymph-glands, 
while  the  lungs  themselves  showed  hardly  any  striking  changes.  One  vagus 
nerve  was  wholly  imbedded  in  the  tubercular  mass  of  the  glands,  and  it  is 
not  impossible  that  the  peculiar  attacks  of  serous  expectoration  were  due  to 
irritation  of  this  nerve.  At  any  rate,  we  should  consider  the  possibility  of  such 
conditions  in  the  future.  It  is  worthy  of  note  that  attacks  of  "  humid  asthma," 
with  expectoration  of  large  amounts  of  serous  sputum,  have  also  been  observed 
in  chronic  nephritis,  especially  in  contracted  kidney  (q.  v.). 

Course  of  the  Disease. — The  course  of  most  chronic  bronchial  catarrhs  is 
very  protracted.  The  disease  usually  lias  frequent  remissions  and  fresh  ex- 
acerbations. The  patient  is  tolerably  well  in  the  pleasanter  time  of  the  year 
if  he  takes  good  care  of  himself,  but  in  autumn  and  winter,  or  after  exposure 
to  various  noxious  influences,  the  catarrh  grows  worse  and  the  patient's  symp- 
toms increase.  If  the  jiisease  has  lasted  for  years,  we  usually  find  symptoms 
in  the  lungs,  such  as  emphysema  or  chronic  tuberculosis,  or  in  the  heart,  such 
as  secondary  dilatation  and  hypertrophy  of  the  right  ventricle,  which  symptoms 
gradually  become  more  severe.  The  details  of  these  conditions  are  to  be  found 
in  the  appropriate  sections. 

Diagnosis. — The  diagnosis  of  chronic  bronchitis  is  not  difficult  in  itself, 
and  may  easily  be  made  by  considering  the  patient's  symptoms  and  by  judging 
of  the  result  of  the  physical  examination.  We  must  always  consider,  however, 
whether  the  bronchitis  is  actually  a  primary  disease  or  a  result  or  a  complica- 
tion of  some  other  chronic  disease.  Therefore,  in  every  case  of  chronic  bron- 
chitis, the  heart  and  the  kidneys  (urine)  must  be  carefully  examined,  as  well 
as  the  lungs. 

In  all  the  severe  cases,  whenever  possible,  an  X-ray  examination  should 
be  made.  By  this  means,  aneurisms,  tumors,  and  the  like  have  not  very 
infrequently  been  discovered  to  be  the  cause  of  an  existing  chronic  bron- 
chitis. 

Prognosis. — Chronic  bronchitis  is  in  most  cases  a  very  stubborn  affection, 
which  frequently,  as  we  have  said,  shows  improvement,  but  from  which  com- 
plete recovery  is  rare.  The  prognosis  also  depends  greatly  upon  the  patient's 
circumstances,  and  upon  the  possibility  of  his  taking  care  of  himself  and  avoid- 
ing all  harmful  exposure.  In  secondary  bronchitis  the  question  whether  the 
bronchitis  is  capable  of  material  improvement  or  not  of  course  depends  mainly 
upon  the  prognosis  of  the  primary  disease. 

The  danger  in  primary  chronic  bronchitis  comes  from  the  final  development 


200  DISEASES   OF  THE   RESPIRATORY   ORGANS 

of  its  sequelae,  especially  from  the  gradual  appearance  of  pulmonary  emphy- 
sema, dilatation  of  the  heart,  secondary  tuberculosis,  etc. 

Treatment. — The  only  hope  of  success  in  severe  cases  in  any  method  of 
treating  chronic  bronchitis  lies  in  removing  the  patient  completely,  at  least  for  a 
time,  from  the  action  of  injurious  influences.  The  favorable  result  of  the  baths 
and  health  resorts  that  are  employed  depends  largely  upon  this,  that  patients 
enjoy  in  them  complete  bodily  rest,  and  are  far  better  protected  from  dust 
and  the  changes  in  the  weather  than  at  home.  We  must  make  the  patient 
comprehend  the  necessity  of  this  condition  as  the  basis  of  any  treatment.  If 
he  cannot  go  to  a  suitable  climate  during  the  cold  season,  he  must  keep  his 
room  in  all  unpleasant  weather,  but  at  other  times  he  may  be  permitted  to 
stay  in  the  open  air.  Furthermore,  the  patient  must  be  warned  to  avoid  as 
completely  as  possible  those  harmful  influences  which  his  calling  and  manner 
of  life  entail,  and  among  which  especially  to  be  mentioned  is  the  bad  air  in 
our  inns  and  restaurants.  Food  should  be  easily  digestible,  and,  in  persons 
inclined  to  corpulence,  sparingly  taken.  Alcohol  is  to  be  permitted  only  in 
a  moderate  degree.  We  combat  the  tendency  to  constipation,  which  is  often 
present,  by  dietetic  remedies,  by  taking  fruit,  especially  grapes,  prunes,  etc., 
honey,  Graham  bread,  or  by  mild  laxatives,  such  as  the  bitter  waters,  Fried- 
richshall,  Ofner,  etc.,  since  jDersistent  constipation  aggravates  the  patient's 
symptoms. 

If  the  circumstances  of  the  patient  permit  and  his  condition  requires  it,  we 
should  send  him  south  in  the  autumn  in  order  to  avoid  the  evils  of  a  northern 
winter,  but  we  must  always  consider  whether  the  patient  has  the  strength  to 
bear  the  burden  and  unavoidable  discomfort  of  such  a  journey  without  per- 
manent harm.  The  rule  is  to  send  patients  with  a  bronchial  catarrh,  when 
there  is  much  secretion,  to  health  resorts  with  a  dry  climate — for  example,  to 
the  western  Riviera,  San  Remo,  Bordighera,  Mentone,  etc.  The  somewhat  dry 
yet  cooler  climate  of  Meran,  Gries,  or  Arco  is  suitable  for  patients  with  a 
stronger  constitution.  Patients  with  dry  bronchitis  usually  find  themselves 
at  their  best  in  a  warm  but  not  too  dry  climate.  If  we  wish  to  be  sure  of 
avoiding  the  winter's  cold,  we  must  choose  Sicily,  Egypt,  or  Madeira  for  a 
residence.  Of  the  more  northern  winter  resorts  we  may  mention  places  on  the 
eastern  Riviera,  especially  Nervi. 

We  must  recommend,  in  bronchitis,  a  suitable  summer  residence,  particu- 
larly for  those  who  dwell  in  large  and  dusty  cities.  Any  private  country  house 
in  a  well-wooded  and  protected  place  is  suitable.  If  we  wish  to  send  patients 
to  a  bath,  Marienbad,  Kissingen,  or  Homburg  are  proper  places  for  corpulent 
people  who  also  suffer  from  digestive  disturbances,  while  we  may  send  weaker 
patients  to  Ems,  Soden,  Badenweiler,  Ischl,  Reichenhall,  etc.  A  summer  resi- 
dence on  the  sea,  best  on  the  Baltic,  is  very  serviceable  for  many  patients. 

The  inhalation  treatment  is  much  employed  in  chronic  bronchitis,  but  we 
should  not  cherish  too  high  hopes  about  its  use.  The  best  inhalations  in  dry 
catarrhs  are  simple  steam,  a  one-  or  two-per-cent  solution  of  common  salt  or 
bicarbonate  of  soda,  Ems  water,  etc.  In  cases  with  marked  secretion,  inhala- 
tions of  oil  of  turpentine  are  most  to  be  praised.  The  simplest  way  is  to  pour 
a  teaspoonful  of  oil  of  turpentine  into  hot  water  and  inhale  the  vapor  as  it 
arises.  The  so-called  turpentine  pipe,  however,  is  more  convenient  and  more 
efficacious  (Fig.  39).     This  consists  of  a  flask,  which  is  filled  to  the  height 


chronic;  bronchitis 


201 


Fig.  39. — Turpentine  pipe. 


of  several  inches  with  water  and  then  will)  a  layer  of  oil  of  turpentine  or  of 
oleum  pini  pumilionis  (P.  (I.).,  some  2  cm.  thick.  Tun  glase  tubes,  open  at 
both  ends,  are  passed  through  the  cork.  One  straight  tube  extends  down  into 
the  layer  of  water:  the  lower  end  of  the  other  is  free  in  the  upper  part 
of  the  flask.  The  outer  portion  of  this  last 
tube  is  bent  at  an  angle  and  is  connected 
with  the  mouthpiece  through  which  the 
patient  inhales.  The  formation  of  turpen- 
tine vapor  is  aided  by  putting  the  flask  in 
hot  water.  We  have  treated  many  pa- 
tients in  this  way,  who,  for  a  number  of 
hours  a  day,  "  smoked "  their  turpentine 
pipes. 

In  treating  chronic  bronchitis  the  pneu- 
matic method  was  considerably  employed 
for  a  time;  that  is,  the  patient  was  made 
to  breathe  artificially  compressed  air,  or  to 
expire  into  air  of  less  than  the  atmospheric 
pressure,  by  means  of  a  movable  pneumatic 
apparatus,  as  proposed  by  Waldenburg  and 
others.  Of  late,  however,  this  method  of 
treatment  has  received  less  favor,  inasmuch 
as  actual  results  have  fallen  decidedly 
short  of  the  benefit  promised.  In  Ems, 
Eeichenhall,  and  other  places,  special  pneumatic  cabinets  have  been  arranged, 
filled  with  compressed  air,  in  which  patients  remain  for  varying  lengths  of  time. 

I  consider  the  exhibition  of  methodically  given  sweat  baths,  and,  above  all, 
the  electric-incandescent-light  baths  (the  so-called  Kellogg  x  incandescent-light 
baths)  far  more  effectual  than  the  pneumatic  treatment.  In  these  baths  the 
patient  is  comfortably  seated  in  the  cabinet,  his  arms  are  free,  and  his  head  is 
outside  the  cabinet  and  covered  with  an  ice  cap  or  cool  cloths.  The  severe 
cases  of  bronchitis  require  especial  care ;  while  the  patients  are  in  bed  they  may 
be  given  localized  electric-light  treatment  to  the  trunk  and  chest  by  means 
of  specially  devised  contrivances.  I  have  seen  very  satisfactory  results  from  this 
method  of  treatment,  even  in  advanced  cases.  The  light  baths  are  given  daily 
for  about  fifteen  to  twenty  minutes  until  there  is  profuse  sweating  all  over  the 
body.  The  patients  are  next  placed  in  a  warm  bath,  are  then  rubbed  dry,  and 
remain  quiet  for  one  to  two  hours.  If  an  electric  incandescent  light  bath  is 
not  at  one's  disposal,  the  usual  steam  cabinets  and  other  diaphoretic  measures 
may  be  employed.  All  these  methods  of  treatment,  of  course,  require  careful 
supervision  of  the  patient  by  the  physician. 

One  of  the  most  serviceable  remedies  in  dry  chronic  bronchitis  is  a  large 
amount  of  warm  drink  (pectoral  tea,  Ems  water,  Seltzer,  etc.).  Iodin  prepa- 
rations (sodium  iodid,  potassium  ioclicl,  sajodin,  etc.)  sometimes  act  favor- 
ably in  making  a  tough  secretion  fluid.  Of  expectorants,  ipecac  and  apomor- 
phin  are  most  recommended  in  this  form  of  bronchitis.  For  distressing  cough 
we  may  give  Dover's  powder,  morphin,  or  codein.     In  bronchial  blennorrhea 


1  [Devised  by  J.  H.  Kellogg,  of  Battle  Creek,  Mich.] 


202  DISEASES  OF   THE   RESPIRATORY   ORGANS 

we  know  empirically  that  the  internal  use  of  balsams  causes  a  distinct  diminu- 
tion of  the  secretion.  Oil  of  turpentine  is  the  most  active,  and  may  be  given 
internally  in  gelatin  capsules,  or  mixed  with  milk,  in  doses  of  10  or  15  drops 
three  or  four  times  a  day.  After  each  dose  of  turpentine  we  should  give  a 
glass  of  milk.  Lepine,  G.  See,  and  other  French  physicians  recommend  ter- 
pin  hydrate  as  still  more  effectual.  This  is  a  derivative  of  turpentine,  and  is 
best  employed  in  pills  containing  1.5  gr.  (gm.  0.1),  of  which  two  or  even 
more  are  to  be  taken  three  times  a  day.  It  may  also  be  given  in  solution 
as  follows:  Terpin  hydrate,  Sijss.  (gm.  10);  alcohol,  q.  s.  ad  sol.  facien-. 
dam;  aq.  dest,  gvij  (gm.  200).  Misce.  Sig. :  Two  or  three  spoonfuls 
daily.  Myrtol  [terebene],  balsam  of  copaiba,  and  balsam  of  Peru  are  also 
used  internally.  The  chief  expectorants  are  infusion  of  senega  root,  liquor 
ammonii  anisatus,  etc.  We  should  be  very  sparing  of  narcotics  at  first,  but  in 
severe  cases  we  cannot  wholly  dispense  with  them. 

[The  iodid  of  potassium  in  doses  of  5  to  10  gr.  thrice  daily  is  sometimes 
distinctly  curative.  An  outdoor  life,  free  diet,  moderate  alcoholic  stimulus, 
tonics,  and  woolen  clothing  do  much  to  promote  recovery.] 

Local  applications  to  the  chest  in  the  form  of  embrocations,  mustard  plas- 
ters, dry  cups,  or  cool  or  warm  wet  compresses  are  to  be  used,  especially  with 
severe  dyspnoea,  or  with  pain  and  a  feeling  of  oppression  in  the  chest. 

In  all  secondary  chronic  catarrhs  our  chief  attention,  beyond  the  sympto- 
matic treatment  of  the  bronchitis,  must  be  directed  to  the  treatment  of  the 
underlying  disease.  If  we  succeed  in  once  more  regulating  the  heart's  action 
by  digitalis  when  there  is  uncompensated  heart  disease,  or  in  establishing 
diuresis  when  there  is  renal  disease,  or  in  improving  the  general  physical  con- 
dition by  proper  dietetic  measures  in  the  corpulent,  gouty,  alcoholic,  etc.,  we 
may  also  in  that  way  cause  improvement  in  the  existing  bronchial  catarrh. 


CHAPTEE    III 

FETID    BRONCHITIS 

(Putrid  Bronchitis) 

iEtiology. — By  putrid  or  fetid  bronchitis  we  mean  that  form  of  bronchitis 
in  which  the  secretion  of  the  mucous  membrane  undergoes  a  putrid  decompo- 
sition, and  in  which,  consequently,  the  expectoration  takes  on  a  peculiar  and 
extremely  foul  odor.  The  special  agents  which  cause  fetid  bronchitis  are  still 
unknown. 

The  opportunity  for  the  agents  of  putrefaction  to  enter  the  bronchi  with 
the  inspired  air  is,  of  course,  often  given,  but  a  fetid  bronchitis  naturally  is 
excited  only  when  they  can  remain  there  and  increase.  Fetid  bronchitis  there- 
fore develops  quite  rarely  in  a  previously  healthy  lung  (primary  fetid  bron- 
chitis). The  retention  and  the  further  development  of  the  bacteria  of  putre- 
faction are  chiefly  favored,  as  we  know,  by  diseased  conditions  which  already 
exist  in  the  bronchi.  A  great  number  of  cases  of  fetid  bronchial  catarrh  there- 
fore develop  secondarily  upon  other  pulmonary  affections  of  longer  standing. 
Thus  the  expectoration  may  quite  suddenly  change  and  take  on  a  fetid  char- 


FETID   BRONCHITIS  203 

actor  in  llie  course  of  a  chronic  or  rarely  of  an  acute  bronchitis  or  of  phthisis. 
Bronchiectasis  (vide  infra)  greatly  favors  the  developmeni  of  this  putrid 
change,  for  in  it  the  retention  and  stagnation  of  large  amounts  of  secretion 
promote  and  occasion  the  putrid  decomposition,  [f  a  putrid  decomposition  of 
the  secretion  begins  in  one  jiart  of  the  bronchial  system,  the  further  extension 
of  the  process  follows  from  direct  infection. 

In  rare  cases  putrid  bronchitis  also  develops  as  a  result  of  an  embolic  pul- 
monary gangrene. 

Symptoms  and  Course;  Anatomical  Changes. — Tf  a  fetid  bronchitis  arises 
in  the  course  of  some  other  chronic  pulmonary  disease,  its  appearance  may  be 
marked  by  a  sudden  impairment  of  tbe  general  condition,  by  high  fever,  often 
associated  with  numerous  chills,  and  by  an  increase  of  the  thoracic  symptoms, 
such  as  pain  and  cough.  Tbe  change  in  the  expectoration,  the  peculiarity  of 
which  was  first  accurately  described  by  Traube,  is  characteristic.  The  expec- 
toration shows  the  same  character  in  cases  of  apparently  primary  fetid 
bronchitis. 

The  sputum  has  a  very  repulsive,  sweetish,  putrid  smell.  The  expectora- 
tion is  usually  quite  abundant;  the  consistence  is  rather  thin.  On  standing, 
the  sputum  shows  a  very  marked  division  into  three  layers.  This  division  is 
due  to  the  abundant  serous  exudation  in  the  bronchial  mucous  membrane  and 
to  the  thin  fluid  character  of  the  expectoration,  which  permits  an  unequal 
division  and  a  settling  of  the  solid  constituents.  The  upper  layer  consists  of 
a  very  frothy,  mucopurulent  stratum,  consisting  in  part  of  individual  masses, 
from  which  a  number  of  coarser  or  finer  fibers  float  down  into  the  middle 
layer.  This  middle  layer  consists  of  a  dirty-green  mucoserous  fluid.  At  the 
bottom  of  the  vessel  is  found  the  third  layer,  which  is  often  the  thickest,  and  is 
composed  entirely  of  pus.  It  consists  of  pus  corpuscles  which  have  sunk  to 
the  bottom,  and  is  of  a  rather  thin,  greasy  consistence.  With  the  naked  eye 
we  generally  recognize  a  number  of  little  whit- 
ish-gray plugs  and  particles  in  it.  These  so- 
called  "  Dittrich's  plugs,"  which  are  easily 
crushed  under  a  cover-glass,  are  quite  charac- 
teristic. Microscopically,  they  consist  of  de- 
composed pus  corpuscles,  detritus,  and  bacteria, 
and  usually  contain  ver}r  many  needles  of  fat 
acids  arranged  in  bundles  (see  Fig.  40).  We 
often  find  also  in  the  sputum  large  masses  of 
fungi,  especially  great  bunches  of  twisted  lep- 
tothrix  fibers,  which,  by  an  unpracticed  eye,  FlG.  40.— Crystals  of  fatty  acids, 
may    readily    be    mistaken    for    elastic    fibers. 

The  latter  are,  of  course,  never  found  in  the  expectoration  of  a  simple 
fetid  bronchitis,  but  only  in  the  deep-seated,  destructive  processes  in  the  lung, 
like  gangrene.  On  chemical  examination  of  the  sputum,  the  ordinary  products 
of  putrefaction  may  be  found — volatile  fat  acids,  especially  butyric  and  vale- 
rianic acids,  also  sulphureted  hydrogen,  leucin,  tyrosin,  etc. 

It  is  very  characteristic  of  many  cases  of  fetid  bronchitis  that  the  sputum 
does  not  have  a  putrid  character  at  all  times.  Sometimes  for  days  the  patient 
coughs  up  a  simple  catarrhal  secretion,  and  then  all  at  once  comes  an  outburst 
of  intolerable   stinking  expectoration.     This  is  probably  because   a  circum- 


204  DISEASES   OF   THE   RESPIRATORY  ORGANS 

scribed  putrid  focus  is  frequently  shut  off,  the  expectoration  coming  solely 
from  the  other  bronchi,  where  there  is  merely  a  simple  catarrh,  until  finally 
the  accumulation  of  putrid  secretion  is  all  at  once  coughed  up  again  in  large 
amount  by  mouthfuls. 

When  fetid  sputum  is  coughed  up,  the  patient's  breath  also  becomes  very 
foul-smelling,  so  that  he  often  becomes  a  burden  to  his  associates. 

The  signs  which  fetid  bronchitis  gives  on  physical  examination  are  those 
of  an  ordinary  bronchitis ;  but  it  is  characteristic  of  many  cases,  in  distinction 
from  ordinary  chronic  bronchitis,  that  the  physical  signs  (rales,  dry  rhonchi) 
are  limited  chiefly  to  a  definite  portion  of  the  lung,  usually  one  lower  lobe. 
In  a  great  number  of  cases  we  also  find  signs  of  consolidation  and  contraction 
of  the  lung,  of  pleurisy,  etc.,  which  do  not  belong  to  fetid  bronchitis  as  such, 
but  are  due  to  complications  or  sequelae. 

The  most  frequent  of  these  sequelae  is  the  development  of  a  "  reactive  " 
lobular  inflammation,  a  genuine  pneumonia  which  follows  a  catarrh  of  the  finer 
bronchi.  These  reactive  inflammations,  in  part  exaggeration  of  the  existing 
bronchitis,  in  part  lobular  pneumonias,  frequently  occur  in  separate  attacks. 
Quite  suddenly,  increased  cough  and  expectoration  appear,  accompanied  by 
darting  pains  in  the  side,  fever,  etc.  After  several  days — sometimes,  however, 
only  after  two  to  three  weeks  or  even  longer — these  manifestations  disappear, 
to  be  followed  by  an  afebrile  period  with  milder  symptoms.  In  the  lobe  of  the 
lung  which  is  the  main  seat  of  the  fetid  bronchitis,  a  chronic  interstitial 
pneumonia,  associated  with  more  or  less  retraction,  pleuritic  adhesions,  etc., 
gradually  develops.  Special  mention  must  be  made  of  the  danger  of  the 
development  of  gangrene.  The  putrefying  agents  having  once  gained  entrance 
into  the  lungs,  any  subsequent  pneumonia  may  be  followed  by  pulmonary 
gangrene.  For  this  reason  we  not  infrequently  find,  post-mortem,  isolated 
smaller  or  larger  gangrenous  foci  in  conjunction  with  a  fetid  bronchitis.  In 
such  cases  the  fetid  bronchitis  is  certainly  the  primary  factor,  and  the  develop- 
ment of  gangrenous  foci  the  secondary  lesion.  It  will  be  shown  later  that 
the  reversed  condition  may  occur.  Fetid  bronchitis  and  gangrene  of  the  lungs 
run  into  each  other  so  often,  both  clinically  and  anatomically,  that  there  is 
no  sharp  line  to  be  drawn  between  them.  If  the  nodules  are  superficial,  and 
reach  the  pleura,  the  infection  attacks  this,  and  we  have  a  purulent  or  even 
an  ichorous  pleurisy. 

The  smaller  and  medium-sized  bronchi  are  almost  always  found  in  a  condi- 
tion of  cylindrical  dilatation  in  long-standing  fetid  bronchitis.  Their  mucous 
membrane  is  intensely  inflamed,  and  often  ulcerated  superficially.  On  its  sur- 
face we  see  in  the  cadaver  the  greasy  purulent  masses  and  the  plugs  which  we 
find  in  the  expectoration  during  life. 

Whatever  may  be  the  case  with  the  general  course  of  fetid  bronchitis,  its 
beginning  is  often  quite  sudden  and  acute,  both  in  the  primary  and  in  the  sec- 
ondary forms,  as  we  have  said.  The  patient  is  attacked  with  fever,  which  may 
often  be  quite  high,  and  with  a  stitch  in  the  side,  cough,  and  expectoration. 
Later,  the  characteristic  peculiarities  described  above  appear.  The  further 
course  of  the  disease  is  almost  always  chronic,  lasting  for  years,  but  subject  to 
many  variations.  Very  often  manifest  improvement,  and  even  apparent  re- 
covery, takes  place,  when  suddenly  there  is  a  new  attack  of  fever  and  thoracic 
symptoms.     The  general  condition  and  nutrition  of  the  patient  may  be  quite 


FETID  BRONCHITIS  205 

good  for  a  long  time,  except  during  the  periods  of  marked  exacerbation  of  the 
disease.  Patients  with  chronic  fetid  bronchitis  of  ten  appear  somewhal  bloated, 
but  also  pale  and  slightly  cyanotic.  Peculiar  clubbed  thickenings  of  the  ter- 
minal phalanges  of  the  fingers,  or  more  rarely  of  the  toes,  gradually  develop, 
as  in  many  cases  of  bronchiectasis.  Slight  oedema  of  the  Lower  extremity 
also  sometimes  present. 

Symptoms  referable  to  other  organs  may  be  wholly  absent.  We  see  most 
frequently  disturbances  of  the  stomach,  loss  of  appetite,  and  nausea,  which 
probably  come  from  swallowing  the  fetid  sputum.  Patients  also  complain  of 
occasional  rheumatic  pains  in  the  muscles  and  joints,  which  are  probably  due 
to  an  absorption  of  septic  matter.  In  conclusion  it  must  be  mentioned  that, 
in  fortunately  rare  cases  of  fetid  pulmonary  disease,  pyogenic  germs  reach  the 
brain  by  metastasis,  and  give  rise  to  purulent  meningitis  or  cerebral  abscess. 

The  danger  of  the  disease,  apart  from  the  exceptional  occurrence  just  men- 
tioned, lies  in  the  possible  extension  of  the  process  to  the  lungs  and  the  develop- 
ment of  pulmonary  gangrene  and  its  sequela?.  We  hardly  ever  find  a  simple 
fetid  bronchitis  in  the  cadaver,  but  we  almost  always  see  other  processes  be- 
sides, which  have  been  mentioned  above — reactive  pneumonia,  pulmonary  gan- 
grene, pleurisy,  etc.  All  these  processes  develop  very  readily,  and  make  rapid 
progress  in  old,  decrepit  persons,  who  live  under  bad  hygienic  conditions,  in 
whom  putrid  processes  in  the  lungs  are  frequent. 

Diagnosis. — The  diagnosis  of  fetid  bronchitis  is  not  difficult  in  itself,  for 
the  diagnosis  of  a  putrid  process  in  the  lung  may  be  made  from  the  stinking 
sputum  alone.  It  may  be  difficult  to  decide  whether  we  have  to  do  merely  with 
a  fetid  bronchitis,  or  with  a  pulmonary  gangrene  also.  Decisive  indications 
of  pulmonary  gangrene  are  derived  from  physical  examination — dullness, 
bronchial  respiration,  and  coarse,  moist  rales,  signs  of  a  cavity — and  also  the 
discovery  of  elastic  fibers  and  fragments  of  parenchyma  in  the  expectoration. 

Prognosis. — The  prognosis  must  be  made  with  care  in  every  case  of  fetid 
bronchitis.  If  the  external  circumstances  of  the  patient  are  favorable,  he  may 
remain  in  tolerable  health  for  years.  We  must  always  be  prepared  for  the 
appearance  of  new  exacerbations  of  the  disease  and  of  affections  of  the  lung 
itself,  and  must  also  bear  in  mind  the  rarer  sequelae  (empyema,  abscess  of  the 
brain).     Complete  cure  is  exceptional. 

Treatment. — The  chief  aim  of  treatment  must  be  to  bring  the  putrid  proc- 
esses in  the  bronchi  to  a  standstill  by  the  death  of  the  agents  of  putrefaction. 
The  difficulty  of  fulfilling  this  task  lies  in  the  impossibility  of  getting  the  dis- 
infecting material  to  act  on  the  bronchial  mucous  membrane  in  the  necessary 
amount  and  concentration.  Nevertheless,  we  can,  without  doubt,  at  least  re- 
lieve a  fetid  bronchitis  and  keep  it  in  check  by  the  judicious  use  of  inhalations. 
Inhalations  of  a  two-per-cent  solution  of  carbolic  acid  are  most  useful,  given 
for  five  or  ten  minutes  several  times  a  day.  These,  however,  are  sometimes 
not  well  borne  if  long  continued,  and  they  may  excite  mild  symptoms  of  car- 
bolic poisoning — such  as  headache,  malaise,  and  dark  carbolic  urine.  We  have 
often  used  with  good  results  the  "carbolic  mask"  recommended  by  Cursch- 
mann,  a  kind  of  respirator  fastened  in  front  of  the  nose  and  mouth,  contain- 
ing cotton  in  a  special  receptacle  impregnated  with  carbolic  acid,  equal  parts 
of  carbolic  acid  and  alcohol,  or  other  remedies  such  as  turpentine  or  creosote. 
Many  patients  can  wear  these  masks,  with  occasional  interruptions,  for  many 


206  DISEASES   OF  THE   RESPIRATORY   ORGANS 

hours  a  day.  Besides  carbolic  acid  we  may  use  inhalations  of  turpentine 
(turpentine  pipe  or  vapor),  oleum  pini  pumilionis,  creosote,  etc.  The  internal 
use  of  these  and  similar  remedies  also  seems  frequently  to  be  of  service  in 
putrid  bronchitis.  We  recommend  especially  the  internal  use  of  turpentine 
(in  gelatin  capsules),  myrtol  (also  in  gelatin  capsules),  also  terpin  hydrate 
(six  to  ten  2-gr.  [gm.  0.1]  pills  a  day),  creosote,  syrupus  kalii  sulphoguaiaco- 
lici  (sirolin),  etc. 

In  other  respects  all  the  general  hygienic  and  symptomatic  methods  of 
treatment  recommended  for  common  chronic  bronchitis  (expectorants,  nar- 
cotics, fresh-air  rest  cures,  climatic  health  resorts,  etc.)  are  also  useful  in 
fetid  bronchitis.  The  sputum  should  be  disinfected  by  putting  strong  carbolic 
acid,  etc.,  into  the  sputum-cup  to  lessen  the  bad  odor.  It  is  a  very  good  plan 
to  keep  the  carbolic  spray  at  work  in  the  patient's  room  as  often  and  as  long 
as  possible ;  or  the  air  may  be  impregnated  with  oleum  pini  pumilionis. 


CHAPTEE    IV 


CROUPOUS    BRONCHITIS 

(Fibrinous  or  Pseudo-membranous  Bronchitis) 


Ceoupous  bronchitis  is  a  peculiar  form  of  disease  of  the  bronchial  mucous 
membrane,  of  very  rare  occurrence,  in  which  there  is  a  formation  of  extensive 
fibrinous  patches  in  the  bronchi.  Only  that  form  of  croupous  bronchitis  which 
occurs  primarily  in  the  bronchi  is  to  be  considered  here,  and  not  the  secondary 
form,  which  on  the  one  side  is  associated  with  diphtheria  in  the  pharynx  and 
larynx,  and  on  the  other  with  croupous  pneumonia. 

^Etiology. — The  aetiology  of  the  disease  is  as  yet  wholly  unknown.  From 
analogy  with  other  well-known  croupous  inflammations  of  mucous  membranes, 
we  must  look  here  for  some  noxious  influence  which  destroys  the  epithelium, 
but  up  to  this  time  we  are  entirely  ignorant  of  its  character.  Individuals  in 
youth  and  middle  age,  somewhere  between  ten  and  thirty  years  old,  are  the 
chief  victims.  Men  are  attacked  somewhat  more  frequently  than  women. 
The  disease  comes  on  either  in  persons  who  were  previously  healthy — the 
essential  fibrinous  or  croupous  bronchitis — or  in  those  who  have  already  suf- 
fered from  some  other  disease,  especially  some  chronic  pulmonary  affection — 
the  symptomatic,  secondary  croupous  bronchitis.  It  is  not  certain  whether 
the  last-named  cases  have  the  same  aetiological  relations  as  the  cases  of  genu- 
ine primary  fibrinous  bronchitis.  Fibrinous  bronchitis  has  been  observed  in 
the  course  of  typhoid  fever  and  other  acute  infectious  diseases. 

Symptoms  and  Course. — Primary  fibrinous  bronchitis  occurs  in  two  forms, 
acute  and  chronic.  The  acute  form  begins  quite  suddenly,  with  fever,  cough, 
pain  in  the  chest,  and,  as  a  rule,  severe  dyspnoea.  The  fibrinous  coagula,  which 
alone  render  the  diagnosis  possible,  appear  in  the  expectoration  either  at 
once,  or  after  the  existence  for  some  days  of  what  is  apparently  simple  catar- 
rhal bronchitis. 

These  coagula  form  complete  casts  of  the  bronchi,  and  are  more  or  less 
branching.     They  are  of  a  whitish  color  and  of  quite  a  dense,  elastic  con- 


CROUPOUS  BRONCHITIS  207 

sistencc.  The  main  stem  may  be  a  centimeter  thick,  and  from  il  the  further 
ramifications  extend,  dividing  diehotomously.  The  largesi  caste  are  L0  or  1~j 
cm.  long.  On  section,  we  usually  find  a  tree  lumen  within,  and  generally 
recognize  a  definite  laminated  structure  in  the  membrane.  In  many  places 
they  are  enlarged  and  swollen.  Microscopically,  we  find  white  blood  corpus- 
cles in  and  upon  the  hyaline  ground  suhstance  of  the  casts,  and  also  red  blood 
corpuscles,  sometimes  epithelial  cells,  and  quite  often  the  peculiar  pointed 
octahedral  crystals  which  are  also  found  in  the  expectoration  in  hronehial 
asthma  (vide  infra).  The  so-called  "spirals"  (vide  infra)  have  also  been 
found  in  the  expectoration  of  fibrinous  bronchitis.  Chemically  the  casts 
apparently  consist  of  coagulated  albumen.  It  is  doubtful  whether  they  actu- 
ally consist  of  fibrin.  Weigert's  fibrin  stain  does  not  affect  them.  Their  solu- 
bility in  alkalies,  especially  in  lime  water,  is  of  therapeutic  importance. 

On  coughing,  the  patient  usually  raises  a  simple  mucous  or  mucopurulent 
expectoration  besides  the  casts,  and  in  this  sputum  the  casts  are  imbedded. 
They  are  often  first  discovered  by  pouring  the  whole  amount  of  sputum  into 
water,  when  they  unfold  and  spread  out.  The  expectoration  also  contains  not 
infrequently  a  slight  admixture  of  blood. 

The  subjective  symptoms  of  the  patient  may  be  very  violent.  The  dyspnoea 
sometimes  attains  a  high  and  alarming  degree.  It  ceases  when  a  large  cast 
is  expectorated  after  a  severe  paroxysm  of  coughing.  Such  attacks  may  recur 
every  day  or  two.  In  other  cases,  however,  the  subjective  symptoms  are  com- 
paratively slight. 

Physical  examination  of  the  lungs  reveals  little  that  is  characteristic. 
In  uncomplicated  cases  percussion  shows  nothing  abnormal,  or  at  most  the 
signs  of  an  acute  emphysema.  Auscultation  gives  the  ordinary  signs  of  bron- 
chitis, not  characteristic  in  themselves,  such  as  rhonchi  or  moist  rales.  If  a 
large  bronchus  is  plugged,  the  respiratory  excursions  and  the  respiratory 
murmur  are  almost  entirely  absent  in  the  corresponding  portion  of  the  lung, 
but  after  the  expectoration  of  a  cast  respiration  becomes  once  more  audible. 

The  duration  of  acute  cases  is  sometimes  only  a  few  days,  at  most  a  few 
weeks.  In  favorable  cases  the  fever,  which  at  times  is  quite  high,  soon  disap- 
pears, the  respiratory  symptoms  grow  milder,  the  expectoration  of  the  casts 
ceases,  and  there  is  a  complete  and  permanent  recovery.  In  severe  cases, 
however,  death  often  ensues  with  all  the  symptoms  of  suffocation.  The  acute 
form  sometimes  becomes  chronic,  but  this  is  rare. 

The  chronic  form  of  fibrinous  bronchitis  may  last  for  years.  Usually  the 
condition  grows  worse  periodically,  at  varying  intervals  of  time,  and  at  each 
exacerbation  casts  are  expectorated,  while  in  the  interval  there  is  apparently 
merely  a  simple  bronchial  catarrh.  Some  observations  are  also  recorded  in 
medical  literature  of  persons  who  have  expectorated  these  casts  at  intervals 
for  years  without  any  special  disturbance  of  their  health  or  their  nutrition. 
In  some  cases  other  chronic  pulmonary  affections,  such  as  tuberculosis,  finally 
develop. 

The  pathological  anatomy  of  fibrinous  bronchitis  is  not  yet  satisfactorily 
known  on  account  of  the  rarity  of  the  affection.  The  changes  in  the  lungs 
found  at  the  autopsy  of  fatal  cases  have  usually  been  complications,  such  as 
pneumonia,  pleurisy,  or  tuberculosis,  which  stood  in  no  direct  relation  to  the 
fibrinous  bronchitis. 


208  DISEASES   OF  THE   RESPIRATORY  ORGANS 

Prognosis. — In  all  acnte  cases  the  prognosis  should  be  guarded,  for  we 
know  that  about  one  fourth  of  the  cases  terminate  fatally.  The  chronic 
cases,  as  has  been  said,  are  usually  very  protracted  and  are  subject  to  frequent 
exacerbations,  but  they  differ  from  the  acute  cases  in  being  much  less  dan- 
gerous. 

Treatment. — We  make  special  use  for  inhalations  of  those  remedies  which, 
as  we  have  said,  have  power  to  dissolve  the  casts.  We  usually  employ  a  two- 
to  five-per-cent  solution  of  carbonate  or  bicarbonate  of  sodium,  and  above  all 
lime  water,  either  pure  or  diluted  with  an  equal  volume  of  water.  The 
internal  administration  of  iodid  of  potassium,  in  doses  of  20  to  45  gr.  (gm. 
1.5  to  3.0)  a  day,  proves  of  advantage  in  many  cases.  Energetic  inunction 
with  mercurial  ointment  is  sometimes  of  service.  In  one  tedious  case  I 
tried  a  course  of  sweating  without  permanent  benefit.  Expectoration  of  the 
casts  may  be  aided  in  many  cases  by  such  drugs  as  senega  and  benzoic  acid, 
or  by  the  timely  use  of  emetics.  We  do  not  know  any  remedies  which  can 
prevent  a  return  of  the  attacks  in  the  chronic  form.  The  treatment,  except 
at  the  time  of  the  attacks,  is  the  same  as  in  ordinary  chronic  bronchial  catarrh. 


CHAPTEE    V 

WHOOPING    COUGH 

(Pertussis.     Tussis  convulsiva) 

iEtiology. — By  the  name  "  whooping  cough  "  we  mean  a  specific  disease 
of  the  mucous  membrane  of  the  air-passages,  which  is  seen  chiefly  in  children, 
and  is  characterized  by  a  peculiar  violent  and  paroxysmal  cough.  Sporadic 
cases  are  of  almost  constant  occurrence  in  large  cities,  but  the  disease  often 
appears  in  epidemic  outbreaks.  Epidemics  of  whooping  cough  follow  epi- 
demics of  measles  with  remarkable  frequency. 

Whooping  cough  is  without  doubt  contagious,  and  therefore  often  attacks 
one  child  after  another  in  the  same  family.  Kindergartens,  orphan  asylums, 
and  day  nurseries  aid  very  much  in  extending  the  disease.  The  contagious 
element  seems  to  be  connected  with  the  air  expired  by  the  patient,  particularly 
with  the  mucous  secretion  coughed  up.  Children  are  most  subject  to  an 
attack  up  to  the  age  of  six  years;  from  that  age  the  liability  to  the'  disease 
decreases  rapidly  with  increasing  years.  Whooping  cough  is  seen,  indeed, 
in  adults,  but  it  is  quite  rare,  and  almost  always  without  the  pronounced  fea- 
tures of  tussis  convulsiva. 

The  epidemic  onset,  the  contagiousness,  and  the  whole  course  of  the  disease 
favor  the  theory  of  its  infectious  nature.  The  presence  of  the  organisms  which 
are  supposed  to  be  the  poison  of  the  disease  has  not  yet  been  certainly  demon- 
strated, although  many  have  claimed  to  discover  characteristic  bacteria  in  the 
sputa  of  patients.  In  an  epidemic  in  Hamburg,  Jochmann  almost  constantly 
found  a  bacillus  present  that  closely  resembled  that  of  influenza.  However, 
the  question  as  to  the  cause  of  whooping  cough  is  not  definitely  solved.  If  a 
patient  has  once  had  the  disease,  he  is  almost  invariably  safe  from  a  second 
attack. 


WHOOPING  COUGH  209 

Symptoms  and  Course  of  the  Disease. — Whooping  cough  begine  with  the 
symptoms  of  a  catarrh  of  the  trachea  and  bronchi,  which  develops  more  or  less 
rapidly,  and  which  at  first  often  shows  nothing  characteristic.  We  can  ;it  this 
period  make  a  tolerably  probable  diagnosis  only  a1  a  time  when  an  epidemic 

is  prevailing,  or  in  case  the  child's  associates  have  already  been  attacked  with 
the  disease.  The  cough  is  often  very  persistent,  obstinate,  and  severe  at  the 
beginning,  but  it  does  not  yet  come  on  in  distinct  paroxysms.  Examination 
of  the  chest  shows  nothing  peculiar  except  a  few  rhonchi.  There  is  often  a 
coryza,  with  frequent  sneezing,  and  there  is  sometimes  a  mild  conjunctivitis. 
The  child  is  restless  and  feverish,  especialy  toward  night.  The  temperature 
may  repeatedly  reach  103°  or  101°  F.  (39°  to  40°  C.)  in  this  initial  fever. 
The  duration  of  this  first  so-called  catarrhal  stage  varies,  but  it  usually  lasts  a 
week  or  ten  days. 

The  catarrhal  stage  gradually  passes  into  the  second,  convulsive  stage, 
without  any  sharp  boundary.  The  cough  becomes  more  violent,  and  comes  on 
in  the  separate  paroxysms  of  whooping  cough  which  are  characteristic  of  the 
disease.  We  do  not  know  the  particular  reason  why  the  cough  has  this  parox- 
ysmal character,  but  a  nervous  factor  probably  plays  the  chief  part  in  it. 

The  peculiarity  of  the  attack  consists  in  the  violent,  paroxysmal  fits  of 
coughing,  which  are  from  time  to  time  interrupted  by  deep,  long-drawn,  loud, 
and  shrill  inspirations,  due  to  the  occurrence  of  a  spasmodic  contraction  of  the 
glottis.  Exceptionally  there  are  cases  without  this  loud  whistling  inspiration. 
The  child  becomes  markedly  cyanotic  during  the  attack,  the  veins  in  the  neck 
swell,  and  tears  come  into  the  eyes.  Hemorrhage  into  the  conjunctiva, 
nosebleed,  and  in  some  cases  hemorrhages  into  other  organs,  as  the  ear  and 
the  skin,  often  come  on  as  a  result  of  this  stasis.  Vomiting  very  often  occurs 
either  during  a  paroxysm  or  at  its  close.  Involuntary  evacuations  of  urine 
and  feces  may  also  follow  from  the  violent  contraction  of  the  abdominal  mus- 
cles. Exceptionally  we  observe  still  more  severe  symptoms  with  a  paroxysm : 
a  complete  spasmodic  cessation  of  respiration  with  imminent  danger  of  suffo- 
cation, or  sometimes  general  convulsions.  In  two  cases  we  have  seen  hemi- 
plegia in  children  which,  according  to  the  positive  statements  of  their  parents, 
came  on  suddenly  during  a  severe  attack  of  whooping  cough.  It  is  still  unde- 
termined whether  these  "  whooping-cough  hemiplegias  "  are  due  to  an  actual 
cerebral  hemorrhage  or  whether  they  come  from  the  enormous  venous  stasis 
in  the  brain. 

The  paroxysms  vary  with  the  severity  of  the  disease,  frequently  appearing 
ten  or  fifteen  times  in  twenty-four  hours ;  sometimes  with  greater  frequency — 
fifty  times  or  more.  They  also  occur  at  night  as  often  or  even  oftener  than 
in  the  daytime.  They  come  on  either  spontaneously  or  from  some  special 
predisposing  cause.  The  attacks  which  come  on  during  eating  cause  the  most 
disturbance,  because  the  food  taken  is  almost  always  vomited  again.  In  chil- 
dren with  whooping  cough  we  can  often  excite  a  spasm  at  any  time — and  this 
is  important  in  diagnosis — by  putting  a  spatula  in  the  mouth,  by  pressing  on 
the  larynx,  or  by  making  the  child  cry.  If  there  are  several  children  with 
whooping  cough  in  the  same  room  and  a  paroxysm  attacks  one  of  them,  the 
others,  as  a  rule,  soon  begin  to  cough,  too.  Some  prodromal  symptoms  often 
precede  the  peculiar  paroxysm,  such  as  general  uneasiness,  rapid  respiration, 
or  vomiting.  At  the  end  of  a  paroxysm  many  children  are  very  feeble  and 
14 


210  DISEASES   OF   THE   RESPIRATORY  ORGANS 

exhausted,  but  others  recover  rapidly,  and  are  playing  again  quite  briskly  a 
few  minutes  after. 

In  general  the  child  feels  quite  well  in  the  interval  between  the  paroxysms, 
but  the  effects  of  the  violent  attacks  of  coughing  ma}r,  of  course,  often  be  seen. 
Besides  the  occasional  hemorrhages  into  the  conjunctiva,  we  find  the  eyelids 
somewhat  swollen,  their  veins  dilated  and  blue,  and  visible  through  the  skin. 
Many  children  grow  very  thin  from  the  repeated  vomiting.  A  small  ulcer  is 
quite  frequently  formed  on  the  frgenum  of  the  tongue,  the  origin  of  which  is 
to  be  referred  to  mechanical  causes.  The  tongue  is  violently  protruded  in  the 
severe  paroxysms  of  coughing,  and  the  fraanum  is  thus  torn,  or  injured  by  the 
sharp  lower  incisors. 

Physical  examination  of  the  lungs  shows  nothing  abnormal  in  uncompli- 
cated cases  except  a  few  moist  rales  or  rhonchi.  Sometimes  the  rhonchi  are 
wanting,  or  are  present  in  small  numbers  only  a  short  time  before  a  paroxysm, 
but  in  other  cases  an  intense  diffuse  bronchitis  is  developed,  which  often  leads 
to  the  development  of  a  lobular  pneumonia  (vide  infra).  Sometimes,  but  not 
always,  there  is  an  acute  catarrhal  inflammation  of  the  bronchi,  and  especially 
of  the  posterior  wall  of  the  larynx. 

The  fever,  which  is  usually  present  in  the  first  or  catarrhal  stage,  is  absent 
in  the  convulsive  stage.  The  child  is  free  from  fever  for  the  most  part.  We 
often  find  a  slight  rise  of  temperature  up  to  100°  or  101°  F.  (38°  to  38.5°  C), 
but  only  toward  night.  Higher  and  more  persistent  fever  points  to  the  devel- 
opment of  complications,  especially  on  the  part  of  the  lungs. 

The  convulsive  stage  seldom  lasts  less  than  three  or  four  weeks,  and  often 
much  longer,  up  to  three  or  four  months.  The  paroxysms  gradually  become 
less  frequent  and  less  violent  (stadium  decremehti),  until  they  finally  disap- 
pear entirely;  but  relapses  and  fresh  exacerbations  also  occur  in  this  stage. 
A  certain  "  irritability "  of  the  bronchial  mucous  membrane  remains  for  a 
long  time  after  whooping  cough.  Finally,  however,  the  disease,  in  uncom- 
plicated cases,  goes  on  to  a  permanent  and  complete  recovery. 

Complications  and  Sequelae. — The  severe  results  which  sometimes  follow 
whooping  cough  are  probably  due  in  part  to  the  direct  action  of  the  specific 
causes  of  the  disease,  and  in  part  to  complications  of  a  secondary  nature  whose 
development  is  merely  favored  by  the  whooping  cough.  The  most  important 
are  complications  in  the  lungs.  A  lobular  catarrhal  pneumonia  often  develops 
after  a  severe  bronchitis  which  involves  the  finer  bronchi.  In  such  cases  the 
respiration  becomes  hurried  and  superficial,  the  fever  higher,  and  the  general 
condition  bad  even  in  the  times  between  the  paroxysms.  On  examination  of 
the  lungs  we  hear  numerous  moist  rales,  especially  over  the  lower  lobes;  and 
we  can  sometimes  make  out  dullness  on  one  or  both  sides,  if  there  is  exten- 
sive pneumonic  infiltration.  Such  cases  are  always  very  protracted,  and  many 
children  succumb,  partly  from  the  disturbance  of  respiration  and  partly  from 
general  weakness  and  inanition. 

Complications  in  other  organs  are  much  rarer.  Among  the  most  frequent 
are  attacks  of  diarrhea  which  impair  the  child's  nutrition.  Many  observers 
have  also  mentioned  the  quite  frequent  occurrence  of  a  croupous  or  diph- 
theritic inflammation  in  the  pharynx  and  larynx  in  the  course  of  whooping 
cough.  Finally,  a  case  under  our  own  observation  may  here  be  mentioned,  in 
which  death  occurred  with  severe  nervous  symptoms,  convulsions,  and  coma. 


WHOOPING    ( 'OIK ill  211 

At  tlio  autopsy   wry    numerous   capillary    hemorrhages    were    found    in    the 
brain. 

Pulmonary  emphysema  is  the  first  thing  to  be  mentioned  among  the 
sequelae  of  whooping  cough.  From  the  marked  pressure  which  the  severe  and 
frequent  outbursts  of  coughing  exert  from  within  upon  the  alveoli  of  the 
lungs,  they  gradually  become  dilated.  An  acute  lobular  emphysema  ("acute 
pulmonary  inflation")  is  set  up,  which  sometimes  passes  into  a  typical 
chronic  pulmonary  emphysema  (q.  v.).  Chronic  bronchial  catarrh  may  also 
remain  for  a  long  time  after  an  attack  of  whooping  cough.  We  have  already 
stated  (see  page  197)  that  many  incurable  cases  of  chronic  bronchitis  in 
adults  are  to  be  referred  to  an  attack  of  whooping  cough  in  childhood. 

A  third  important  sequel  of  whooping  cough  is  pulmonary  tuberculosis. 
The  bronchitis  and  lobular  pneumonia  which  occur  during  whooping  cough 
sometimes  do  not  improve,  especially  in  weak  children  with  a  tuberculous 
tendency.  The  fever  continues  high,  the  child  grows  thin,  and  constantly 
becomes  more  and  more  miserable.  At  the  autopsy  we  find  cheesy  nodules 
in  the  lungs,  cheesy  bronchial  glands,  and  at  times  tuberculosis  of  other  organs. 
These  cases  signify  that  when  a  tuberculous  infection  is  present,  but  is  still 
latent,  the  whooping  cough  acts  as  an  exciting  cause  for  the  outbreak  of  the 
disease,  or  that  a  greater  receptivity  to  infection  with  tuberculous  poison  is 
created  by  the  whooping  cough.  Mobius  has  lately  reported  the  occurrence, 
in  a  few  cases,  of  paralysis  as  a  sequel  of  whooping  cough.  This  usually  begins 
in  the  lower  and  extends  to  the  upper  extremities,  and  is  due  apparently  to 
neuritis. 

Diagnosis. — The  diagnosis  of  whooping  cough  cannot  be  made  with  cer- 
tainty, as  we  have  said,  until  the  second  or  convulsive  stage.  It  is  easy  then, 
however,  since  the  characteristic  attacks  occur  in  no  other  affection  of  the 
lungs  in  like  manner  and  with  like  frequency  and  duration.  If  we  have  no 
opportunity  to  observe  the  attack  itself,  and  have  to  depend  upon  the  descrip- 
tion of  the  friends,  the  diagnosis  is  sometimes  more  uncertain;  but  the  ac- 
counts of  the  occurrence  of  cough,  in  individual  paroxysms  associated  with 
vomiting,  are  usually  so  characteristic  that  errors  are,  on  the  whole,  rare. 
Furthermore,  the  child  between  the  paroxysms  usually  presents  certain  signs : 
he  has  a  bloated  aspect,  or  we  may  find  slight  hemorrhages  into  the  conjunc- 
tiva, or  ulcers  on  the  frsenum  of  the  tongue,  which  make  the  diagnosis  highly 
probable.  Under  some  circumstances  we  may  also  make  the  attempt  to  bring 
on  the  paroxysm  artificially  (vide  supra).  In  adults,  as  we  have  said,  the 
attacks  are  rarely  as  characteristic  as  in  children.  There  are  usually  the 
symptoms  of  a  more  or  less  severe  bronchitis  with  obstinate  paroxysmal  cough, 
but  without  the  characteristic  attacks  and  usually  without  vomiting.  The 
diagnosis  of  whooping  cough,  therefore,  rests  mainly  upon  the  existence  of 
special  astiological  conditions  (the  coexistence  of  the  disease  in  children,  etc.). 

Prognosis. — The  prognosis  is  favorable  with  the  majority  of  children  if 
they  are  previously  strong  and  healthy.  Very  young  children  are  in  more 
danger  than  older  ones.  [Under  two  years  there  is  great  danger,  and  over 
five  scarcely  any.  It  has  been  said  that  whooping  cough  causes  one  fourth  the 
total  mortality  of  children  in  London.]  There  is  danger  if  secondary  pneu- 
monia develops,  and  if  the  general  nutrition  and  strength  of  the  child  suffer. 
As  soon  as  the  diagnosis  is  certain  we  must  call  the  attention  of  the  parents 


212  DISEASES   OF  THE   RESPIRATORY   ORGANS 

to  the  probable  long  duration  of  the  disease.  Eegard  must  also  be  paid  to 
the  possibility  of  the  development  of  sequela?,  especially  in  weak  children 
susjDectecl  of  tuberculosis.  I  am  convinced  that  many  cases  of  lifelong  chronic 
bronchitis  are  referable  in  the  tinal  analysis  to  an  attack  of  whooping  cough 
in  childhood. 

Treatment. — Since  the  disease  is  protracted  and  is  not  devoid  of  danger, 
it  is  our  duty,  when  an  epidemic  of  whooping  cough  prevails,  to  guard  chil- 
dren from  it  as  far  as  possible.  If  one  child  in  a  family  is  taken  ill,  the 
other  children  must  be  rigorously  kept  away  from  him.  If  circumstances 
permit,  it  is  better  to  send  them  away  to  another  place  free  from  whooping 
cough. 

With  regard  to  the  treatment  of  the  disease,  we  must  first  endeavor  to 
fulfill  general  dietetic  and  hygienic  indications.  The  child  should  breathe 
good,  pure  air,  and  for  this  reason  it  is  often  advisable  to  transfer  the  patient 
to  a  larger  room,  with  as  much  air  and  sunlight  as  possible.  The  atmosphere 
should  not  be  too  dry,  and  it  is  advisable  to  employ  a  spray  of  water  (carbolic 
solution)  frequently,  or  to  hang  up  moist  sheets  in  the  room.  In  good  weather 
the  child  should  be  out  of  doors  a  large  part  of  the  time,  provided  fever  has 
ceased.  City  children  are  to  be  sent,  if  possible,  into  the  country.  The  food 
should  be  good  ar.d  nourishing,  but  dry  and  crumbly  articles  should  be 
avoided,  being  apt  to  excite  cough.  "Warm  or  lukewarm  baths  frequently  prove 
very  beneficial,  particularly  when  there  is  considerable  bronchitis,  as  they 
lessen  the  danger  of  a  lobular  pneumonia. 

The  medicinal  treatment  of  whooping  cough  has  not  yet  shown  brilliant 
results  despite  the  large  number  of  remedies  recommended.  During  the 
catarrhal  stage  it  is  usually  sufficient  to  give  a  simple  expectorant  (ipecac, 
etc.)  and  plenty  of  warm  drink.  In  the  convulsive  stage  the  best  remedies 
to  try  are  quinin,  antipyrin,  belladonna,  bromid  of  potassium,  and  bromo- 
form.  The  latter  has  been  much  recommended  of  late.  Quinin  is  given  in 
powders  of  1.5  to  8  gr.  (gm.  0.1  to  0.5)  several  times  a  day,  either  in  cap- 
sules, or,  in  the  case  of  smaller  children,  with  chocolate.  The  earlier  this 
remedy  is  employed  the  more  prompt  is  said  to  be  its  beneficial  influence. 
Antipyrin  is  at  present  used  more  frequently  than  quinin,  and  in  doses  of  4 
to  8  gr.  (gm.  0.25  to  0.5)  several  times  a  day  it  often  produces  distinct 
improvement.  Belladonna  is  prescribed  in  powders  containing  yV  to  ^  gr. 
(gm.  0.005  to  0.01)  of  the  extract  of  belladonna,  giving  three  to  five  such 
powders  a  day.  This  remedy  has  often  seemed  to  the  author  to  diminish  the 
number  and  violence  of  the  paroxysms.  Bromid  of  potassium  is  employed 
in  an  aqueous  solution  in  the  dose  of  15  to  45  gr.  per  diem  (gm.  1  to  3).  Its 
efficacy  is  probably  due  to  its  power  to  diminish  reflex  excitability.  The  same 
drug  employed  in  an  atomizer  often  has  a  palliative  effect.  Bromoform  is 
the  remedy  most  used  of  late;  two  to  five  drops  or  more  are  given  several 
times  a  day  in  sweetened  water  or  fruit  juice.  It  is  readily  taken,  and  it 
seems  to  act  favorably  both  on  the  severity  of  the  individual  attacks  and  on 
-the  whole  course  of  the  disease.  Finally,  we  might  mention  a  recent  prepara- 
tion called  "  pertussin  "  that  has  been  widely  praised  for  its  results.  It  is 
a  fluid  extract  of  thyme,  and  is  given  in  teaspoonful  doses  three  or  four  times 
a  day.  Pyrenol  (gr.  v  [gm.  0.3]  three  times  a  day)  is  also  said  to  be 
effectual. 


BRONCHIECTASI 8  213 

If  the  paroxysms  are  very  violent  we  may  cautiously  administer  small  doses 
of  morphin  or  codeia.  [nhalations  of  chloroform  and  ether  have  also  been 
recommended.    The  following  mixture  is  a  suitable  one: 

1$  Chloroformi    5.J       (30c.c); 

iEtheris   rjij      (60c.c.); 

01.   terebinthinaa    3ijss.  (lOc.c.). 

M. 

Sig.  One  or  two  teaspoonfuls  to  be  poured  upon  a  pocket  handkerchief  for 
inhalation.  >-  t  .    - 

Finally,  efforts  have  been  repeatedly  made  to  lessen  the  frequency  and  the 
severity  of  the  attacks  by  anaesthetizing  the  pharynx  and  larynx  by  painting 
with  a  ten-  to  fifteen-per-cent  solution  of  coca  in.  Michael  advocates  the 
daily  insufflation  into  the  nostrils  of  powdered  benzoin.  Neither  method  of 
treatment  has  succeeded  in  establishing  itself  in  practice.  Numerous  attempts 
have  been  made  to  reduce  the  number  of  paroxysms  by  inhalations  of  the  most 
diverse  remedies.  Because  of  the  infectious  nature  of  the  disease,  frequent 
inhalations  of  one-  to  two-per-cent  solutions  of  carbolic  acid  were  employed. 
The  results  were  not  striking,  and  the  danger  of  poisoning  (as  evidenced  by 
the  urine)  must  not  be  lost  sight  of.  Turpentine  or  benzine,  20  to  30  drops 
poured  on  a  sponge  moistened  with  hot  water,  is  more  to  be  recommended. 
Inhalations  of  bromid  and  salt  solution  (sodii  bromidi,  sodii  chloridi,  aa 
gr.  xxxviij  [gm.  2.5],  aq.  destillat.,  §vij  [gm.  200])  are  also  worthy  of  trial. 
Turpentine  and  especially  terpin  hydrate  (gr.  vij,  gm.  0.5,  thrice  daily) 
are  also  given  internally.  [Farlow  and  others  report  marked  success  from 
spraying  the  upper  air-passages  with  a  two-per-cent  solution  of  resorcin.] 

In  many  cases  we  finally  content  ourselves  with  taking  good  general  care 
of  the  child,  and,  if  the  weather  permit,  with  keeping  him  as  much  as  possible 
in  the  open  air.  For  the  detailed  treatment  of  the  complications  and  sequelae 
of  whooping  cough  the  reader  is  referred  to  the  appropriate  chapters  of  this 
book. 


CHAPTER    VI 

BRONCHIECTASIS 

(Bronchial  Dilatation) 

Dilatation  of  the  bronchi  is  usually  not  a  separate  disease^  but  it  is  a 
result  of  various  affections  of  the  lungs  and  bronchi.  Nevertheless,  we  will 
speak  of  it  briefly  in  this  connection  since  many  cases  actually  present  a  very 
characteristic  clinical  picture. 

We  distinguish  anatomically  the  cylindrical  and  saccular  bronchiectases. 

CYLINDRICAL   BRONCHIECTASIS 

Cylindrical  bronchiectasis  consists  of  a  uniform  dilatation  of  a  bronchial 
tube,  and  occurs  most  frequently  in  the  medium-sized,  or  rarely  in  the  finer 


214  DISEASES   OF  THE   RESPIRATORY   ORGANS 

bronchi  of  one  or  more  lobes  of  the  lung.  We  usually  find  at  the  autopsy 
that,  on  slitting  up  the  bronchi,  the  point  of  the  scissors  can  easily  be  pushed 
through  the  dilated  bronchial  tube  close  up  to  the  pleura.  Cylindrical  bronchi- 
ectasis is  usually  due  to  a  long-continued  bronchitis,  and  develops  most  fre- 
quently in  cases  of  emphysema,  and  also  in  whooping  cough,  measles,  and 
sometimes  in  phthisis,  etc.  The  primary  process  is  probably  always  the  atrophy 
which  follows  the  catarrh,  and  the  diminished  resistance  of  the  bronchial  walls 
thus  occasioned.  The  dilatation  of  the  lumen  of  the  bronchus  is  produced 
gradually,  partly  by  the  traction  of  the  thorax  during  inspiration,  and  still 
more  hj  the  increased  pressure  in  the  bronchi  due  to  the  frequent  and  violent 
fits  of  coughing,  and  finally,  perhaps,  by  the  constant  pressure  of  the  stagnat- 
ing secretion. 

The  diagnosis  of  C3dindrical  dilatation  of  the  bronchi  is  only  a  probable 
one.  We  suspect  that  a  bronchiectasis  has  formed  if  the  conditions  are  ful- 
filled which  we  know  lead  to  it.  In  the  chronic  bronchial  catarrh  of  emphy- 
sema we  judge  that  there  is  cylindrical  dilatation  of  the  bronchi  if  the  secre- 
tion is  very  abundant  and  comparatively  thin,  and  separates  into  layers  on 
standing  in  a  sputum-cup.  The  dilatation  is  usually  emptied  by  a  severe 
paroxysm  of  coughing,  such  as  is  apt  to  occur  in  the  morning  if  the  secretion 
collects  in  great  quantity  during  the  night.  Physical  examination  usually 
gives  numerous,  feeble,  fine,  and  medium  nonresonant  moist  rales,  especially 
in  the  lower  lobes.  The  respiratory  murmur  sometimes  loses  its  vesicular 
character  in  marked  cylindrical  bronchiectasis,  and  has  a  more  indefinite  and 
blowing  or  whispering  quality.  Sometimes  it  is  quite  obscured  in  the  lower 
part  of  the  lung  by  the  abundant  rales. 

SACCULAR   BRONCHIECTASES 

Saccular  bronchiectases  are  spherical  or  oval  dilatations  which  are  usually 
confined  to  a  definite  portion  of  the  bronchial  tree.  Several  larger  and  smaller 
bronchiectases  are  generally  found;  the  larger  are  usually  not  bigger  than 
a  cherry  or,  at  most,  a  walnut.  The  bronchus  passes  suddenly  or  gradually 
into  the  dilatation,  and  it  is  often  obliterated  so  that  the  bronchiectasis  forms 
a  completely  closed  cavity.  The  wall  of  a  saccular  bronchiectasis  loses  in  great 
measure  the  character  of  the  normal  bronchial  wall.  As  a  rule  it  is  atrophied 
to  a  high  degree,  the  atrophy  involving  not  only  the  mucous  glands,  but  also 
the  muscular  fibers,  the  elastic  elements,  and  even  the  cartilages,  so  that  the 
bronchiectatic  cavities  seem  lined  with  nothing  but  a  thin  membrane.  The 
occurrence  of  many  dilated  vessels  in  the  walls  of  a  bronchiectasis  is  due  per- 
haps to  an  atrophy  of  the  vessel  walls  and  is  a  symptom  of  clinical  importance 
(vide  infra).  In  other  cases,  however,  we  find  hypertrophic  processes,  which 
involve  the  connective  tissue  of  the  mucous  membrane,  and  lead  to  band- 
like projections  and  swellings.  Finally,  ulcerative  processes  may  develop  on 
the  inner  surface  of  a  bronchiectasis  and  attack  the  surrounding  lung  tissue, 
and  change  the  bronchiectatic  cavity  into  a  typical  ulcerating  cavity. 

Only  rarely,  for  example  in  emphysema,  clo  we  find  a  single  saccular 
bronchiectasis  surrounded  by  tolerably  normal  lung  tissue.  Its  origin,  then, 
is  to  be  referred  to  causes  like  those  which  have  been  given  above  for  the 
commoner  cylindrical  bronchiectases.     In  the  great  majority  of  cases  we  find 


BRONCHIECTASIS  215 

saccular  bronchiectases,  singly  or  in  large  numbers,  surrounded  by  indurated 
ami  contracted  lung  tissue.  They  form  one  of  the  complications  of  "pul- 
monary contraction"  [fibroid  phthisis],  which  is  almost  always  associated 
with  contraction  of  the  pleura.  Since  Corrigan's  day  we  have  with  good 
reason  looked  upon  this  contraction  as  the  chief  cause  for  their  origin.  By  the 
gradual  shrinking  and  retraction  of  the  lung,  which,  as  a  rule,  has  become 
adherent  to  the  costal  pleura,  a  traction  is  exerted  upon  the  bronchial  walls 
from  without  to  which  they  gradually  yield.  In  like  manner  increased 
inspiratory  efforts  as  well  as  the  stagnation  and  pressure  of  the  secretion 
work  at  the  same  time  to  dilate  the  bronchial  tube,  especially  where  the 
bronchial  wall  is  abnormally  yielding  as  a  result  of  disease. 

^Etiology. — The  question  of  the  origin  of  bronchiectasis  is  thus  directly 
associated  with  that  of  primary  pulmonary  contraction.  In  this  connection, 
careful  inquiry  into  the  past  history  of  cases  shows  that  the  disease  in  very 
many  instances  is  referable  to  some  previous  acute  inflammatory  condition. 
This  often  is  an  acute  croupous  pneumonia,  or  sometimes  a  broncho-pneu- 
monia after  measles,  influenza,  whooping  cough,  etc.  These  pulmonary  affec- 
tions are  followed  by  chronic  interstitial  inflammation  with  secondary  bron- 
chiectatic  developments.  Inasmuch  as  pleurisy  is  so  often  associated  with  the 
original  pneumonia,  earlier  observers  (Laennec,  for  example)  concluded  that 
the  disease  started  in  the  pleura,  and  from  there  extended  to  the  lung.  This 
view,  however,  cannot  be  maintained.  Whenever  the  vestiges  of  a  previous 
pleurisy  can  be  demonstrated,  this  has  been  invariably  either  a  metapneumonic 
pleurisy  or  an  empyema.  In  some  cases  the  evidences  of  bronchiectasis  fol- 
low upon  a  pneumonia  so  rapidly  that  we  may  actually  speak  of  an  "  acute 
bronchiectatic  formation"  (vide  Criegern).  Here  we  are  probably  dealing 
with  circumscribed  metapneumonic  abscesses,  which,  after  discharging  their 
contents  into  the  bronchi,  become  permanent  cavities.  In  all  but  a  small 
percentage  of  bronchiectatic  cases  it  is  possible  to  demonstrate  an  acute  pneu- 
monic origin.  In  these  exceptional  instances  we  have  to  assume  that  the 
process  from  its  incipiency  was  of  a  chronic  inflammatory  nature,  somewhat 
similar  to  that  resulting  from  the  inhalation  of  dust,  foreign  bodies,  and  the 
like.  It  is  worthy  of  note  that  bronchiectasis  develops  oftenest  in  early  life. 
Corresponding  to  the  most  frequent  location  of  pneumonia,  bronchiectasis 
generally  occurs  in  the  lower  lobes  of  the  lungs,  less  frequently  in  the  right 
middle  lobe,  and  far  more  rarely  in  the  upper  lobes.  As  a  rule,  the  disease  is 
unilateral,  or,  at  least,  involves  one  lung  to  a  much  greater  extent  than  the 
other.  In  the  less  affected  lung  only  slight  secondary  changes  (emphysema, 
bronchitis)  are  to  be  found. 

"  Pure  "  cases  of  bronchiectasis  have  nothing  to  do  with  tuberculosis.  Be- 
fore the  discovery  of  the  tubercle  bacillus  there  was,  of  course,  confusion  be- 
tween bronchiectatic  and  chronic  contraction  of  the  lungs;  but  we  must 
remember  that,  under  some  circumstances,  chronic  tuberculosis  may  lead  to 
the  formation  of  bronchiectasis,  and  that,  on  the  other  hand,  in  bronchiectatic 
processes  there  is  not  infrequently  a  secondary  development  of  tuberculosis. 
There  are  cases  in  which  it  is  hard  to  decide,  even  at  the  autopsy,  whether  an 
existing  chronic  contraction  in  a  portion  of  the  lung,  with  induration  of  tissue 
and  the  formation  of  bronchiectasis,  was  originally  tubercular  or  of  some  other 
nature. 


216  DISEASES   OF   THE   RESPIRATORY   ORGANS 

Symptoms  and  Course  of  the  Disease. — The  symptoms  of  saccular  bronchi- 
ectasis are  obtained  in  part  from  physical  examination  and  in  part  from 
observation  of  the  sputum  and  of  the  general  course  of  the  disease.  If  great 
bronchiectatic  cavities  lie  near  the  chest  wall,  they  may  give  the  same  physical 
signs  that  we  shall  learn  to  recognize  later  in  the  description  of  tuberculous 
cavities.  Bronchiectases  lying  within  the  lung,  however,  are  often  devoid  of 
definite  physical  signs,  so  that  at  most  we  may  suspect  them  from  other  symp- 
toms, such  as  the  peculiarities  of  the  sputum.  The  more  abundant  the  forma- 
tion of  bronchiectases  the  more  does  the  respiration  lose  its  vesicular  charac- 
ter and  become  harsh  and  finally  bronchial.  Inasmuch  as  there  is  usually  a 
very  considerable  secretion  of  mucus,  we  generally  find,  upon  auscultation, 
abundant  medium  and  even  coarse  moist  rales.  But  the  rales,  of  course,  vary 
in  number  and  in  quality,  according  to  the  expectoration  and  the  amount  of  se- 
cretion. Where  there  are  dense  pleural  adhesions  the  respiratory  murmur  i& 
very  feeble,  and  often  then  only  coarse,  indefinite  bronchial  rales  are  audible. 
The  percussion  note  over  the  bronchiectatic  j)ortion  of  the  lung  is  usually  dull 
or  dull-tympanitic,  a  result  of  the  chronic  interstitial  pneumonia  about  the 
bronchiectasis.  The  whole  thorax  near  an  extensive  bronchiectasis  is  often 
much  retracted  and  distorted.  In  consequence  the  heart  and  the  mediastinum 
may  be  greatly  displaced.  X-ray  examination  gives  us  very  valuable  informa- 
tion concerning  the  general  situation  of  the  thoracic  organs. 

The  expectoration  is,  as  a  rule,  very  abundant,  and  it  is  often  raised  by 
large  mouthfuls.  On  standing,  as  a  result  of  its  thin  fluid  character,  it  ex- 
hibits a  distinct  division  into  an  upper  frothy,  mucopurulent  layer,  a  middle 
mucoserous  layer,  and  a  lower  purulent  layer.  It  usually  has  a  peculiar  stale, 
sweetish  odor,  but  it  may  be  fetid.  The  latter  characteristic  is  almost  always 
associated  with  stagnation  of  the  secretion.  So  long  as  the  expectoration  is 
loose  and  easily  evacuated,  it  is  not  fetid  and  the  patient  feels  well.  Then  a 
cessation  of  the  expectoration  may  ensue.  The  patient  feels  poorly,  there 
may  be  a  slight  rise  of  temperature,  and  the  expectoration  becomes  scanty  and 
has  a  stinking  fetid  character.  Periods  of  improvement  may  thus  alternate 
with  exacerbations.  It  is  a  favorable  sign  when  the  amount  of  the  expectora- 
tion decreases,  provided  that  it  does  not  become  fetid  and  that  the  patient 
does  not  feel  worse.  Since  bronchiectasis  may  give  rise  to  a  permanent  fetid 
bronchitis,  and  since,  on  the  other  hand,  as  we  have  said,  fetid  bronchitis 
itself  often  leads  to  the  formation  of  bronchiectasis,  we  can  understand  the 
manifold  interrelations  and  transitions  which  the  two  forms  of  disease  present. 

Sometimes  large  quantities  of  secretion  collect  during  the  night  or  the 
day,  and  then  finally  the  expectoration  becomes  particularly  profuse.  Certain 
positions  or  postures  (such  as  stooping)  also  induce  strong  paroxysms  of 
coughing.  Quincke  has  shown  that  by  lowering  the  upper  part  of  the  thorax 
and  placing  the  patient  in  a  lateral  posture,  one  can  often  artificially  empty 
a  bronchiectatic  cavity  in  the  lower  lobe  of  the  lung  (Quincke's  procedure). 
This  is  of  some  diagnostic  value. 

The  not  infrequent  pulmonary  hemorrhages  in  bronchiectasis  are  of  great 
clinical  importance.  A  few  red  blood  cells  are  almost  invariably  found  in  the- 
sputum.  A  mucoid  sputum  resembling  raspberry  jelly  is  sometimes  coughed 
up;  such  sputum  is  intimately  mixed  with  blood.  Larger  hemorrhages  are 
due  to  rupture  of  the  dilated  vessels  (vide  supra)  in  the  walls  of  the  bron- 


BRONCHIECTASIS  217 

chiectasis.  They  may  also  be  due  to  ulcerative  processes.  Slight  precursors 
may  precede  a  severe  hemoptysis.  The  hemorrhage  may  be  very  abundant, 
and  it  may  be  repeated  during  a  Long  period— several  weeks — so  that  tin- 
patient  becomes  extremely  anaemic.  Finally,  the  hemorrhages  cease  and  the 
patient  improves  quite  rapidly.  Such  attacks  of  hemoptysis  may  be  repeated 
very  often  in  the  course  of  the  year.  When  we  hear  comparatively  well-nour- 
ished patients  with  lung  disease  say  that  they  have  suffered  for  years  from 
frequent  and  severe  hemoptyses,  we  can  usually  infer,  from  such  statements, 
that  there  is  a  saccular  bronchiectasis. 

The  whole  course  of  the  disease  is  very  variable,  but  it  usually  lasts  for 
many  years.     It  is  doubtful  whether  a  saccular  bronchiectasis  can  actually  lie 


Fig.  41. — Drumstick  fingers  in  a  case  of  bronchiectasis  (personal  observation). 

cured;  but  if  no  more  serious  sequela  occur,  many  patients  may  live  for 
years  in  a  tolerable  condition,  and  may  even  reach  an  advanced  age.  The  gen- 
eral nutrition  often  remains  very  good,  although  a  certain  very  characteristic, 
anaemic,  cyanotic,  pale  tinge  of  the  skin  gives  even  to  corpulent  patients  an 
unmistakable  morbid  appearance.  A  very  characteristic  sign,  present  in 
nearly  all  cases,  is  that  the  terminal  phalanges  of  the  fingers  gradually 
become  clubbed  and  thickened,  and  the  nails  are  much  bent,  and  often  have  a 
peculiar  glossiness  (see  Fig.  41).  The  cause  of  these  changes  is  to  be  sought 
for  in  the  action  of  absorbed  toxic  and  septic  material.  On  this  basis,  the 
attempt  has  even  been  made  to  explain  the  extensive,  chronic  bone  and  joint 
hyperplasias  ("  osteoarthropathie  hypertrophiante  "  of  P.  Marie)  observed  in 
bronchiectasis.  Acute  "  rheumatoid  "  joint  swellings  also  are  not  very  rarely 
seen  in  this  disease. 

Complications. — Intercurrent  febrile  complications  from  secondary  acute 
pneumonic   processes,   pleurisy,   gangrene,   and   the   like,    sometimes    set   in. 


218  DISEASES   OF   THE   RESPIRATORY   ORGANS 

Such  complications  may  frequently  recur  in  the  course  of  years,  until  they 
finally  lead  to  an  incurable  and  serious  state.  Some  patients  are  also  in 
danger  because  of  their  hearts  (secondary  hypertrophy  of  the  right  ventricle), 
and  oedema  may  set  in.  Amyloid  disease  of  the  internal  organs,  especially 
the  kidneys,  develops  in  some  cases.  Finally,  metastatic  brain  abscess  should 
be  mentioned  as  a  rare  complication. 

Diagnosis. — In  most  instances  the  diagnosis  of  the  chronic  pulmonary  affec- 
tion, as  such,  is  easy.  An  exact  conclusion  is  sometimes  difficult,  however, 
especially  as  regards  a  differentiation  from  chronic  pulmonary  tuberculosis. 
The  special  features  to  take  into  consideration  are  the  general  appearance,  the 
clubbed  fingers,  the  nature  of  the  sputum  (absence  of  tubercle  bacilli),  the 
seat  of  the  disease  in  the  lower  lobes  of  the  lungs,  and  the  general  course  of 
the  disease.    A  careful  anamnesis  is  important. 

We  will  refer  to  the  appropriate  chapters  for  the  relations  of  bronchiec- 
tasis to  fetid  bronchitis,  pulmonary  gangrene,  etc. 

Treatment. — Treatment  should  provide  first  of  all  for  the  best  possible 
hygienic  conditions  (i.e.,  rest,  fresh  air,  nourishment,  and  climate),  and  also 
should  be  directed  toward  the  amelioration  of  the  secretion  and  expectoration. 
To  diminish  the  secretion  and  to  prevent  or  lessen  fetid  decomposition  of 
the  same  inhalations  of  turpentine,  Curschmann's  carbolic  mask  and  similar 
measures  are  especially  recommended.  The  internal  administration  of  creo- 
sote preparations  (guaiacol,  sirolin)  is  often  of  advantage.  In  addition  to 
the  usual  expectorants,  we  may  try  mechanically  to  assist  the  discharge  of 
the  secretion  by  means  of  Quincke's  inclined  posture.  All  complications 
(hemorrhages,  secondary  pneumonia,  pleurisy,  empyema)  should  naturally 
receive  special  treatment.  The  drainage  of  bronchiectatic  cavities  by  surgical 
means  has  been  repeatedly  attempted,  but  the  results  have  not  as  yet  proved 
particularly  encouraging.     [See  remarks  on  page  339.] 


CHAPTEE    VII 

STENOSIS  OF  THE  TRACHEA  AND  BRONCHI 

{Tracheal  and  Bronchial  Stenosis) 

TRACHEAL   STENOSIS 

etiology. — Stenosis  of  the  trachea  may  be  caused  either  by  diseases  in  the 
vicinity  of  the  trachea,  or  by  diseases  of  the  trachea  itself.  The  first-named 
mode  of  origin  is  the  more  frequent.  To  this  are  due  all  the  stenoses  of  the 
trachea  from  compression.  Enlargements  of  the  thyroid  gland  from  simple 
struma  and  new  growths,  aneurisms  of  the  arch  of  the  aorta  and  of  the  in- 
nominate artery,  tumors  and  abscesses  in  the  anterior  mediastinum,  swelling  of 
the  lymph-glands  at  the  bifurcation  of  the  trachea,  abscess  on  the  anterior 
surface  of  the  cervical  vertebra?,  etc.,  may  exert  so  great  a  pressure  on  the 
trachea  from  without  that  its  lumen  is  made  narrower.  Besides  the  direct 
action  of  pressure,  in  most  cases,  a  gradual  atrophy  and  a  softening  of  the 
rings  of  cartilage,  due  to  pressure,  sometimes  play  an  important  part,  accord- 
ing to  Eose,  in  the  occurrence  of  stenosis.    A  collapse  of  the  trachea  may  arise 


STENOSIS  OF  THE  TRACHEA    AND   BRONCHI  219 

from  this  "flaccid  softening,"  which  may  come  on  quite  suddenly,  and  a 
cause  many  of  the  cases  of  sudden  "  death  due  to  goiter." 

Changes  in  the  trachea  itself  leading  to  stenosis  are  quite  rare.  Cicatricial 
stenosis  as  a  result  of  syphilitic  ulcerations  is  relatively  the  most  frequent. 
New  growths  in  the  trachea  are  also  to  be  mentioned,  such  as  polypi  and 
cancer,  the  latter  almost  always  having  invaded  the  trachea  from  the  adjacenl 
parts.  Very  rarely  acute  and  chronic  inflammatory  processes  such  as  peri- 
chondritis lead  to  a  swelling  of  the  mucous  membrane  sufficient  to  cause  ste- 
nosis. In  conclusion,  we  may  mention  that  stenosis  of  the  trachea  may  he 
due  to  the  presence  of  foreign  bodies. 

Symptoms. — If  the  stenosis  is  so  extreme  that  there  is  a  real  hindrance 
to  respiration,  a  very  striking  modification  of  the  breathing  occurs.  It  is  diffi- 
cult and  labored,  and  is  performed  only  by  the  help  of  the  accessory  mua 
Both  expiration  and  inspiration  are  protracted,  long  drawn,  and  accompanied 
by  a  loud  stridor.  In  many  cases  inspiration  is  more  difficult  than  expiration, 
so  that  there  is  accordingly  a  preponderating  inspiratory  dyspnoea,  and  the 
number  of  respirations  a  minute  is  diminished.  If  the  entrance  of  air  into  the 
lungs  is  incomplete  in  spite  of  the  lengthening  of  the  respirations,  we  see  an 
inspiratory  retraction  of  the  lower  part  of  the  thorax,  and  sometimes  of  the 
throat  and  the  supraclavicular  fossas.-  In  tracheal  stenosis  the  larynx, 
however,  shows  little  or  no  to-and-fro  movement  on  respiration.  This  fact 
is  of  value  in  diagnosis  in  distinguishing  tracheal  from  laryngeal  stenosis, 
for  in  the  latter  the  respiratory  movements  of  the  larynx  are  quite  well 
marked. 

We  sometimes  notice  in  the  pulse  during  inspiration  a  marked  fall  in  ten- 
sion and  in  the  height  of  the  pulse  waves,  the  pulsus  paradoxus.  With  the 
sphygmograph  we  can  show  still  more  plainly  the  changes  in  blood  pressure, 
which  vary  quite  markedly  with  the  respiration.  The  frequency  of  the  pulse 
is  usually  a  little  increased,  but  sometimes  it  is  diminished. 

The  symptoms  of  the  disease  just  described  may  form  so  characteristic  a 
picture  that  we  can  recognize  it  at  the  first  glance.  More  precise  information 
as  to  the  seat  of  the  stenosis,  or  the  accurate  differentiation  of  tracheal  stenosis 
from  the  very  similar  picture  presented  by  laryngeal  stenosis,  demands  a  direct 
laryngoscopy-  examination  of  the  larynx  and  trachea,  which,  of  course,  is 
hardly  practicable  in  a  patient  with  a  high  degree  of  dyspnoea. 

BRONCHIAL   STENOSIS 

etiology. — Narrowing  of  a  primary  bronchus,  which  is  the  only  form  to 
be  mentioned  here,  arises  most  frequently  as  a  result  of  the  presence  of  foreign 
bodies — e.  g.,  bits  of  bone,  plum  stones,  buttons,  etc.  These  may  enter  the 
air-passages  by  means  of  a  deep  inspiration,  especially  while  eating  or  during 
sleep.  We  know  that  foreign  bodies  get  into  the  right  bronchus,  which  is 
wider,  somewhat  more  frequently  than  they  do  into  the  left.  Stenosis  of  the 
main  bronchi  from  pressure  also  arises  from  aneurisms  of  the  aorta,  medias- 
tinal tumors,  enlarged  bronchial  lymph-glands,  etc.  Stenosis  of  the  left  bron- 
chus from  the  pressure  of  the  greatly  dilated  left  auricle  has  been  observed 
in  mitral  stenosis.  Direct  narrowing  of  the  larger  bronchi  most  frequently 
results  from  bronchial  carcinoma. 


220  DISEASES   OF  THE   RESPIRATORY   ORGANS 

Symptoms. — The  symptoms  are  not  equally  distinct  in  all  instances.  They 
depend  upon  the  shutting  off  of  the  corresponding  part  of  the  lung.  The 
dyspnoea  is  usually  very  evident,  especially  in  acute  cases.  The  respiratory 
excursions  are  much  less  on  the  affected  side  than  on  the  sound  side.  The 
percussion  note  remains  clear;  sometimes  it  is  very  deep,  because  the  lung 
beyond  the  narrowed  bronchus  is  constantly  inflated.  Auscultation  shows 
complete  absence  of  the  vesicular  respiratory  murmur.  We  either  hear  noth- 
ing or  we  sometimes  hear  over  the  whole  side  a  loud  whistling  or  humming 
sound,  the  vibration  of  which  can  in  some  cases  be  felt  by  the  hand  applied 
to  the  chest  wall.  The  vocal  fremitus  is  diminished  on  the  affected  side.  A 
vicarious  emphysema  soon  develops  in  the  other  lung. 

Lobular  pneumonia  frequently  develops  as  a  result  of  the  entrance  of  for- 
eign bodies  into  a  bronchus,  because  the  agents  of  inflammation  have  entered 
at  the  same  time  with  these  bodies,  and,  as  the  expectoration  can  be  evacuated 
only  with  difficulty,  and  hence  is  more  or  less  stagnant,  the  germs  can  readily 
establish  themselves  in  it.  In  stenosis  from  pressure  the  condition  may  of 
course  be  modified  in  many  ways  by  the  primary  disease. 

PROGNOSIS   AND   TREATMENT 

The  prognosis  and  treatment  of  tracheal  and  bronchial  stenosis  depend  en- 
tirely upon  the  nature  of  the  primary  disease.  General  statements  as  to  treat- 
ment, therefore,  need  not  be  given  here.  A  direct  mechanical  treatment  of 
tracheal  stenosis  in  appropriate  cases,  such  as  cicatricial  stenosis,  may  be  un- 
dertaken according  to  the  different  modes  of  dilatation  above  enumerated. 
The  methods  for  removing  foreign  bodies  from  the  larger  air-passages  belong 
to  the  domain  of  surgery.  The  employment  of  an  emetic  has  met  with  distinct 
success  in  such  cases,  but  it  is  not  without  danger,  .for  the  foreign  body  may 
wedge  itself  into  the  glottis  during  the  act  of  vomiting  and  occasion  danger  of 
instant  suffocation. 


CHAPTEE    VIII 

BRONCHIAL    ASTHMA 

{Exudative  Bronchiolitis.     Asthmatic  Bronchiolitis) 

Definition  and  Causes  of  the  Disease. — Bronchial  asthma  is  the  name  we 
give  to  a  morbid  condition  whose  chief  symptom  is  a  special  form  of  severe 
d}"spncea.  The  characteristic  features  of  the  dyspnoea  of  bronchial  asthma  are, 
first,  that  it  occurs  in  paroxysms,  or  at  least  that  it  groAvs  worse  paroxysmally, 
and,  second,  its  peculiar  manner  of  onset.  Every  case  of  true  bronchial  asthma 
is  due  to  an  extensive  and  usually  quite  sudden  contraction  of  the  smaller  and 
smallest  bronchial  branches.  This  always  gives  rise  to  a  form  of  distress  for 
breath  which  differs  materially  from  every  other  form  of  dyspnoea. 

The  question  as  to  the  origin  of  bronchial  asthma  coincides,  then,  with  that 
of  the  origin  of  diffuse  stenosis  of  the  bronchioles.  Earlier  authors,  especially 
Trousseau  and  Biermer,  explained  the  suddenly  developing  stenosis  of  the 
lumen  of  the  bronchioles  on  the  basis  of  a  tonic  cramp  of  the  circular  mus- 


BRONCHIAL  ASTHMA  221 

culature  of  the  smaller  bronchi.  Aside  from  the  fad  that  such  a  spasm  has 
never  been  directly  demonstrated,  and  is  also  aol  to  be  easily  explained  theo- 
retically, this  view-point  seems  to  me  to  be  furthermore  unsatisfactory,  because 
it  does  not  explain  the  peculiar  appearance  of  the  sputum  during  and  after 
an  asthmatic  attack.  On  the  other  hand,  the  characteristics  of  the  sputum, 
which  will  be  described  in  detail  below,  point  with  greal  certainty  to  a  special 
morbid  process  affecting  the  mucous  membrane  of  the  bronchioles.  The  fre- 
quent recurrence  and  the  ofttimes  brief  duration  of  individual  asthmatic  at- 
tacks render  impossible  the  supposition  of  true  inflammatory  disease.  We 
must,  therefore,  accept  the  theory  of  a  purely  secretory  disturbance  which  is 
either  located  in  the  mucous  membrane  and  its  secretory  cells  alone,  or  i- 
dependent  upon  nervous  influences.  Favoring  the  nervous  nature  of  many 
cases  of  asthma  is,  first,  the  fact  that  the  disease  is  not  infrequently  observed 
in  persons  of  a  decided  general  neuropathic  constitution,  and  secondly,  that 
an  asthmatic  attack  is  sometimes  excited  by  reflex  action.  There  are,  for 
example,  some  asthmatics  whose  attacks  are  induced  b}r  certain  odors  and  in- 
halations (ipecac,  violets,  roasted  coffee,  etc.).  Pathological  alterations  of  the 
nasal  mucous  membrane  (hypertrophy  of  the  turbinate  bones,  polypi,  chronic 
catarrh)  are  sometimes  found  in  asthmatics;  irritation  of  such  lesions  may 
even  lead  to  an  artificially  induced  asthmatic  attack,  Avhile  their  removal 
may  result  in  a  disappearance  of  the  attacks.  Some  physicians,  in  fact,  have 
been  inclined  to  refer  most  cases  of  bronchial  asthma  to  a  primary  disease 
within  the  nasal  cavities.  In  this  there  has  been  great  exaggeration,  and  yet 
the  possibility  of  asthma  originating  "  from  the  nose  "  cannot  he  disputed. 
It  is  very  doubtful  if  asthma  can  be  caused  by  reflex  stimuli  from  other  or- 
gans. The  asserted  association  of  asthma  with  diseases  of  the  pharynx  (hyper- 
trophy of  the  tonsils)  is  deserving  of  the  most  credence.  But  one  should  be 
very  skeptical  in  accepting  statements  concerning  the  occurrence  of  asthmatic 
attacks  in  cases  of  diseases  of  the  ear,  the  stomach  ("  dyspeptic  asthma"),  the 
intestine,  the  female  sexual  organs,  etc.  In  these  conditions,  true  asthma  is 
usually  confused  with  other  dyspnceic  conditions  (hysterical  asthma,  cardiac 
weakness,  and  the  like). 

A  reflex  origin  cannot  be  demonstrated  in  the  majority  of  cases  of  asthma. 
Apparently  the  asthmatic  attacks  and  the  underlying  acute  swelling  of  the 
mucous  membrane  of  the  bronchioles  begin  spontaneously,  or,  at  most,  origi- 
nate through  certain  external  influences,  such  as  the  inhalation  of  cold  air, 
dust,  etc.  If  the  attack  is  only  of  brief  duration,  and  is  followed  by  an  entirely 
normal  condition  of  the  lungs  and  bronchi,  we  then  speak  of  a  purely  nervous 
form  of  bronchial  asthma.  Not  infrequently,  however,  asthmatic  attacks  are 
combined  with  a  permanent  inflammatory  and  catarrhal  condition  of  the  finer 
bronchi.  The  relations  between  asthma  and  bronchiolitis  are  not  always  the 
same.  Sometimes  chronic  bronchiolitis  only  develops  gradually,  a  long  time 
after  the  asthmatic  attacks  have  existed.  Under  such  circumstances,  we  are 
dealing  with  a  secondary,  chronic,  inflammatory  disease  on  the  basis  of  a 
specially  predisposed  mucous  membrane.  In  many  cases,  however,  we  appear 
to  be  dealing  with  a  particular  form  of  primary,  chronic  disease  of  the  bron- 
chioles, in  which  the  characteristic  asthmatic  attacks  are  to  be  considered  as 
exacerbations  of  the  continuous  chronic  morbid  process.  Curschmann,  to 
whom  we  are  indebted  for  the  first  accurate  clinical  studies  of  this  form  of 


222  DISEASES   OF  THE   RESPIRATORY   ORGANS 

bronchial  asthma,  terms  the  underlying  bronchial  disease  "  exudative  bron- 
chiolitis." We,  however,  prefer  the  name  "  asthmatic  bronchiolitis  "  for  this 
condition.  By  these  terms,  a  peculiar  disease  of  the  finer  bronchi  and  the 
bronchioles  is  designated.  It  is  characterized  by  the  peculiar  appearance  of 
the  sputum  and  by  intercurrent,  characteristic  "  asthmatic  "  attacks.  Very 
probably,  reflex  nervous  influences,  too,  favor  the  onset  of  individual  asthmatic 
attacks  in  asthmatic  bronchiolitis.  Here,  again,  I  am  inclined  to  attach  far 
greater  importance  to  the  varying  amount  of  swelling  of  the  bronchial  mucous 
membrane  than  to  a  possible  tonically  contracted  state  of  the  musculature  of 
the  bronchioles.  Some  authors  have  also  found  an  aetiology  for  asthmatic 
dyspnoea  in  spasm  of  the  diaphragm.  This  assumption  is,  however,  without 
facts  to  support  it,  and  is  directly  refuted  by  the  demonstrable  fact  (shown 
also  by  the  X-ray  examination)  that  the  diaphragmatic  excursions  are  unem- 
barrassed during  asthmatic  attacks.  Inhalations  of  dust  (wool  dust,  flower 
dust,  and  the  like)  sometimes  play  a  demonstrable  role  in  the  causation  of 
asthmatic  bronchiolitis.  In  addition,  previous  attacks  of  acute  bronchitis 
must  be  especially  taken  into  consideration.  Some  cases  are  referable  to  a 
severe  bronchitis  complicating  measles  or  whooping  cough  during  childhood. 

The  "  pure  "  cases  of  asthma,  which  owe  their  origin  to  a  special  predis- 
position of  the  mucous  membrane  to  acute  swelling,  acquire  a  general  patho- 
genetic interest  because  of  similar  processes  that  occur  in  other  mucous  mem- 
branes and  tissues.  Thus,  a  certain  analogy  may,  for  example,  be  drawn 
between  bronchial  asthma  and  urticaria,  as  well  as  between  bronchial  asthma 
and  certain  secretory  disturbances  of  the  intestine  (mucous  colitis,  q.v.).  All 
such  anomalies  may  be  considered  as  the  expression  of  a  peculiar  pathological 
tendency  to  exudative  disturbances  (the  "exudative  diathesis"  of  Czerny). 
Indeed,  a  careful  investigation  will  not  infrequently  demonstrate  various  mani- 
festations of  this  "  diathesis "  in  different  organs  of  the  same  individual. 
Perhaps  the  observations  of  artificial  urticaria  in  asthma,  made  by  Lenhartz 
and  myself,  are  associated  with  this  "  diathesis."  That  is,  we  have  noticed 
that  mechanical  irritation  of  the  skin  (with  the  handle  of  a  percussion  ham- 
mer, for  example)  not  uncommonly  gives  prompt  rise  to  an  active  reddening 
and  urticaria-like  wheals  along  the  line  of  irritation.  The  possible  association 
of  this  "  exudative  diathesis "  with  the  general  neuropathic  condition  is  of 
interest,  but  as  yet  quite  obscure. 

Symptoms  and  Course  of  the  Disease. — We  will  begin  the  account  of  the 
symptomatology  by  a  description  of  the  asthmatic  "  attack."  In  its  purest 
form  "  nervous  "  bronchial  asthma  consists,  in  fact,  of  single  attacks  of  dysp- 
noea, differing  in  frequency  and  duration,  which  occur  at  least  without  special 
cause  or  without  any  discoverable  reason  in  persons  otherwise  apparently 
healthy.  In  the  intervals  between  the  attacks  the  patient  is  perfectly  well, 
and,  in  particular,  shows  no  signs  of  disease  of  the  respiratory  organs.  In 
most  cases  of  "  bronchial  asthma,"  however,  the  attacks,  as  we  have  said,  are 
only  more  or  less  sudden  exacerbations  of  a  condition  which  in  the  intervals 
is  not  perfectly  normal.  While  ordinarily  only  the  signs  of  a  chronic  bron- 
chitis are  present,  often  associated  with  pulmonary  emphysema,  from  time  to 
time  exacerbations  occur,  usually  in  the  form  of  long-continued  asthmatic 
dyspnoea,  lasting  for  days  or  weeks.  It  is  this  latter  form  especially  which 
can  be  explained  only  by  the  assumption  of  a  true  bronchiolitis. 


BRONCHIAL  ASTHMA  223 

The  asthmatic  attack  either  begins  quite  suddenly,  or  is  preceded  for  a 
shorter  or  longer  period  by  prodromata.  These  consisl  in  a  general  feeling  of 
discomfort,  in  abnormal  sensations  in  the  Larynx  or  epigastrium,  sometimes  in 
remarkably  frequent  gaping,  and  often  in  a  marked  coryza  associated  with  a 
good  deal  of  secretion  and  frequenl  sneezing  (compare  the  relation  between 
many  attacks  of  asthma  and  diseases  of  the  nose,  stated  above).  The  attack 
begins  in  most  cases  at  night  (before  midnight).  The  patient  wakes  up  with 
an  intense  feeling  of  pressure  and  anxiety.  Sometimes  he  emu  plains  of  a 
feeling  of  pain  in  the  chest.  He  has  to  sit  up  straight,  and  in  severe  cases 
even  to  get  out  of  bed.  He  often  hurries  to  an  open  window  in  order  to  "get 
air."  His  expression  is  anxious;  his  skin  becomes  pale  and  cyanotic,  and 
sometimes  is  covered  with  a  cold  sweat.  On  objective  examination  we  are  at 
once  struck  by  the  characteristic  change  in  the  respiration.  Both  inspiration 
and,  especially,  expiration  are  almost  always  accompanied  by  a  high-pitched 
whistling  sound,  audible  at  a  distance.  Both  respiratory  acts  are  labored, 
requiring  the  aid  of  the  accessory  muscles.  On  inspiration,  only  the  upper 
part  of  the  thorax  is  elevated  to  any  extent.  We  see  in  the  neck  the  inspiratory 
contraction  of  the  sterno-cleido-mastoids,  the  scaleni,  etc.  Still  more  striking, 
however,  is  the  labored,  panting,  long-protracted  expiration,  during  which  the 
abdominal  muscles  are  contracted  to  a  board-like  hardness.  We  therefore  rec- 
ognize the  disturbance  of  respiration  in  asthma  as  essentially  an  expiratory 
dyspnoea.  The  frequency  of  respiration  is  in  many  cases  normal,  or  even  some- 
what diminished,  yet  we  have  repeatedly  counted  thirty  or  forty  respirations 
a  minute. 

On  physical  examination  of  the  lungs  during  the  paroxysm,  we  find  the 
percussion  note  normal  or  even  strikingly  loud  and  deep — the  "  box-tone." 
The  lower  boundary  of  the  lung  is  usually  found  one  or  two  intercostal  spaces 
lower  than  normal.  Not  only  is  this  condition  shown  in  the  cases  with  a  perma- 
nent pulmonary  emphysema,  but  during  the  asthmatic  attack  itself  there  oc- 
curs an  acute  inflation  of  the  lung.  The  latter  is  probably  explained  by  the 
fact  that  the  lung  is  much  stretched  by  the  strenuous  inspirations  which  are 
made  by  aid  of  the  accessory  muscles,  while  the  weaker  expiratory  force  is  not 
enough  wholly  to  drive  out  the  air  again  through  the  contracted  bronchioles. 
Therefore  it  happens  in  bronchial  asthma,  as  in  every  other  bronchial  disease, 
that  the  expiration  is  usually  more  labored  and  protracted  than  the  inspiration. 
On  auscultation,  high-pitched  whistling  and  creaking  sounds,  which  quite  ob- 
scure the  vesicular  murmur,  are  heard  over  most  of  the  lung,  especially  during 
the  long  expirations.  In  many  places,  indeed,  where  the  bronchioles  are 
almost  completely  closed,  the  respiratory  murmur  is  entirely  absent,  or  we 
hear  only  a  low  whistle  on  expiration.  Toward  the  end  of  the  paroxysm  the 
noises  become  deeper  and  more  booming,  and  sometimes  we  hear  a  few  moist 
rales. 

In  the  intervals  between  individual  attacks,  the  respiratory  murmur,  in  the 
cases  of  "  pure  nervous  asthma,"  is  quite  normal.  In  cases  of  asthmatic  bron- 
chiolitis, even  during  the  intervals,  there  are  abnormal  auscultatory  signs  (iso- 
lated bronchial  rales,  suppressed  and  weakened  inspiration,  prolonged  expira- 
tion, etc.). 

In  brief  paroxysms  there  may  be  scarcely  any  cough  or  expectoration.  In 
most,  particularly  in  the  tedious  cases  of  true  asthmatic  bronchiolitis,  there  is, 


224  DISEASES   OF  THE   RESPIRATORY   ORGANS 

however,  a  scanty  tough  mucous  expectoration.  In  this  are  found,  besides  the 
ordinary  constituents  of  simple  bronchitis  sputum,  larger  or  smaller  numbers 
of  characteristic  clumps.  These  may  be  yellow  or  greenish-yellow,  or,  on  the 
other  hand,  gray.  The  yellowish  masses,  which  are  usually  very  tough,  and 
often  consist  of  a  bunch  of  thready  matter,  represent  swollen  and  fatty-degen- 
erated pus  corpuscles,  between  which  are  very  frequently  interspersed  a  con- 
siderable number  of  pointed  octahedral  crystals.  These  crystals  were  first 
described  by  Leyden  in  the  sputum  of  asthmatic  patients,  and  are  usually 
termed  asthma  crystals  (see  Fig.  42).  Chemically  they  are  identical  with 
"  Charcot's  crystals,"  which  are  found  in  the  leukemic  spleen,  the  bone  mar- 
row, etc.,  and  they  probably  represent  the  phosphoric-acid  salt  of  an  organic  base 
(Schreiner's  base,  C2H5N),  although  this  has  lately  been  questioned.  As  soon 
as  the  paroxysms  cease  the  number  of  crystals  in  the  sputum  usually  begins  to 
diminish  rapidly,  and  it  is  often  possible  to  observe  in  them  evident  signs  of 
disintegration.  Nothing  is  known  as  to  the  origin  of  these  crystals.  Their 
presence  probably  bears  some  relation  to  the  eosinophile  cells  of  the  sputum 
(vide  infra).  At  any  rate,  Charcot's  crystals  are  also  found  wherever  degen- 
erated eosinophile  cells  are  to  be  seen.  Not  infrequently,  also,  numerous  cili- 
ated epithelial  cells  are  found,  in  addition  to  the  crystals,  in  the  yellow  masses. 
The  gray  plugs  in  the  sputum  of  asthmatic  patients  consist  mainly  of  clumps 
of  thready  mucus,  and  contain  the  peculiar  "spirals"  which  were  first  de- 
scribed by  TTngar  and  by  Curschmann.  Many  of  these  spiral  threads  are  visible 
to  the  naked  eve,  but  others  demand  the  microscope  for  their  recognition, 


i*^ 


Fig.  42. — Asthma  crystals  and  Curschmann's  spirals  (a,  central  fiber). 

through  which  they  are  seen  as  brilliant  forms  composed  entirely  of  various 
sized  bands  and  threads  collected  in  spirals  (see  Fig.  42).  Sometimes  a 
brilliant  central  thread  of  small  diameter  is  seen  in  the  midst  of  the  spiral. 
Around  the  spirals  are  found  round  cells,  drops  of  fat  and  myelin,  and  some- 
times ciliated  epithelium,  and  epithelial  cells  from  the  pulmonary  alveoli.  As 
to  the  precise  way  in  which  the  spirals  and  their  central  thread  develop,  the 
question  is  not  yet  settled,  but  it  is  certain  that  the  spirals  represent  casts  of 
the  minutest  spirally  twisted  branches  of  the  bronchi,  and  therefore  clearly 
indicate  the  existence  of  a  peculiar  disease  of  the  finest  terminal  bronchial 
twigs.  The  origin  of  the  central  thread  is  to  be  sought,  perhaps,  in  the  expul- 
sive cough. 


BRONCHIAL   ASTHMA  225 

Of  the  other  peculiarities  of  the  sputum  in  bronchia]  asthma  we  may 
mention,  first  of  all,  the  alraosl  invariable  occurrence  of  very  many 
eosinophilous    cells    in    the    sputum,    and    also,    apparently,    in    the    blood 

(see  Fig.  43).  The  significance  of  this 
fact  is  still  unknown.  We  occasionally 
find  in  the  sputum  of  asthmatics  crys- 
tals of  calcic  oxalate  and  calcic  phos- 
phate. 

The    pulse    is    usually    accelerated 
during    the    asthmatic    paroxysm,    the  ^  :-ap  'T,.*  z.. 


arteries    contracted;    the    bodily    tem- 
perature is  normal,  or  sometimes  even 

subnormal.      In  protracted  attacks   we     FlG  43._EoSinophile  cells  in  the  sputum  in 
have    repeatedly    seen    a    slight    febrile  bronchial  asthma, 

movement  up  to  about  102°  F.  (39°  C). 

The  duration  of  the  asthmatic  paroxysm  is  very  different  in  individual 
cases,  as  has  already  been  said.  Sometimes  it  lasts  only  a  few  hours,  but  some- 
times it  lasts  several  days,  and  even  weeks.  Marked  exacerbations  and  remis- 
sions of  the  disease  usually  alternate.  The  frequency  of  the  paroxysms  in  ordi- 
nary asthma  also  varies  exceedingly.  Sometimes  they  come  on  almost  every 
night,  and  then  there  are  long  pauses  of  months  and  years,  so  that  we  cannot 
make  any  general  statements  as  to  the  course  of  the  disease.  Many  asthmatic 
patients  make  very  remarkable  statements  as  to  the  individual  exciting  causes 
of  their  attacks.  Many  patients  claim,  for  example,  that  the  attacks  occur  only 
in  certain  places,  while  in  other  places  they  are  wholly  free  from  the  trouble, 
that  they  can  live  only  in  the  upper  stories  of  the  house,  etc.  Such  statements 
should  not  remain  unheeded,  although  it  is  certain  that  they  are  often  due  to 
imagination.  In  mild  cases,  cures  are  not  infrequent ;  the  possibility  of  recur- 
rences must,  however,  always  be  remembered.  Only  rarely  can  a  complete  cure 
of  the  severer  cases  of  asthmatic  bronchiolitis  be  expected,  though  a  decided 
improvement  can  often  be  obtained.  In  asthma  of  long  standing,  chronic  pul- 
monary emphysema  with  its  sequelae  almost  invariably  develo|>s.  The  occur- 
rence of  a  secondary  pulmonary  tuberculosis  has  also  been  repeatedly  observed. 

Diagnosis. — The  diagnosis  of  the  bronchial  asthmatic  condition  as  such  is 
not  difficult  if  we  limit  ourselves  strictly  to  the  characteristic  type  of  the  dis- 
ease :  the  strenuous  respiration  with  wheezing  that  can  be  heard  at  a  distance, 
the  labored,  prolonged  expiration,  the  characteristic  physical  signs  in  the  lungs, 
and  the  peculiar  sputum.  Usually  we  can  easily  distinguish  bronchial  asth- 
matic dyspnoea  from  cardiac  asthma  (q.  v.),  spasm  of  the  glottis  (q.  v.),  and 
also  from  hysterical  dyspnoea  with  its  superficial  and  very  rapid  respiration 
and  normal  conditions  in  the  lungs.  This  latter  distinction  of  true  bronchial 
asthma  from  "  hysterical  asthma  "  is  very  important  both  in  prognosis  and 
treatment,  since  the  two  are  frequently  confounded.  If  we  are  sure  that  we 
are  dealing  with  true  asthmatic  attacks,  the  next  question  is  whether  it  is  a 
"  purely  nervous  "  reflex  asthma  or  an  asthmatic  exudative  bronchiolitis.  Here, 
of  course,  we  can  decide  only  after  a  careful  and  thorough  examination  of  the 
patient  (especially  of  the  nasal  cavities)  and  after  observing  the  course  of  the 
disease.  Finally,  we  must  also  consider  the  possibility  of  a  purely  symptomatic 
asthma  in  chronic  pulmonary  emphysema,  in  the  chronic  bronchitis  of  renal 


226  DISEASES   OF  THE   RESPIRATORY   ORGANS 

disease  or  arthritis,  etc.  We  must,  however,  confine  our  use  of  the  term 
"  s}rmptomatic  bronchial  asthma  "  to  those  cases  in  which  we  actually  have  a 
dysjmcea  with  air  the  characteristic  peculiarities  of  true  bronchial  asthma. 

Treatment. — In  every  case  of  asthma  the  first  thing  to  be  thought  of  is 
whether  there  is  not  a  definite  cause  whose  removal  may  cure  the  disease.  In 
this  connection  we  should  examine  the  nose  carefully,  since  numerous  recent 
observations  have  shown  that  a  previously  existing  asthma  may  wholl}r  disap- 
pear or  at  least  be  materially  relieved  after  the  treatment  of  some  nasal  disease 
which  may  be  present,  such  as  the  removal  of  polypi,  the  destruction  of  the 
erectile  bodies  by  the  galvano-cautery,  etc.  Of  course  these  results  should  not 
be  overestimated.  It  has  repeatedly  been  claimed  by  nasal  specialists  that  in 
many  asthmatic  patients  we  can  find  a  definite  spot  in  the  nose  and  excite  an 
asthmatic  attack  by  touching  it  with  a  probe.  This  spot  must  then  be  treated 
first  of  all.  We  will  not  wholly  reject  these  statements,  but  we  are  somewhat 
skeptical  in  regard  to  them.  At  any  rate,  the  nose  should  be  treated,  in  our 
opinion,  only  when  it  presents  actual  morbid  changes. 

If  we  cannot  satisfy  the  causal  indication  in  this  way,  we  should  always  try 
next  a  remedy  which  must  pass  for  a  direct  specific  against  certain  forms  of 
asthma — ioclid  of  potassium.  In  doses  of  20  to  45  gr.  a  day  (gm.  1.5  to  3.0), 
or  even  more,  if  necessary,  this  usually  causes  a  rapid  improvement,  which 
of  course  is  not  always,  although  it  is  frequently,  permanent.  In  asthmatic 
bronchiolitis,  especially,  iodid  of  potassium  in  large  doses  often  acts  excel- 
lently. It  seems  to  make  the  tough  secretion  more  fluid,  to  ease  the  expectora- 
tion, and  in  this  way  to  lessen  the  stenosis  of  the  bronchioles.  Of  course  a 
permanent  and  complete  cure  is  only  rarely  obtained  from  iodid  of  potassium. 
Next  to  potassium  iodid,  I  consider  an  energetically  pursued  methodical  dia- 
phoretic treatment  the  most  effectual  therapy.  By  the  use  of  the  electric-light 
baths,  as  well  as  by  the  other  generally  employed  diaphoretic  agents,  I  have 
usually  obtained  good  results,  and  occasionally,  even  apparent  cures  in  cases 
of  nervous  asthma  and  of  asthmatic  bronchiolitis.  The  patients  are  placed 
daily  in  the  electric-incandescent-light  bath,  in  which  they  remain  from  ten  to 
fifteen  minutes  at  the  beginning  of  the  treatment,  and  later  from  twenty-five 
to  thirty  minutes.  The  incandescent-light  bath  is  followed  by  an  ordinary 
warm  bath,  after  which  the  patients  rest  for  one  or  two  hours.  In  many  cases, 
after  four  or  five  treatments,  a  decided  improvement  is  already  observed.  The 
attacks  cease,  breathing  becomes  freer,  and  the  respiratory  murmur  clearer. 
An  apparently  con^lete  cure  may  be  attained  in  three  to  four  weeks.  If  iodid 
of  potassium  and  the  above  diaphoretic  treatment  have  been  used  in  vain,  we 
must  turn  to  the  other  remedies  which  have  been  employed  against  asthma, 
although  their  action  is  often  quite  uncertain.  We  may  mention  here  the 
nitrite  of  sodium  (2  parts  in  120  of  water,  two  to  three  teaspoonfuls  a  day) 
and  nitroglycerin,  which  has  an  analogous  action  (20  drops  of  a  one-per-cent 
alcoholic  solution  in  ovjss.  (gm.  200)  of  water,  a  tablespoonful  two  or 
three  times  a  clay)  ;  also  pyrenol,  bromid  of  potassium,  belladonna,  atropin, 
etc.  In  some  cases  pneumatic  treatment,  such  as  the  inhalation  of  compressed 
air,  has  been  successful,  and  sometimes,  too,  electricity  (galvanization  and  fara- 
dization of  the  neck),  or  hydrotherapy,  has  been  claimed  to  give  relief.  Change 
of  climate  may  sometimes  be  of  distinct  service.  Many  patients  bear  the  sea-air 
Avell,  while  with  others  a  mountain  residence  exerts  a  favorable  influence.    Spe- 


PULMONARY   EMPHYSEMA  227 

•cial  reports  (Marienbad,  Kissingen,  ferruginous  baths,  etc.)  may  often  be  rec- 
ommended with  advantage  if  appropriate  to  the  patient's  genera]  constitution. 

In  severe  cases  a  special  symptomatic  treatment  of  the  attack  itself  is  often 
necessary.  Narcotics  are  without  doubt  the  mosl  effecl  ive,  especially  chloral  and 
morphin.  In  severe  attacks  we  cannot  avoid  injections  of  morphin,  but  we 
must  always  be  cautious  in  order  that  the  patient  may  not  form  the  habit  of 
using  this  to  excess.  Chloral  hydrate  (gr.  xv  to  xxx  [gm.  1.0  to  '<!.<)  |  )  often  re- 
lieves the  individual  attack.  Among  other  s3Tnptomatic  remedies  we  may  men- 
tion mustard  plasters  to  the  chest  and  calves,  putting  the  hands  and  feel  into 
hot  water,  inhalations  of  nitrite  of  amy],  turpentine,  chloroform,  pyridin,  etc. 
Fumigation  with  saltpeter  paper — unsized  paper  dipped  in  a  concentrated  solu- 
tion of  nitrate  of  potassium  and  dried — and  the  stramonium  cigarettes  to  be 
had  in  most  drug  stores,  are  much  praised.  The  patient  may  also  smoke  witli 
occasional  benefit  stramonium  or  belladonna  leaves  which  have  previously  been 
dipped  in  a  solution  of  saltpeter  and  then  dried.  Many  patients  praise  highly 
the  different  asthma  cigarettes  and  smoke-producing  powders  or  pastilles,  which 
are  sold  as  secret  remedies.  We,  ourselves,  usually  employ  a  mixture  of  equal 
parts  of  powdered  stramonium  leaves  and  powdered  nitrate  of  potassium. 

[Potassium  iodid  is  more  likely  to  prevent  recurrence  if  it  is  given  continu- 
ously, for  several  months,  at  least,  and  it  should  not  be  thrown  aside  as  useless 
until  it  lias  been  pushed  to  the  limit  of  toleration  without  avail.  A  convenient 
form  of  administration  is  in  saturated  aqueous  solution,  a  minim  of  which 
rejiresents  about  a  grain  of  the  drug. 

The  sirup  of  hydriodic  acid  may  he  substituted  for  potassic  iodid  in  cases 
of  intolerance  of  the  latter.  Grindelia  robusta,  a  drachm  of  the  fluid  extract 
three  or  four  times  a  da)r,  serves  sometimes  to  prevent  recurrence  of  attacks. 
Marked  alleviation  of  the  paroxysms  is  often  obtained  from  the  inhalation  of 
15  to  30  drops  of  the  iodid  of  ethyl.] 


SECTION   IV 
Diseases  of  the  Lungs 

CHAPTER    I 

PULMONARY    EMPHYSEMA 

(Alveolar  Ectasis.      Volumen  pulmonum  auctum) 

Nature  and  etiology  of  the  Disease. — Pulmonary  emphysema,  the  abnor- 
mal inflation  and  dilatation  of  the  lungs,  either  develops  in  separate  parts  of 
the  lung,  in  which  case  it  is  subordinate  to  other  pathological  changes  which 
coexist  in  the  lungs,  or  involves  almost  the  whole  extent  of  both  lungs,  and 
then  presents  the  symptoms  of  a  characteristic  affection,  which  it  is  usually 
easy  to  recognize. 

Attention,  however,  should  be  called  to  the  fact  that  emphysematous  ex- 
pansion of  the  lungs  is  usually  a  secondary  condition,  developing  as  a  sequel 
15 


228  DISEASES   OF   THE   RESPIRATORY   ORGANS 

to  previously  existing  diseases.  Pulmonary  emphysema  is  by  no  means  com- 
mon as  a  primary  affection. 

The  essence  of  pulmonary  emphysema,  the  condition  from  which  most 
symptoms  are  immediately  derived,  is  the  loss  of  elasticity  in  the  lungs.  If 
we  compare  the  sound  lung,  with  its  normal  elastic  force,  to  a  new  and  very 
tense  rubber  band,  the  emphysematous  lung  must  be  compared  to  an  old  and 
lax  band  that  is  stretched  and  pulled  out.  We  therefore  see  why  the  emphy- 
sematous lung  takes  up  a  greater  space  than  the  sound  one,  for,  on  account 
of  its  lack  of  elasticity,  it  can  no  longer  contract  to  its  former  volume.  We 
may  therefore  call  emphysema  a  permanent  inspiratory  distention  of  the  lung 
from  which  it  can  no  longer  return  to  its  expiratory  condition.  If  we  open  the 
thorax  of  a  subject  with  normal  lungs,  they  contract,  as  is  well  known,  but  the 
emphysematous  lungs  remain  in  their  inflated  condition  after  the  thorax  has 
been  opened. 

If  we  inquire  into  the  factors  which  cause  this  loss  of  elasticity  in  the  lung, 
we  find  that  they  are  the  same  kind  of  influences  which  tend  to  diminish  the 
elasticity  of  any  other  elastic  body.  As  a  rubber  band,  by  much  pulling  and 
stretching,  gradually  gets  longer  and  less  elastic,  so  the  lungs,  as  a  result  of 
their  abnormally  frequent  and  severe  distention,  gradually  become  inelastic 
and  emphysematous.  Emphysema  in  many  cases  is  a  true  wearing  out  of  the 
lung.  The  normal  traction  of  inspiration,  which  is  continually  making  new 
demands  on  the  elastic  powers  of  the  lungs,  finally  leads  to  a  loss  of  elasticity 
in  them.  In  advanced  age  most  lungs  become  more  or  less  inelastic.  The 
lungs  of  an  old  man  are  like  an  elastic  band  which  has  done  its  work  for  years 
but  which  has  finally  given  out.  We  therefore  class  emphysema  of  the  lungs 
in  old  age  rather  among  the  states  of  involution,  such  as  develop  in  almost  all 
organs  in  advanced  life,  than  among  special  pathological  changes.  We  distin- 
guish, moreover,  most  lungs  with  senile  emphysema  from  other  emphysematous, 
lungs  by  the  fact  that  their  volume  as  a  whole  is  not  increased,  but  is  rather 
diminished  below  that  of  the  healthy  lung,  since  we  find  in  them  the  extensive 
atrophic  processes  of  old  age. 

The  condition  becomes  pathological,  however,  if  the  elasticity  of  the  lung  is 
deficient  in  earlier  years  and  independently  of  the  action  of  the  special  in- 
jurious influences  which  will  soon  be  mentioned.  In  such  cases  of  emphysema, 
developing  in  middle  life  or  even  in  youth,  the  idea  of  a  congenital  weakness  of 
the  elastic  elements  in  the  lungs  cannot  be  set  aside.  It  probably  consists  in  a 
quantitative  or  a  qualitative  defect  of  the  elastic  tissue.  Some  observations 
seem  to  justify  the  statement  that  a  disposition  to  emphysema  may  be  present 
in  several  members  of  the  same  family. 

If  a  lung  whose  elasticity  is  previously  subnormal  cannot  persistently  sat- 
isfy the  ordinary  demands  upon  it,  a  normal  lung,  on  the  other  hand,  also  loses 
its  elasticity  if  the  demands  made  upon  it  are  greater  than  it  can  perform. 
This  is  the  reason  why  pulmonary  emphysema  is  in  some  instances  to  be  re- 
garded as  a  vocational  disease.  We  mean  here  not  only  those  influences  which 
lead  to  chronic  bronchitis  and  thus  later  to  emphysema  (vide  infra),  but  more 
especially  the  abnormal  demands  upon  the  lungs  in  all  those  callings  which 
necessitate  severe  physical  labor.  We  must  not  only  regard  the  deeper  and 
more  rapid  respirations,  but  also  the  increased  pressure  during  expiration  to 
which  the  lungs  are  often  exposed  in  the  raising  of  heavy  weights,  etc.    This 


PULMONARY  EMPHYSfcMA  229 

explains  the  common  occurrence  of  emphysema  in  the  Laboring  classes,  and 
also  its  greater  frequency  in  men  than  in  women.  Besides  this,  we  must  arid 
that  in  certain  callings,  such  as  glass-blowing  and  horn-blowing,  the  overstrain- 
ing of  the  lungs  is  much  more  direct.  In  all  such  cases  emphysema  may  be 
termed  simply  a  premature  exhaustion  of  the  lungs. 

In  very  many  cases — in  most  cases,  I  mighl  say — emphysema  develops  a3 
a  result  of  chronic  bronchitis.  Dry  catarrh  of  the  medium-sized  and  finer 
bronchi  when  of  long  duration  leads,  as  a  rule,  to  pulmonary  emphysema.  The 
abnormal  mechanical  influences  to  which  the  lungs  are  thus  exposed  act  both 
in  inspiration  and  in  expiration.  Since  the  entrance  of  air  to  the  alveoli  is 
rendered  more  difficult  by  the  swelling  of  the  mucous  membrane  of  the  smaller 
bronchi,  abnormally  deep  and  strong  inspirations  are  necessary,  with  a  marked 
expansion  of  the  alveoli,  in  order  to  draw  a  sufficienl  quantity  of  air  into  the 
alveoli.  The  alveolar  walls  are  therefore  exposed  to  an  abnormal  traction  at 
each  inspiration.  On  expiration,  a  pressure  from  within,  which  is  perhaps  even 
more  injurious,  acts  on  the  alveoli.  The  ordinary  expiration,  which  usually 
needs  only  the  elastic  power  of  the  lungs,  is  not  sufficient  in  chronic  bronchitis 
to  drive  the  air  out  of  the  alveoli  through  the  narrowed  bronchi.  Thus  arise 
the  difficulty  and  delay  in  expiration  which  are  present  in  chronic  bronchitis, 
and  which  lead  to  the  active  participation  of  the  muscles  of  expiration,  the 
abdominal  group  of  muscles.  On  forced  expiration,  however,  the  pressure 
does  not  act  simply  upon  the  contents  of  the  alveoli,  but  much  more  upon  the 
smaller  bronchi  themselves.  The  channel  of  exit  for  the  air  from  the  alveoli, 
therefore,  becomes  still  narrower.  Since  the  air  cannot  at  once  escape,  the 
pressure  within  the  alveoli  is  raised  by  the  efforts  at  expiration,  and  the  alveo- 
lar wall  is  thus  again  abnormally  expanded.  The  cough,  which  is  often  present 
in  chronic  bronchitis,  is  a  further  factor,  which  acts  in  a  precisely  similar 
injurious  fashion.  The  act  of  coughing  begins  with  a  forced  contraction  of 
the  muscles  of  expiration,  which  follows  the  closure  of  the  glottis.  Until  the 
glottis  opens,  therefore,  the  lower  parts  of  the  lung  especially  are  put  under 
strong  pressure.  The'  air  in  them,  which  cannot  escape  outward,  is  driven  into 
the  upper  parts  of  the  lung,  and  there  leads  to  expansion  of  the  alveoli,  and 
finally  to  emphysema. 

We  accordingly  see  that  a  number  of  injurious  influences  cooperate  in  the 
gradual  development  of  emphysema  from  chronic  bronchitis,  and  that,  sooner 
or  later,  these  influences  have  as  their  result  the  gradual  dilatation  of  the  lungs. 
Here,  too,  we  must  bear  in  mind  the  individual  differences  in  the  resisting 
power  of  the  lungs. 

Conditions  precisely  similar  to  those  in  chronic  bronchitis  occur  in  other 
diseases,  and  lead  in  like  manner  to  pulmonary  emphysema.  We  very  often  see 
the  development  of  emphysema  in  severe  and  persistent  whooping  cough.  The 
worst  factor  here,  besides  the  existing  bronchitis,  are  the  frequent  paroxysms 
of  coughing.  Many  cases  of  pulmonary  emphysema  and  chronic  bronchitis 
may  be  ultimately  referred  to  such  a  severe  bronchial  disease  occurring  in 
childhood.  We  have  already  mentioned,  in  the  description  of  bronchial  asth- 
ma, both  the  acute  emphysema,  which  occurs  during  the  attacks,  and  the  final 
development  of  a  permanent  emphysema. 

In  conclusion,  we  must  here  consider  a  theory  advanced  by  Freund,  which 
would  make  the  development  of  an  emphysema  dependent  upon  a  "  primary 


230  DISEASES   OF   THE   RESPIRATORY   ORGANS 

rigid  dilatation  of  the  thorax."  It  is  indeed  conceivable  that  from  certain 
pathological  changes  in  the  costal  cartilages,  as  Freund  claims,  a  thorax,  which 
had  become  fixed  in  the  position  of  inspiration,  might  exert  a  constant  abnor- 
mal traction  on  the  lungs  and  so  give  rise  to  an  emphysema.  The  occurrence 
of  this  hypothetical  primary  disease  of  the  cartilages,  however,  has  up  to  the 
present  time  not  been  established.  It  is  rather  considered  by  the  majority  of 
authors  as  a  secondary  change,  developing  as  a  result  of  emphysema  or  else 
simultaneously  with  it.  On  the  other  hand,  it  is  certainly  remarkable  that 
we  sometimes  observe  in  children  the  "  emphysematous  -habit "  of  the  thorax 
and  neck,  which  will  be  more  fully  described  farther  on,  and  that  in  fact  we 
can  often  discover  in  such  children  a  beginning  emphysema  early  in  life.  We 
might  perhaps  imagine  a  congenital  failure  of  harmony  between  the  size  of  the 
thorax  and  the  size  of  the  lungs,  whereby  the  latter  are  from  the  start  in  con- 
stant hypertension. 

Besides  the  already  described  essential  or  substantial  emphysema,  which  is 
a  special  disease  attacking  both  lungs  uniformly,  we  distinguish  a  so-called 
vicarious  or  complementary  emphysema.  If,  by  any  disease,  certain  portions 
of  the  lungs  are  incapacitated  in  their  functions,  the  parts  which  remain 
healthy  must  then  assume  the  whole  business  of  respiration.  The}r  become 
excessively  expanded  on  inspiration,  and  as  a  result  they  become  emphysema- 
tous. Thus  we  see  emphysema  of  the  upper  lobes  in  affections  of  the  lower 
lobes.  Emphysema  of  one  lung  is  most  frequently  observed  clinically  when 
the  other  lung  is  extensively  diseased,  especially  in  unilateral  chronic  contrac- 
tion of  the  lung  and  pleura,  usually  seen  in  tuberculosis.  Vicarious  emphy- 
sema may  also  be  confined  to  quite  small  portions  of  the  lung,  but  then  it  is 
merely  of  pathological  and  not  of  clinical  interest. 

Pathological  Anatomy. — As  we  have  seen,  the  actual  abnormality  of  the 
lung  in  emphysema  is  not  due  to  an  anatomical  change,  but  to  a  change  in  its 
physical  conditions.  The  loss  of  elasticity  of  the  lung  is  shown  in  its  greater 
volume,  in  its  lack  of  contractility,  and  in  its  persistence  in  a  position  of 
inspiration. 

The  single  alveoli  are,  of  course,  just  as  much  expanded  as  the  whole  lung, 
but  their  walls  show  at  first  no  histological  changes.  We  have  here,  then,  a 
condition  which  Traube  has  called  "  increased  volume  of  the  lungs,"  and  has 
distinguished  from  the  "  pulmonary  emphysema  "  proper.  This  distinction  is 
without  doubt  justified  anatomically,  but  clinically  it  cannot  well  be  main- 
tained. As  the  distention  is  constant,  the  alveolar  walls  cannot  withstand  the 
constant  traction  and  pressure.  This  leads  to  progressive  atrophy  of  their 
tissue  from  pressure — that  is,  it  leads  to  a  real  disappearance  of  the  elastic 
elements  of  the  lung.  The  atrophy  begins  quite  gradually.  The  partition 
walls  of  the  alveoli  are  first  perforated,  and  then  they  partly  or  wholly  break 
down.  The  neighboring  alveoli  run  more  and  more  into  one  another,  and 
thus  finally  arise  alveolar  ectasis  and  infundibular  ectasis,  which  can  be  made 
out  with  the  naked  eye,  and  which  may  attain  a  diameter  of  TV  to  f  of  an  inch 
(0.5  to  2  cm.)  or  more.  If  single  air  bubbles  enter  the  interlobular,  interstitial, 
or  subpleural  connective  tissue,  which  may  happen  perhaps  in  severe  fits  of 
coughing,  we  speak  of  an  interstitial  or  interlobular  emphysema,  in  distinction 
from  the  ordinary  vesicular  or  alveolar  emphysema. 

The  tissue  atrophy  in  the  septa  of  the  alveoli  affects  not  only  the  elastic 


PULMONARY  EMPHYSEMA  231 

tissue,  however,  but  also  the  branches  of  the  pulmonary  capillaries  in  the  al 
lar  walls.  The  affection  of  the  elastic  tissue  adds  no  new  conditions  to  the  dis- 
turbed functions  of  the  emphysematous  lung,  which  we  have  jus!  described. 
The  destruction  and  final  atrophy  of  the  pulmonary  capillaries,  however,  is 
the  second  important  factor  in  the  pathology  of  pulmonary  emphysema,  for, 
with  the  destruction  of  so  great  a  part  of  the  vascular  area  in  the  lungs,  the 
outflow  from  the  right  side  of  the  heart  is  considerably  impeded.  There  must 
therefore  necessarily  be  a  stasis  in  the  pulmonary  arteries  and  the  right  side 
of  the  heart,  and  the  right  side  of  the  heart  can  overcome  the  increased  resist- 
ance only  by  increased  work,  and  thus  in  chronic  pulmonary  emphysema  there 
must  finally  arise  a  dilatation  and  consecutive  hypertrophy  of  the  right  ven- 
tricle with  their  further  consequences. 

Symptoms  and  General  Course  of  the  Disease. — Although  a  pulmonary  em- 
physema may  sometimes,  as  in  whooping  cough,  develop  in  a  comparatively 
short  time,  still,  its  course  is  always  very  chronic.  In  most  cases  the  origin 
of  the  disease  is  quite  gradual,  as  in  all  those  instances  in  which  emphysema 
develops  from  chronic  bronchitis  or  asthma,  or  as  a  result  of  some  injurious 
occupation.  The  symptoms  gradually  and  insidiously  associate  themselves 
with  those  of  the  chronic  bronchitis. 

The  symptoms  of  emphysema  usually  begin  in  middle  or  advanced  life,  but 
marked  emphysema  may  occur  even  in  youth  and  childhood.  The  disease 
always  lasts  for  years,  unless  some  fatal  intercurrent  disease  arises. 

The  objective  and  subjective  symptoms  are  due  either  to  the  chronic  bron- 
chitis, which  very  often  coexists,  or  to  the  emphysema  itself.  As  we  have  seen 
above,  chronic  bronchitis  is  nearly  always  the  primary  disease  from  which  em- 
physema gradually  develops.  On  the  other  hand,  to  be  sure,  emphysema  can 
lead  to  a  stasis  of  the  pulmonary  circulation  (vide  infra),  and  in  this  manner 
favor  the  development  or  the  increase  of  a  chronic  bronchitis.  At  any  rate,  the 
two  diseases,  emplrysema  and  chronic  bronchitis,  are  closely  connected  clin- 
ically. 

Bronchitis  causes  its  well-known  symptoms — cough,  expectoration,  moderate 
dyspnoea,  and  a  feeling  of  pressure  in  the  chest.  The  bronchiectases,  which  are 
often  gradually  formed,  especially  in  the  lower  lobes,  may  lend  a  peculiar  stamp 
to  the  cough  and  expectoration  (vide  page  198).  Emphysema  increases  the 
patient's  dyspnoea  to  a  degree  which  can  only  rarely  be  caused  b}^  chronic  bron- 
chitis alone.  The  emphysematous  lungs  soon  become  incapable  of  satisfying 
any  extraordinary  demands  of  respiration.  Many  patients  are  only  slightly 
conscious  of  the  difficulty  in  breathing  so  long  as  they  keep  quiet,  but  when- 
ever they  make  a  trifling  physical  exertion,  go  upstairs,  or  take  a  little  longer 
walk  than  usual,  the  dyspnoea  comes  on. 

The  variations  in  the  intensity  and  extent  of  the  bronchitis  correspond  to 
the  frequent  and  quite  marked  variations  in  the  patient's  feelings.  These 
variations  depend  upon  the  condition  of  the  patient,  his  circumstances,  and 
the  possibility  of  his  taking  care  of  himself ;  the  change  of  seasons,  too,  has  an 
influence  on  him.  In  pleasant  weather  many  patients  live  in  tolerable  com- 
fort, but  autumn  and  winter  bring  an  aggravation  of  all  their  symptoms  with 
the  increase  in  their  bronchitis. 

The  last  stage  of  the  disease  is  characterized  by  the  appearance  of  disturb- 
ance of  compensation  in  the  heart.     We  have  seen  above  that  the  cause  of  the 


232  DISEASES  OF  THE   RESPIRATORY   ORGANS 

impairment  of  the  pulmonary  circulation,  and  of  the  resulting  lrypertrophy  of 
the  right  ventricle,  is  the  closure  of  numeroiis  pulmonary  capillaries.  A  fur- 
ther reason  for  the  impairment  of  the  circulation  .comes  from  the  disturbance 
of  respiration  itself,  since  the  influence  of  the  respiratory  movements  on  the 
circulation  is  well  known.  The  appearance  of  a  marked  disturbance  of  the 
circulation  may  be  deferred  for  some  time  by  the  increased  efforts  of  the  right 
ventricle.  The  cyanosis  of  most  patients,  however,  is  due  not  only  to  incom- 
plete oxidation  but  to  the  blood  stasis  which  extends  backward  from  the  right 
side  of  the  heart  into  the  veins  of  the  body.  Finally,  the  right  ventricle  be- 
comes more  and  more  feeble,  the  stasis  in  the  veins  increases,  oedema  of  the 
extremities  and  transudation  into  the  various  cavities  of  the  body  ensue,  and 
after  long  suffering  "the  patient  succumbs  to  dropsy. 

Emphysema  is  frequently  combined  in  its  later  stages  with  other  chronic 
diseases.  Pulmonary  emphysema  with  its  sequelae  is  seldom  found  at  the 
autopsy  as  a  single  lesion,  but  we  discover  in  the  cadaver  coexisting  disease  of 
the  heart,  the  blood  vessels,  or  the  kidneys,  all  a  genuine  wearing  out  of  the 
aging  body.  Pulmonary  tuberculosis  is  often  a  final  development  in  emphy- 
sema, but  it  is  usually  of  the  chronic  indurated  form,  and  is  not  very  extensive. 

Physical  Examination.  1.  Inspection. — In  many  patients  we  can  detect 
the  disease  with  considerable  certainty  at  the  first  glance ;  we  are  therefore 
justified  in  speaking  of  an  emphysematous  habit.  (See  Fig.  44.)  The  pa- 
tients are  usually  quite  well  nourished,  at  least  in  the  early  stages  of  the  dis- 
ease, and  are  often  rather  corpulent.  They  appear  plump  or  even  somewhat 
bloated,  and  their  faces  are  more  or  less  markedly  cyanotic.  The  configuration 
of  the  neck  and  thorax  is  especially  characteristic.  The  neck  is  usually  short 
and  thick;  the  sterno-cleido-mastoid  muscles,  which  have  to  act  as  auxiliaries 
in  inspiration,  are  tense  and  hypertrophied,  especially  during  the  inspiratory 
contraction.  The  inspiratory  contraction  of  the  scaleni  may  also  be  seen  and 
felt.  The  veins  in  the  neck  are  visibly  dilated,  and  in  severe  cases  are  swollen 
to  thick  blue  cords,  and  we  sometimes  see  in  them  evident  undulating  or  jml- 
sating  movements.  The  thorax  is  rather  short,  but  broad  and  strikingly  deep 
— the  "  barrel-shaped  thorax."  The  intercostal  spaces  are  narrow,  and  the 
lower  ribs  incline  only  a  little  downward.  The  epigastric  angle  is  therefore 
obtuse,  and  sometimes  becomes  almost  a  straight  line.  The  respiratory  move- 
ments are  almost  always  accelerated  in  severe  cases.  Inspiration  becomes  short 
and  labored.  The  excursions  of  single  ribs  are  therefore  slight,  and  the  thorax 
is  raised  rigidly  and  more  as  a  whole.  Expiration  is  distinctly  prolonged. 
There  may  be  a  noticeable  retraction  of  the  intercostal  spaces  on  inspiration, 
in  the  lower  and  lateral  portions  of  the  thorax. 

This  characteristic  form  of  the  thorax  in  emphysema  is  regarded  as  a 
constant  inspiratory  position  of  the  ribs,  and  corresponds  to  the  permanent  in- 
spiratory dilatation  of  the  lungs.  The  peculiar  rigidity  of  the  thorax  is  prob- 
ably due  to  the  changes  in  the  costal  cartilages  already  described,  which,  ac- 
cording to  Freund,  are  primary.  In  many  cases  the  emphysematous  form  of 
the  thorax  gradually  develops  in  the  course  of  the  disease,  but  in  other  cases 
it  seems  to  depend  on  some  original  predisposition  to  the  disease  {vide 
supra). 

In  conclusion,  we  must  state  that  the  above  description  corresponds  to  the 
typical  form  of  emphysema,  from  which  we  may  have  many  deviations.     In 


PULM  ONA  RY   EMPH  YSE  .\  I A 


233 


the  paralyzed  thorax,  for  instance,  we  may  meel  with  a  high  degree  of  '  --ential 
emphysema  of  the  lungs,  which  may  give  rise  to  errors  in  diagnosis. 

2.  Percussion. — Percussion  gives  very  decided  results  in  the  diagnosis  of 
pulmonary  emphysema.  We  find  the  inferior  holder  of  the  lunge  one  or  two 
intercostal  spaces  lower  than  under  normal  conditions,  corresponding  to  their 


Fig.  44. — Advanced  pulmonary  emphysema.     (Breslau  Medical  Clinic.) 

permanent  inspiratory  inflation.  Clear  pulmonary  resonance  on  the  right 
front  in  the  line  of  the  nipple  extends  to  the  lower  border  of  the  seventh,  and 
sometimes  of  the  eighth,  rib.  On  the  left  front  it  extends  to  the  fifth  or  sixth 
rib,  so  that  the  cardiac  dullness  is  lessened.  The  area  of  cardiac  dullness 
can  often  not  be  made  out  at  all ;  or,  at  most,  on  strong  percussion,  it  is  made 
out  in  a  limited  extent  as  relative  dullness.  The  pulmonary  resonance  ex- 
tends on  both  sides  in  the  back  to  the  first  or  second  lumbar  vertebra.  These 
results  of  percussion  in  emphysema,  however,  are  frequently  altered,  because 
other  conditions,  such  as  passive  congestion  of  the  liver,  meteorism,  and  ascites, 
may  be  present  at  the  same  time,  and  push  up  the  diaphragm.     Thus  the 


234  DISEASES   OF   THE   RESPIRATORY  ORGANS 

detection  of  emphysema  by  percussion  is  made  decidedly  difficult.  An  in- 
crease in  the  lung  area  is  also  absent  in  the  emphysema  of  old  age  (senile 
atrophy  of  the  lungs). 

Qualitative  changes  in  the  percussion  note  may  be  entirely  wanting  in  em- 
physema. The  pitch  is  sometimes  remarkably  loud  and  deep — the  "  box  tone  " 
[tympanitic  resonance] ;  but  in  other  cases,  especially  in  the  back,  we  find  it 
somewhat  dull.  This  may  depend  in  part  upon  the  poor  vibratory  conditions 
in  the  rigid  chest  walls,  but  in  other  cases  it  is  caused  by  the  retention  of  an 
abundant  secretion  in  the  lower  lobes. 

On  inspiration,  the  lower  edge  of  the  lung  moves  downward  very  little  or 
not  at  all.  This  is  an  important  sign  in  diagnosis.  Since  the  lung  is  always  in 
a  state  of  abnormal  inspiratory  distention,  and  since  the  entrance  of  air  is 
impeded  by  the  accompanying  catarrh  of  the  bronchi,  the  difference  between 
the  inspiratory  and  expiratory  expansion  of  the  lung  is  much  diminished.  The 
difference  caused  by  respiration  in  the  lower  limit  of  the  lung  affords  a  good 
measure  of  the  respiratory  disturbance  in  the  lower  lobes. 

The  detection  of  dilatation  and  hypertrophy  of  the  right  ventricle  by 
percussion  is  in  many  cases  difficult,  because  the  lungs  cover  the  heart.  A 
positive  result  can  be  obtained  only  by  carefully  defining  the  relative  cardiac 
dullness.  [For  this  purpose  some  prefer  vigorous  percussion  and  others  very 
light  strokes.]  The  epigastric  pulsations  frequently  seen  in  emphysema,, 
and  also  the  marked  undulating  and  pulsating  movements  in  the  jugular 
veins,  are  to  be  regarded  as  quite  certain  signs  of  dilatation  of  the  right  side 
of  the  heart. 

3.  Auscultation. — The  characteristic  auscultatory  sign  of  emphysema  is 
the  prolonged  expiration.  As  a  flabby  rubber  band,  when  it  is  stretched  and 
then  let  loose,  no  longer  snaps  back  quickly  and  strongly,  so  the  emphysema- 
tous lung,  when  it  has  been  stretched  in  inspiration,  comes  back  again  only 
slowly.  We  hear  with  it  a  somewhat  aspirated,  sonorous  sound,  which  plainly 
exceeds  the  vesicular  inspiratory  sound  in'  duration.  The  vesicular  murmur 
itself  often  undergoes  a  modification  in  pulmonary  emphysema.  It  has  a  sharp 
sound,  as  if  the  breath  were  sucked  in,  or  in  other  cases  it  is  rougher  and 
more  indefinite.  In  a  high  degree  of  emphysema  the  vesicular  respiration  is 
sometimes  very  faint  and  obscure,  because  the  inspiratory  current  of  air  is- 
reduced  to  a  small  amount  in  the  lungs,  which  are  already  excessively  dilated. 
In  many  cases  we  hear  rhonchi  beside  the  respiratory  murmur,  dry  whistling,, 
buzzing,  and  creaking  sounds  on  inspiration  and  expiration.  If  cylindrical 
bronchiectases  have  already  formed,  we  hear,  especially  over  the  lower  lobes,, 
numerous  fine  and  medium  moist  rales,  but  no  sonorous  rhonchi.  The  adven- 
titious sounds  may  wholly  conceal  the  respiratory  murmur.  With  a  marked 
retention  of  secretion  we  sometimes  hear  nothing  but  a  low,  suppressed  rat- 
tling. 

The  heart  sounds  are  usually  rather  feeble,  because  the  heart  is  covered 
by  the  lung.  The  "  functional  systolic  murmur  of  emphysema  "  at  the  apex, 
described  by  some  writers,  we  have  heard  much  less  frequently  than  we  should 
expect  after  the  statements  relating  to  it.  If  present,  it  is  probably  due  to- 
coexisting  valvular  changes.  The  pulmonic  second  sound  in  emphysema  is, 
as  a  rule,  markedly  accentuated,  as  a  result  of  the  stasis  in  the  pulmonary 
circulation. 


PULMONARY   EMPHYSEMA  235 

The  diminution  of  the  expiratory  pressure  in  emphysema  may  be  meas- 
ured with  the  manometer,  or  with  Waldenburg's  "  pneumatometer."  The  nor- 
mal expiratory  pressure  of  110  to  130  mm.  sinks  in  emphysema  to  loo  or  80 

mm.  As  we  should  expect.,  the  spirometer  shows  a  diminution  of  tin-  vital 
lung  capacity,  which  can  be  readily  explained.  The  normal  lung  capacity  of 
about  3,500  c.c.  falls  to  2,000  or  1,000  c.c. 

Other  Symptoms  in  the  Lungs  and  in  Other  Organs. — In  regard  to  the  other 
symptoms  in  the  lungs  we  have  only  a  little  to  add  to  what  has  already  been 
said.  The  intensity  of  the  cough  naturally  varies  in  individual  cases  accord- 
ing to  the  degree  of  the  existing  bronchial  catarrh.  Many  patients  are  trou- 
bled by  a  dry  cough,  while  others  have  abundant  expectoration.  There  is 
nothing  characteristic  of  emphysema  in  the  composition  of  the  latter.  All 
the  kinds  of  sputa  which  are  found  in  the  different  forms,  of  chronic  bronchitis 
are  also  found  in  pulmonary  emphysema.  The  dyspnoea,  whose  predomi- 
nantly expiratory  character  we  have  already  mentioned,  increases  in  advanced 
cases  to  a  most  marked  degree.  Sometimes  the  increase  shows  itself  by  the 
appearance  of  distinctly  paroxysmal  dyspnoea.  This  is  often  really  to  be 
regarded  as  a  symptomatic  bronchial  asthma,  but,  on  the  other  hand,  we  must 
not  overlook  the  fact  that  a  temporary  increase  of  the  bronchitis,  retention 
of  secretion,  and  cardiac  failure,  may  also  excite  attacks  of  dyspnoea,  which 
cannot  properly  be  termed  asthma. 

The  important  changes  in  the  heart  resulting  from  emphysema  have 
already  been  described.  The  exhausted  right  ventricle  can  no  longer  overcome 
the  increased  resistance  in  the  pulmonary  circulation.  The  difficulty  of 
respiration  is  still  greater,  from  the  passive  congestion  of  the  pulmonary  ves- 
sels. The  skin  becomes  still  more  cyanotic,  and  finally  oedema  and  general 
dropsy  develop.  The  failure  of  compensation  is  indicated  by  the  smallness 
of  the  pulse,  its  increased  frequency,  and  sometimes  by  its  irregularity;  [and 
also  by  the  fact  that  the  pulmonary  second  sound  ceases  to  be  accentuated]. 
The  difficulty  of  an  objective  examination  of  the  heart  in  emphysema  has 
been  spoken  of  above. 

The  appearances  of  blood  stasis  in  the  internal  organs  are  shown  especially 
in  the  liver  and  kidneys.  The  liver  is  swollen,  and  its  increase  in  size  (the 
liver  of  passive  congestion)  can  frequently  be  made  out  by  percussion  or  pal- 
pation. The  pains  in  the  hepatic  region,  of  which  many  patients  complain, 
are  perhaps  due  sometimes  to  the  stretching  of  the  capsule  of  the  liver, 
but  they  are  probably  more  often  muscular  pains  excited  by  the  frequent 
coughing. 

In  the  kidneys  the  effect  of  stasis  is  first  shown  by  a  diminished  excretion 
of  urine.  The  urine  is  more  scanty  in  amount,  more  concentrated,  of  a 
higher  specific  gravity,  and  of  a  darker  color.  It  generally  gives  an  abundant 
sediment  of  urates,  and  it  may  contain  a  small  amount  of  albumen.  Micro- 
scopically we  may  find  a  few  hyaline  casts,  and  a  few  red  and  white  blood 
corpuscles.  It  is  evident  that  this  diminished  activity  of  the  kidneys  favors 
the   development   of   dropsy. 

The  spleen  is  not  infrequently  found  congested  at  the  autopsy.  The  evi- 
dence of  this,  however,  is  often  uncertain  during  life,  for  percussion  of  the 
spleen  is  difficult  on  account  of  the  emphysema,  and  palpation  is  difficult 
from  the  anasarca, 


236  DISEASES   OF  THE   RESPIRATORY   ORGANS 

Gastro-intestinal  symptoms  may  be  present  in  emphysema.  The  appetite 
seldom  remains  good  throughout  the  disease.  Many  patients  suffer  from 
chronic  constipation;  and  more  rarely  there  is  a  tendency  to  diarrhea. 

Fever  is  not  present  in  simple  pulmonary  emphysema.  Whenever  fever 
exists  for  a  long  time  it  depends  on  other  complications,  such  as  severe  bron- 
chitis, pneumonia,  or  tuberculosis. 

Complications. — Complications  of  emphysema  with  other  chronic  diseases 
are  frequent.  The  old  opinion  that  emphysema  and  tuberculosis,  and  emphy- 
sema and  chronic  heart  disease,  were  antagonistic  to  each  other  is  entirely 
false.  These  complications  are  not  very  rare.  We  may  also  mention  the 
complication  with  general  arteriosclerosis  and  with  chronic  nephritis,  espe- 
cially the  contracted  kidney.  Among  acute  diseases  we  must  mention  particu- 
larly the  acute  accidental  pulmonary  complications,  to  which  emphysematous 
patients,  particularly  of  the  lower  classes,  are  much  exposed  as  a  result  of 
overexertion,  exposure  to  cold,  etc.  Acute  febrile  bronchitis  and  lobular  pneu- 
monia cause  marked  exacerbations,  and  attacks  of  true  influenza  and  croupous 
pneumonia  in  aged  patients  are  not  infrequently  dangerous  to  life. 

Diagnosis. — The  diagnosis  of  emphysema  can  be  made  directly  from  the 
results  of  the  physical  examination,  and  usually  presents  no  difficulties.  We 
think  it  important  merely  to  say  that  too  much  stress  should  not  be  laid 
upon  a  low  position  of  the  lower  edge  of  the  lung  alone.  Many  men  appar- 
ently have  dilated  lungs  but  no  symptoms  at  all.  The  chief  thing,  therefore 
(besides  the  dilatation  of  the  lungs),  is  the  presence  of  delayed  and  difficult 
expiration  and  lessened  power  of  inspiration.  The  last-named  symptoms  alone 
render  a  diagnosis  of  senile  atrophy  of  the  lungs  (the  emphysema  of  old  age) 
possible.  For,  as  indicated  above,  the  lungs  are  not  distended,  but  rather  are 
shrunken  and  atrophic.  When  a  pronounced  emphysema  is  associated  with 
decided  thoracic  symptoms,  the  question  always  arises  as  to  whether  the 
emphysema  is  the  sole  cause  of  these  manifestations,  or  whether  there  is  not, 
in  addition,  some  disease  of  the  heart,  the  blood  vessels,  or  the  kidneys  (con- 
tracted kidney).  The  contracted  kidney  is  generally  recognizable  by  a  care- 
ful urinary  examination.  It  is  more  difficult  to  judge  of  the  heart  and  the 
aorta,  especially  in  the  presence  of  pulmonary  distention.  In  previous  years 
the  diagnosis  of  "  pulmonary  emphysema  "  was  far  more  frequently  made  than 
at  the  present  time,  when  much  more  attention  is' paid  to  muscular  diseases 
of  the  heart  and  to  sclerosis  of  the  aorta,  and  when  the  X-ray  examination 
furnishes  us  with  a  new  and  exceedingly  valuable  means  for  the  recognition 
of  these  conditions.  At  any  rate,  Rontgen-ray  examination  should  never  be 
omitted  in  any  severe  case  of  emphysema.  The  diagnosis  may  also  offer  great 
difficulties  when  a  patient  with  emphysema  is  not  examined  until  the  final, 
dropsical  stage.  In  such  cases  it  is  often  very  difficult  to  avoid  confusion 
with  heart  disease  (myopathic  hypertrophy,  myocarditis,  mitral  stenosis), 
contracted  kidney,  etc.  It  is  often  difficult,  also,  to  come  to  a  decision  in 
those  cases  in  which  there  are  evident  signs  of  coexisting  cardiac  or  renal 
disease  besides  the  emphysema.  In  such  cases  it  is  often  hardly  possible  to 
decide  upon  which  of  the  different  organic  changes  the  chief  stress  is  to  be 
laid.  In  all  such  cases  we  must  place  especial  confidence  in  an  accurate  his- 
tory as  well  as  a  careful  physical  examination,  including  the  X-rays.  The 
special  nature  and  the  sequence  in  development  of  the  individual  symptoms 


PULMONARY    EMPHYSEMA  237 

often  afford    valuable  data    for  ;i  correct  appreciation   of  the  whole  clinical 

picture. 

Prognosis. — Pulmonary  emphysema  of  acute  origin — thai  is,  acute  infla- 
tion of  the  lung — like  that  resulting  from  whooping  cough  and  analogous 
affections,  may  be  recovered  from  in  many  cases.  Otherwise,  as  regards  the 
final  curability  of  the  disease,  the  prognosis  is  wholly  had.  The  duration 
of  the  disease  and  the  intensity  of  the  symptoms  are,  of  course,  very  different 
in  individual  cases.  Here  almost  everything  depends  upon  the  worldly  cir- 
cumstances and  hygienic  surroundings  of  the  patient.  With  sufficient  care 
the  disease  may  be  tolerably  well  borne  for  many  years,  but  without  it  the 
first  symptoms  of  respiratory  and  cardiac  insufficiency  appear  much  earlier. 
The  final  termination  is  usually  due  to  complications  (vide  supra). 

Treatment. — Since  emphysema  itself  is  only  slightly  amenable  to  treat- 
ment, most  of  our  therapeutic  remedies  are  directed  to  that  accompanying 
condition  upon  which  the  greater  part  of  the  symptoms  depend — the  chronic 
bronchitis.  If  we  succeed  in  improving  this,  or  even  in  wholly  removing  it, 
we  always  obtain  a  decided  improvement  in  all  the  patient's  symptoms.  The 
therapeutic  agents  mentioned  in  the  description  of  chronic  bronchitis  are 
therefore  of  frequent  use  in  emphysema. 

In  the  first  place,  we  must  seek  the  best  hygienic  conditions  for  the 
patient,  and  remove  him  from  all  injurious  influences,  such  as  dust,  bad  air, 
and  great  physical  exertion.  In  dry  catarrh  we  should  use  the  alkaline  min- 
eral waters,  and  when  there  is  abundant  mucous  secretion  the  balsams,  such 
as  turpentine  internally  and  by  inhalation.  The  most  valuable  expectorants 
are  iodid  of  potassium,  apomorphin,  and  ipecac  when  the  expectoration  is 
tough,  and  liquor  ammonii  anisatus  and  senega  when  it  is  abundant.  A 
widely  employed  mixture  ("emphysema  drops")  is  the  following:  Liq. 
ammonii  anis.,  tinct.  stramonii,  tinct.  opii  simpl.,  aa  oijss.  (10  gm.),  the 
dose  being  15  to  20  drops  three  times  daily.  (For  further  formulae,  consult  the 
Appendix.)  The  action  of  these  drugs,  of  course,  too  often  fails  of  the  desired 
result,  so  that  we  frequently  have  to  change  our  remedies.  When  there  is  a 
troublesome  cough,  disturbing  the  sleep,  we  cannot  dispense  with  narcotics, 
such  as  morphin,  codein,  or  Dover's  powder.  If  severe  dyspnoea  comes  on, 
we  may  try  to  obtain  relief  by  mustard  plasters  to  the  chest,  or  by  immersing 
the  hands  and  feet  in  hot  water.  With  asthmatic  attacks  we  may  try  iodid 
of  potassium,  besides  the  other  remedies  mentioned  for  asthma.  A  mixture 
of  3  gr.  (0.2  gm.)  of  the  sodium  salicylate  of  caffein,  and  12  gr.  (0.8  gm.) 
of  antipyrin,  or  the  stramonium  preparations,  may  also  be  of  occasional  value. 
Here,  too,  we  must  finally  resort  to  narcotics. 

We  must  carefully  watch  the  condition  of  the  heart,  and  use  digitalis 
when  there  are  signs  of  beginning  disturbance  of  compensation  and  the  pulse 
grows  small  and  irregular,  and  this  drug  may  prove  very  useful.  If  symp- 
toms of  dropsy  set  in,  we  may  sometimes  prescribe  diuretic  remedies,  such 
as  juniper  tea,  acetate  of  potassium,  diuretin,  theocin,  calomel,  etc.,  besides 
digitalis.  When  there  is  persistent  weakness  of  the  heart,  we  should  also  use 
digitalis  and  other  stimulants    (strophanthus,  camphor,  wine,  etc.). 

Besides  the  purely  symptomatic  treatment  thus  described,  the  attempt  has 
been  made  to  meet  the  causal  indications  in  emphysema,  and  especially  to  aid 
the  patient  in  expiration,  and  thus  to  improve  the  power  of  the  lung  to  con- 


238  DISEASES   OF  THE   RESPIRATORY   ORGANS 

tract,  where  it  is  possible.  To  this  end  Gerhardt  has  recommended  assist- 
ing expiration  mechanically  by  compression  of  the  thorax.  This  compression 
must  be  done  methodically  by  another  person,1  about  five  or  ten  minutes 
every  day,  by  the  aid  of  both  hands  laid  flat  on  the  lower  lateral  portions  of 
the  thorax.  The  effect  of  this  manipulation  in  diminishing  the  dyspnoea  and 
making  expectoration  easier  is  in  many  cases  very  satisfactory.  The  "  breath- 
ing chair  "  made  by  Eossbach  has  a  similar  mechanical  action. 

The  employment  of  the  pneumatic  treatment  has  also  become  quite  gen- 
eral, especially  since  the  introduction  of  Waldenburg's  portable  apparatus. 
The  expiration  into  rarefied  air,  which  meets  the  causal  indication,  may  procure 
great  relief  for  the  patient  in  many  cases,  and  sometimes,  too,  may  result  in 
an  improvement  of  the  emphysema  which  can  be  demonstrated  on  physical 
examination.  Inhalations  of  compressed  air  are  also  employed  when  there  is 
severe  bronchial  catarrh.  Still,  too  much  must  not  be  anticipated  from  pneu- 
matic treatment. 


CHAPTEE    II 

PULMONARY    ATELECTASIS 

(Compression  of  the  Lungs.     Aplasia  of  the  Lungs  in  Cases  of  Kyphoscoliosis) 

iEtiology. — Atelectasis  of  the  lungs  is  a  condition  the  direct  opposite  of 
emphysema.  While  in  the  latter  the  lungs  are  abnormally  inflated,  in  the 
former  they  are  abnormally  collapsed.  The  air  has  disappeared  from  the 
alveoli  and  lesser  bronchi,  and  in  the  most  advanced  cases  even  from  the 
larger  bronchi.  The  atelectatic  portions  of  the  lung  are  not  altered  histo- 
logically, but  are  changed  to  a  firm  tissue,  deprived  of  air — so-called  spleniza- 
tion  or  carnification. 

The  atelectasis  of  the  newborn  is  due  simply  to  deficient  respiration  and 
to  the  consequent  imperfect  entrance  of  air  into  the  lung.  In  weak  children, 
who  die  soon  after  birth,  we  often  find  the  lower  lobes  wholly  or  in  part  in 
a  fetal,  uninflated  condition — that  is,  atelectatic.  By  artificial  inflation  we 
can  readily  expand  the  lungs  to  their  normal  extent.  In  many  cases  of  weak, 
newborn  infants  there  is  at  first  an  atelectasis  of  parts  of  the  lung  which 
gradually  disappears  entirely  and  is  replaced  by  normal  conditions. 

Acquired  atelectasis  occurs  in  two  ways.  We  may  mention,  as  the  first 
and  most  frequent  setiological  factor,  the  plugging  of  the  smaller  bronchi. 
If  a  complete  closure  of  a  bronchus  arises  from  the  accumulation  of  secre- 
tion, as  may  easily  happen  in  the  narrow  bronchi  of  children,  the  air  can 
no  longer  enter,  on  inspiration,  into  that  portion  of  lung  supplied  by  the 
plugged  bronchus.     The  air  which  is  shut  up  in  it  is  gradually  absorbed  by 

1  One  of  the  author's  patients  at  the  polyclinique  in  Leipsic  made  a  very  simple  but  very  effective 
apparatus  for  producing  this  compression  of  the  thorax  on  himself  by  the  aid  of  two  narrow  boards, 
which  are  fastened  together  at  one  end  by  a  cord  of  suitable  length.  These  boards,  which  are  fur- 
nished with  a  pad  at  this  end  fitted  to  the  wall  of  the  chest,  are  laid  flat  on  the  two  sides  of  the 
thorax  so  that  their  free  ends  project  forward  some  six  inches  or  a  foot,  and  serve  as  a  one-armed 
lever.  By  pressing  them  together  the  patient  himself  can  thus,  without  any  strain,  exert  a  con- 
siderable pressure  on  his  thorax  with  each  expiration. 


PULMONARY   ATELECTASIS  239 

the  blood.  The  adjacent  parts  of  the  lung  expand,  and  the  portion  that  is 
excluded  from  respiration  collapses,  leaving  a  circumscribed  pulmonary  atelec- 
tasis, usually  rich  in  blood  but  devoid  of  air.  Such  atelectases,  in  greater  or 
less  number  and  extent,  are  very  often  found  in  the  bodies  of  children  who 
have  suffered  from  severe  bronchitis,  especially  after  measles,  whooping  cough, 
or  diphtheria.  Besides  the  direct  action  of  the  plugging  of  the  bronchus, 
the  weakness  of  the  respiratory  movements  and  the  inability  to  cough 
vigorously,  conditional  upon  the  constitutional  condition,  play  a  significant 
part. 

The  second  very  frequent  and  important  cause  of  pulmonary  atelectasis  is 
compression  of  the  lung.  In  all  the  diseases  which  diminish  the  space  for  the 
expansion  of  the  lungs,  the  lungs  are  compressed  to  a  greater  or  less  extent, 
whereby  the  air  is  squeezed  out  of  them.  Thus  arise  the  atelectases  from 
pressure  in  pleuritic  effusion,  hydrothorax,  pneumothorax,  in  marked  cardiac 
hypertrophy,  pericardial  effusion,  and  aneurism  of  the  aorta.  Atelectasis  of 
the  lower  lobes  also  arises  in  the  same  way  from  great  upward  pressure  on 
the  diaphragm  by  ascites,  meteorism,  abdominal  tumors,  etc. 

That  form  of  pulmonary  atelectasis  which  arises  from  deformities  of  the 
thorax  is  of  great  practical  importance.  In  severe  kyphoscoliosis,  the  half 
of  the  thorax  corresponding  to  the  convexity  of  the  vertebral  column  is  much 
narrowed.  The  lungs  are  materially  hindered  in  their  expansion,  and  even 
in  their  growth,  if  the  deformity  occurs  in  youth.  This  is  called  "  aplasia 
of  the  lungs,"  a  condition  which  may  give  rise  to  grave  results  (vide 
infra). 

Symptoms. — In  the  majority  of  cases  the  symptoms  of  atelectasis  are  sub- 
ordinate to  the  disturbance  caused  by  the  primary  disease.  This  is  especially 
true  in  most  of  the  atelectases  from  pressure,  although  the  most  dangerous 
factor  lies  in  the  compression  of  the  lung. 

The  atelectasis  of  the  lungs  developing  as  a  result  of  diffuse  capillary 
bronchitis,  especially  in  children,  can,  of  course,  not  be  detected  by  physical 
examination  until  it  is  of  great  extent.  The  respiration,  in  extensive  forma- 
tion of  atelectasis,  often  shows  a  very  striking  and  characteristic  deviation 
from  the  ordinary  type,  especially  when  the  atelectasis  develops  in  the  lower 
lobes.  It  is  accelerated  and  labored,  and  is  performed  chiefly  by  the  upper 
and  anterior  portions  of  the  thorax.  In  the  lower  portions  we  see  marked 
inspiratory  retractions,  which  are  caused  in  part  by  the  external  pressure  of 
the  air,  and  in  part  by  the  exaggerated  contraction  of  the  diaphragm. 

Physical  examination  can,  of  course,  reveal  abnormal  conditions,  espe- 
cially dullness  on  percussion,  only  when  the  atelectasis  is  extensive.  Dullness, 
however,  is  usually  hard  to  make  out  in  children.  Auscultation  gives  signs  of 
existing  bronchitis;  and  sometimes,  too,  with  more  extensive  consolidation, 
there  is  bronchial  respiration.  In  other  cases,  as  may  be  easily  seen,  the 
respiratory  murmur  is  much  diminished  or  wholly  absent.  Thus,  the  physical 
signs  of  atelectases  are  not  easily  distinguishable  from  those  of  pneumonia, 
especially  of  lobular  pneumonia.  In  fact,  a  sharp  distinction  between  atelec- 
tatic nodules  and  nodules  of  lobular  pneumonia  in  the  lung  cannot  be  drawn 
clinically. 

Aplasia  of  the  lungs  in  kyphoscoliosis  demands  a  special  description,  be- 
cause it  is  of  great  practical  significance.     Many  patients  with  kyphoscoliosis 


240  DISEASES   OF   THE   RESPIRATORY   ORGANS 

may  live  for  years  without  special  respiratory  disturbance.  Careful  observa- 
tion, of  course,  usually  shows  a  somewhat  labored  and  hurried  respiration, 
but  the  patients  have  not  paid  much  attention  to  it.  In  other  cases  the  diffi- 
culty in  breathing  is  more  noticeable.  The  person  affected  is  incapable  of  any 
severe  physical  exertion;  he  always  feels  short  of  breath,  and  often  suffers 
from  cough  and  expectoration.  In  the  cases  first  mentioned,  however,  which 
for  years  have  had  little  or  no  trouble,  disturbances  in  respiration  sometimes 
come  on  quite  suddenly.  They  may  also  frequently  arise  without  any  special 
cause,  and  may  attain  a  very  threatening  degree.  The  condition  may  improve, 
or  it  may  lead  to  comparatively  or  even  absolutely  sudden  death.  Examina- 
tion of  the  lungs  during  life  usually  shows  nothing  but  the  signs  of  an  exten- 
sive bronchitis.  By  careful  percussion  we  may  quite  frequently  detect  an 
increase  of  cardiac  dullness  to  the  right.  Sometimes  a  moderate  oedema 
develops.  In  such  cases  the  autopsy  shows  nothing  as  the  cause  of  death  but 
the  changes  in  the  chest.  The  lungs  are  deficient  in  air,  small,  and  com- 
pressed, but  in  circumscribed  portions,  on  the  contrary,  emphysematous  and 
expanded.  The  right  side  of  the  heart  in  the  great  majority  of  cases  is  dilated 
and  hypertrophied.  There  can  scarcely  be  a  doubt,  therefore,  that  the  cause 
of  the  onset  of  severe  symptoms  and  the  final  cause  of  death  is  to  be  sought 
in  the  cardiac  failure. 

Finally,  it  is  worthy  of  mention  that  there  is  a  frequent  form  of  mild 
atelectasis  in  the  lower  lobes,  which  occurs  in  very  sick  and  bedridden  patients 
who  usually  keep  in  one  position— on  the  back — as  in  typhoid  fever.  On 
making  such  patients  sit  up  Ave  hear  during  the  first  inspirations  exquisite 
crepitant  rales  over  the  lower  lobes,  which  sometimes  disappear  after  a  few 
deep  inspirations.  Here  we  have  to  do  with  a  mild  atelectatic  condition,  with 
a  temporary  collapse  of  the  alveoli  and  smallest  bronchi. 

Treatment. — The  treatment  of  atelectasis  coincides  in  great  measure  with 
the  treatment  of  the  primary  disease,  and  is  tberefore  to  be  looked  for  in  the 
corresponding  chapters.  The  prophylaxis  of  atelectasis,  by  constant  attention 
to  the  respiration,  is  of  great  practical  importance.  We  should  try  to  keep 
the  patient  from  lying  continually  on  his  back,  and  we  should  make  him  take 
deep  inspirations.  The  timely  use  of  tepid  baths,  with  effusions,  is  a  special 
preventive  of  the  development  of  atelectasis,  and  it  may  bring  about  a  recovery 
when  atelectasis  is  already  present. 

Tepid  baths  may  also  be  used  with  care  in  the  treatment  of  dyspnoea 
caused  by  kyphoscoliosis.  The  condition  of  the  heart,  however,  deserves 
especial  attention  (stimulants  and  digitalis).  The  reader  is  referred  to  the 
consideration  of  the  general  treatment  of  circulatory  disturbances  in  the 
chapters  on  diseases  of  the  heart.  In  other  respects  the  symptomatic 
treatment  by  expectorants,  etc.,  is  the  same  as  in  other  chronic  pulmonary 
affections. 

For  a  long  time  I  have  entertained  the  impression  that  it  might  be  possi- 
ble to  give  the  compressed  lungs,  in  cases  of  Pott's  disease,  freer  play  by  per- 
forming an  extensive  resection  of  the  ribs.  To  my  knowledge  such  a  pro- 
cedure has  never  been  practiced. 


PULMO.v\]<Y  (EDEMA  241 

CHAPTER    IIJ 

PULMONARY    (EDEMA 

etiology  and  General  Pathology. — We  have  in  pulmonary  oedema  the 
dation  of  a  highly  albuminous  fluid,  usually  somewhat  hemorrhagic,  nol  only 
into  the  interstitial  tissue,  but  also  into  the  alveoli  themselves.  The  danger 
of  the  condition  is  easily  understood  from  the  high  degree  of  dyspnoea  which 
immediately  ensues  from  it.  In  fact,  pulmonary  oedema  is  in  many  cases  a 
terminal  symptom,  which  comes  on  in  all  forms  of  acute  and  chronic  disease. 
Many  patients  are  said  to  die  with  the  signs  of  pulmonary  oedema,  especially 
patients  with  heart  disease,  pulmonary  and  renal  disease,  and  also  with  other 
affections  of  the  most  varied   kinds. 

In  rare  cases  pulmonary  oedema  is  a  transitory  symptom.  Repeated  attacks 
of  it  may  occur,  especially  in  heart  disease  and  chronic  renal  disease,  and,  for 
a  time,  at  least,  the  patient  recover  from  them. 

In  spite  of  much  clinical  and  experimental  work,  the  special  causes  of 
pulmonary  oedema  are  still  quite  obscure.  For  one  class  of  cases  the  work  of 
Cohnheim  and.  Welch  shows  that  pulmonary  oedema  is  to  be  considered  as 
purely  the  result  of  stasis.  Pulmonary  oedema  takes  place  when  the  outflow 
of  venous  blood  in  the  lung  meets  an  obstacle  which  can  no  longer  be  over- 
come by  the  mechanical  force  of  the  right  ventricle.  The  obstacle  which 
plays  the  most  significant  part  here,  and  which  may  occur  in  all  possible 
forms  of  disease — of  course  more  readily  in  those  mentioned  above  than  in 
others — is  paralysis  of  the  left  ventricle.  If  the  further  progress  of  the  blood 
is  much  hindered  by  this,  the  overfilling  of  the  pulmonary  circulation  and 
a  consequent  pulmonary  oedema  will  necessarily  follow,  in  spite  of  the  most 
vigorous  action  of  the  right  ventricle.  Many  cases  of  terminal  pulmonary 
oedema  seem  to  depend  upon  the  fact  that  the  left  ventricle  is  paralyzed  in  its 
action  sooner  than  the  right. 

The  paralysis  of  the  left  ventricle,  however,  is  certainly  not  the  only  factor 
to  be  considered  in  the  origin  of  pulmonary  oedema.  We  must  also  consider 
the  condition  of  the  walls  of  the  blood  vessels  in  the  lungs.  In  many  cases, 
especially  in  renal  disease,  pulmonary  oedema  seems  to  depend  upon  local 
changes  in  the  vessel  walls  (Sahli).  This  form  of  pulmonary  oedema  is  some- 
what akin  to  true  inflammatory  oedema.  The  latter  is  found  chiefly  in  the 
vicinity  of  portions  of  lung  infiltrated  with  pneumonia ;  it  is  usually  of  limited 
extent,  and  therefore  it  is  of  subordinate  importance  as  a  cause  of  disturbances 
in  respiration  compared  with  the  diffuse  oedema  of  stasis. 

In  very  rare  cases,  as  we  have  ourselves  seen,  an  apparently  primary  acute 
pulmonary  oedema,  with  a  speedily  fatal  termination,  develops  in  men  who 
are  apparently  perfectly  healthy,  and  the  autopsy  gives  no  explanation  of  its 
origin.  We  perhaps  have  to  do  in  these  cases  with  the  sudden  failure  of  the 
left  ventricle,  but  probably  with  acute  vascular  changes  as  well. 

Symptoms. — Marked  dyspnoea  is  the  most  striking  symptom  in  pulmonary 
oedema.  It  is  subordinate  only  when  the  patient  is  found  in  the  death  agony 
and  is  no  longer  fully  conscious. 

In  pulmonary  oedema  the  respiration  is  hurried,  labored,  and  rattling.    All 


242  DISEASES   OF   THE   RESPIRATORY   ORGANS 

the  accessory  muscles  of  respiration  are  called  into  play.  The  patient  usually 
sits  upright  in  bed.  We  see  on  his  lips  and  cheeks  a  gradually  and  constantly 
increasing  cyanosis,  and  we  often  hear  at  a  distance  the  moist  rales  originating 
in  the  larger  bronchi. 

On  examination  of  the  lungs,  the  percussion  is  essentially  normal,  if  there 
is  no  other  disease  of  the  lungs.  Sometimes  the  percussion  note  is  a  little 
higher  in  pitch,  and  often  it  is  slightly  tympanitic.  On  auscultation,  we  hear 
everywhere  many  fine  and  medium  moist  rales.  If  the  patient  can  still 
expectorate,  he  raises  a  large  amount  of  frothy,  serosanguineous  sputum.  The 
whole  picture  of  the  disease  is  so  characteristic  that  the  condition  is  but  rarety 
mistaken. 

Treatment. — Since  in  most  eases  pulmonary  oedema  is  not  so  much  the 
cause  as  a  symptom  of  approaching  death,  our  remedies  against  it  are  apt  to 
prove  powerless,  but  it  must  always  be  our  duty,  at  least  in  all  cases  that  are 
not  absolutely  hopeless,  to  try  to  relieve  the  pulmonary  circulation.  .From 
the  pathogenesis  of  pulmonary  cedema  it  follows  that  we  must  pay  particular 
attention  to  the  condition  of  the  heart,  especially  of  the  left  ventricle.  Hence 
we  should  use  energetic  stimulants,  especially  subcutaneous  injections  of  cam- 
phor or  ether,  every  half  hour  or  hour.  Internally  we  give  first  strophanthus 
(10  drops  of  the  tincture  every  hour)  and  also  camphor,  wine,  and  very  strong 
cafe  noir.  Besides  that,  we  apply  strong  irritants  to  the  chest,  such  as  large 
mustard  plasters  or  hot  sponges.  Sometimes  a  decided  improvement  of  the 
respiration,  when  it  has  nearly  stopped,  may  be  obtained  by  a  bath  with  cold 
douching.  When  there  is  marked  general  cyanosis,  if  the  patient  is  on  the 
whole  strong  and  well  nourished,  venesection  is  sometimes  of  manifest  benefit. 
Emetics,  however,  accomplish  little,  and  are  even  dangerous  on  account  of  the 
collapse  which  is  apt  to  come  on  after  them.  Expectorants  (benzoin,  liquor 
ammonii  anisatus)  are  more  frequently  prescribed,  and  an  energetic  "  deriva- 
tion to  the  intestines,"  by  senna,  calomel,  or  enemata  of  vinegar,  seems  some- 
times to  be  really  of  service.  Acetate  of  lead  in  large  doses,  1  or  2  gr.  (gm. 
€.05  to  0.10),  in  powder,  every  hour,  employed  empirically  by  Traube,  is 
deserving  of  trial. 

In  this  way,  especially  in  acute  diseases  like  typhoid  and  pneumonia,  we 
in  fact  sometimes  succeed  in  averting  the  danger  of  pulmonary  cedema  by 
rapid  and  energetic  action.  In  the  cases  of  oedema  occurring  in  incurable 
chronic  diseases  of  the  heart  and  kidneys,  the  remedies  employed  are,  of  course, 
unfortunately  incapable  of  preventing  death. 


CHAPTER    IV 

CATARRHAL    PNEUMONIA 

(Broncho-pneumonia .      Lobular  Pneumonia) 

etiology. — Catarrhal  pneumonia  is  neither  astiologically  nor  anatomically 
one  single,  absolutely  independent  disease,  but  from  a  clinical  standpoint  we 
are  perfectly  justified  in  grouping  together  the  catarrhal,  lobular  pneumonias, 
which  are  usually  secondary  to  other  diseases,  and  especially  to  a  previous 


CATARRHAL  PNEUMONIA  243 

bronchitis,  and  in  contrasting  them  with  croupous,  lobar,  "genuine"  pneu- 
monia. In  the  great  majority  of  catarrhal  pneumonias  the  belief  i-  certainly 
correct  that  the  agents  of  inflammation  do  aol  enter  the  pulmonary  alveoli 

directly  from  without,  but  that  tlie  inflammatory  pmri'.-.-  i-  situated  originally 
in  the  bronchi,  and  from  this  point  extends  downward  to  the  Bpecial  respira- 
tory parenchyma  of  the  lung.  This  extension  of  the  inflammation  may  take 
place  entirely  by  continuity,  or  it  may  skip  some  part,  as  the  germs  are  often 
inhaled  from  the  bronchi  directly  into  the  infundibula  and  alveoli.  The 
last-mentioned  parts  must,  however,  possess  considerable  power  of  resisting 
germs,  since  the  danger  of  an  extension  of  bronchitis  to  the  alveoli  generally 
exists  only  in  the  severer  and  more  extensive  cases  of  bronchitis  or  under 
other  peculiar  conditions.  This  extension  of  the  process  is  not  uniform  in 
all  parts,  but  it  occurs  first  in  the  distribution  of  some  small  branches  of  the 
bronchi,  and  this  is  the  reason  why  the  pneumonic  infiltration  affects  first 
only  a  few  bronchial  areas — that  is,  individual  lobules. 

In  opposition  to  this  generally  accepted  theory  of  the  method  of  origin  of 
the  true  "  lobular "  or  "  broncho-pneumonic "  foci,  the  attempt  has  re- 
cently been  made  to  show  that  the  inflammatory  process  can  pass  through 
the  walls  of  a  small  bronchus  directly  into  the  neighboring  parenchyma  of 
the  lung,  and  that  it  may  then  extend  farther  along  the  lymph-channels. 
Clinically,  however,  we  cannot  yet  distinguish  this  form  of  focal  pneumonia 
from  the  ordinary  catarrhal  pneumonia. 

If  we  ask  what  are  the  conditions  under  which  we  are  most  apt  to  observe 
the  development  of  lobular  pneumonia,  we  must  first  mention  a  number  of 
acute  infectious  diseases,  in  which  the  air-passages  are  primarily  affected, 
or  in  which  they  may  very  readily  be  involved  sympathetically.  Chief  among 
these  are  measles  and  whooping  cough,  and  next  diphtheria,  influenza,  small- 
pox, etc.  In  all  these  diseases  there  is  either  a  bronchitis  at  the  beginning, 
or  else  it  can  develop  very  easily  in  them.  It  is  in  these  same  diseases,  also, 
that  simple  bronchitis  comparatively  often  develops  into  lobular  pneumonia. 

Furthermore,  in  almost  all  severe  acute  and  in  many  chronic  diseases  the 
conditions  favor  the  development  of  secondary  bronchitis  and  subsequently,  at 
times,  of  lobular  pneumonia.  Everywhere  in  the  air-passages,  as  well  as  in 
the  cavities  of  the  mouth  and  pharynx,  saliva,  mucus,  etc.,  readily  collect  if  the 
patient  is  very  ill.  Expectoration  is  imperfect,  and  the  constant  dorsal  decu- 
bitus favors  the  accumulation  of  secretion,  especially  in  the  lower  lobes.  The 
mouth  and  pharynx  are  harder  to  keep  clean  than  under  normal  conditions. 
Fungi  and  bacteria  collect  in  the  secretion  itself,  as  well  as  in  the  epithelium 
and  particles  of  food  which  are  left  in  the  mouth,  and  these  excite  and  keep 
up  processes  of  decomposition.  The  inflammatory  agents,  which  are  carried 
into  the  air-passages  with  the  inspired  air,  find  everywhere  favorable  condi- 
tions for  colonization  and  further  development.  From  the  upper  portions 
they  are  drawn  farther  downward.  From  the  larger  bronchi  the  process 
invades  the  alveoli,  and  leads  to  catarrhal  pneumonia.  It  is  probably  of  sig- 
nificance, too,  that  in  such  very  sick  persons  the  vital  resistance  of  the  tissues 
has  suffered,  and  that  the  development  of  such  secondary  inflammation  is 
consequently  facilitated.  We  must  also  bear  in  mind  that  many  patients  who 
are  very  ill  have  difficulty  in  swallowing.  They  get  choked,  and  particles  of 
food,  with  the  germs  of  inflammation  clinging  to  them,  are  carried  into  the 
16 


244  DISEASES  OF  THE  RESPIRATORY  ORGANS 

air-passages.  These  particles,  which  a  healthy  person  could  easily  cough  up 
again,  remain  there,  are  decomposed,  and  give  rise  to  bronchitis  and  lobular 
pneumonia. 

This  is  the  explanation  of  the  frequent  development  of  lobular  pneumonia 
in  the  course  of  diseases  which  are  entirely  dissimilar.  We  observe  it  espe- 
cially in  severe  bedridden  cases,  in  all  patients  with  stupor,  in  severe  infec- 
tious diseases,  in  meningitis,  and  also  in  cases  of  nervous  disease,  in  which 
coughing  and  deglutition  are  impaired  as  a  result  of  bulbar  affections.  In 
all  such  cases  lobular  pneumonia  is  to  be  considered  a  complication,  and 
with  reference  to  its  origin  deserves  the  name  of  inhalation  pneumonia  or 
deglutition  pneumonia.  We  shall  soon  see  that  this  form,  under  some  circum- 
stances, may  pass  into  circumscribed  gangrene. 

Although  in  the  preceding  we  have  always  spoken  of  "  agents  of  inflam- 
mation "  in  general,  the  precise  variety  is  not  necessarily  the  same  in  all  cases. 
In  the  lobular  pneumonias  occurring  in  the  course  of  measles,  whooping  cough, 
influenza,  etc.,  it  is  possible  that  the  original  specific  germs  may  penetrate  as 
far  as  the  alveoli,  and  there  cause  an  inflammatory  exudation;  but  this  is 
certainly  not  always  the  case,  and  there  are  many  reasons  why  in  these  affec- 
tions, as  well  as  in  all  the  others  mentioned  above,  catarrhal  pneumonia  should 
be  regarded  as  a  secondary  complication,  dependent  upon  the  secondary  in- 
vasion of  other  varieties  of  agents  which  cause  inflammation.  Different 
microorganisms  may  probably  act  as  such  agents.  So  far  as  our  present 
investigations  go,  streptococci  seem  most  frequently  to  be  the  special  cause  of 
bronchopneumonia,  and  sometimes  in  other  cases  staphylococci,  diplococci, 
etc.  Clinically,  we  cannot  at  present  make  a  complete  separation  on  a  strictly 
astiological  basis. 

The  development  of  lobular  pneumonia  from  bronchitis  is  most  frequent, 
as  we  know,  in  children  and  old  people.  The  frequency  of  catarrhal  pneu- 
monia in  childhood  is  due  in  part  to  the  limited  dimensions  of  the  bronchi. 
Besides  that,  however,  the  diseases  in  which  it  is  especially  frequent — namely, 
measles  and  whooping  cough — are  children's  diseases.  In  old  people  its  com- 
paratively easy  development  is  due  to  imperfect  expectoration,  and  perhaps 
to  the  diminished  resistance  of  the  tissues. 

The  mild  cases  of  primary  bronchitis  scarcely  ever  lead  to  lobular  pneu- 
monia, but  sometimes  in  children,  and  less  often  in  adults,  a  severe  febrile 
bronchitis  may  occasion  the  formation  of  pneumonic  foci.  In  Erlangen,  the 
author  has  seen  a  good  many  cases  which  cannot  be  regarded  otherwise  than 
as  primary  catarrhal  pneumonia.  We  may  also  state  that  the  inhalation  of 
irritating  chemicals  may  occasion  lobular  pneumonia  as  well  as  bronchitis. 

Pathological  Anatomy. — It  is  characteristic  of  catarrhal  pneumonia  that 
the  inflammation  is  usually  plainly  circumscribed  (vide  supra),  being  lim- 
ited to  the  territory  of  a  small  bronchus.  Hence  the  name  of  "  lobular " 
pneumonia  or  broncho-pneumonia,  in  distinction  from  croupous  lobar  pneu- 
monia. An  atelectasis  (vide  supra)  of  the  affected  lobule,  arising  from  the 
plugging  of  the  bronchus  leading  to  it,  often,  but  not  always,  precedes  the  in- 
flammation. The  atelectasis,  of  course,  becomes  pneumonia  only  in  case  germs 
enter  the  atelectatic  spot.  The  inflammatory  process  itself  consists  in  the  exu- 
dation of  a  scanty  fluid,  which  usually  does  not  coagulate,  and  of  numerous 
pus  corpuscles  (white  blood  corpuscles)  into  the  lumen  of  the  alveoli.    With 


CATARRHAL   PNEUMONIA  245 

this  is  usually  associated  more  or  less  marked  desquamation  of  the  alveolar 
epithelium,  in  which  we  often  find  necrosis  or  tatty  degeneration.  The 
alveolar  cavities  are  completely  filled  with  leucocytes  and  epithelium;  few 
if  any  red  blood  corpuscles  are  to  he  seen,  although  in  some  cases  they  may 
be  more  abundant.  The  vessels  of  the  alveolar  walls  are  hyperacute,  and  the 
connective  tissue  also  contains  a  few  wandering  leucocytes. 

The  inflamed  lobules  are  readily  apparent  to  the  eve  and  the  touch  by, 
their  firm  consistence,  being  devoid  of  air.  Their  color  at  first,  from  the 
blood  contained  in  the  inflamed  part,  is  dark  red  ("  splenization  "),  but 
later  it  becomes  more  grayish.  A  bit  of  such  an  inflamed  spot,  cut  out  with 
scissors,  does  not  float  in  water  but  sinks,  because  it  contains  no  air.  The 
lobular  boundary  of  the  individual  nodules  is  usually  easily  distinguished 
from  the  neighboring  healthy  tissue,  but,  by  confluence  of  adjacent  nodules, 
large  portions  of  the  lung,  and  even  whole  lobes,  may  become  infiltrated 
throughout — generalized  lobular  pneumonia. 

Symptoms. — 1.  Primary  Catarrhal  Pneumonia  of  Adults. — The  primary 
catarrhal  pneumonia  which  infrequently  occurs  in  adults  usualty  begins  with 
the  same  phenomena  as  a  severe  attack  of  acute  bronchitis.  The  patient  feels 
prostrated, '  and  has  cough,  dyspnoea,  and  pain  on  the  side  which  is  chiefly 
affected.  There  is  almost  never  a  pronounced  initial  chill,  as  in  croupous 
pneumonia.  The  fever  is  usually  not  very  high,  from  101°  to  103°  F.  (38.5° 
to  39.5°  C),  but  higher  temperatures  sometimes  occur,  especially  at  the 
beginning  of  the  disease.  The  expectoration  is  simply  catarrhal  or  muco- 
purulent, never  mucosanguineous,  as  in  croupous  pneumonia.  The  physical 
examination  gives  almost  invariably  in  one  lower  lobe  many  moist  rales  and 
a  slight  tympanitic  or  dull  tympanitic  percussion  note.  Marked  dullness 
and  definite  bronchial  breathing  are  rare.  In  the  lower  lobe  on  the  other, 
unaffected  side,  we  often  find  signs  of  a  slight  bronchitis;  but  in  general  the 
unilateral  character  of  the  symptoms  is  characteristic  of  primary  catarrhal 
pneumonia,  in  distinction  from  ordinary  bronchitis  and  secondary  broncho- 
pneumonia. In  mild  cases  the  fever  lasts  from  four  to  eight  days,  but  the 
disease  may  last  two  or  three  weeks  or  more.  There  is  never  a  crisis ;  the  fever 
ends  gradually  by  lysis. 

The  setiology  of  primary  catarrhal  pneumonia  has  been  little  studied. 
Many  cases  may  be  streptococcus  pneumonia;  we  must  also  consider  the  influ- 
enza bacilli,  since  catarrhal  pneumonia  is  especially  common  at  the  time 
of  an  influenza  epidemic. 

2.  Secondary  Catarrhal  Pneumonia. — Most  of  the  cases  of  catarrhal  pneu- 
monia develop,  as  we  have  already  said,  secondarily  in  the  course  of  other 
affections,  hence  the  symptoms  are  frequently  overshadowed  by  those  of  the 
other  diseases.  There  are  often  found  at  autopsy  a  few  foci  of  lobular  pneu- 
monia in  the  lower  lobes  which  gave  rise  to  no  clinical  symptoms  whatever. 

In  other  cases,  however,  the  development  of  extensive  lobular  pneumonia  is 
of  the  greatest  clinical  significance.  In  many  cases  of  chronic  bronchitis, 
pulmonary  emphysema,  pulmonary  tuberculosis,  etc.,  in  which  the  patient 
suddenly  grows  worse  with  a  rise  of  temperature,  the  cause  is  certainly  the 
development  of  foci  of  lobular  pneumonia.  Such  complications  may  after  a 
time  completely  disappear,  or  may  cause  a  permanent  aggravation  of  the 
original  condition  (e.g.,  tuberculosis).     The  onset  of  lobular  pneumonia  in 


246  DISEASES   OF  THE   RESPIRATORY   ORGANS 

other  acute  diseases  is  very  important.  The  disturbance  of  respiration  forms 
the  most  striking  symptom  of  the  disease  during  the  patient's  life,  and  at  the 
autopsy  lobular  pneumonia  is  shown  to  be  the  immediate  cause  of  death.  The 
largest  part  of  the  fatal  cases  of  measles  and  whooping  cough,  and  no  very 
small  part  of  those  of  diphtheria,  scarlet  fever,  typhoid,  smallpox,  influenza, 
etc.,  are  due,  in  the  last  instance,  to  the  disturbance  of  respiration  dependent 
upon  lobular  pneumonia. 

Since  a  diffuse  bronchitis,  extending  into  the  finer  bronchi,  almost  always 
precedes  the  development  of  lobular  pneumonia,  and  since  it  may  also  give 
rise  in  itself  to  marked  disturbance  in  respiration,  there  is  no  sharp  boundary 
to  be  drawn  clinically  between  diffuse  capillary  bronchitis  and  lobular  pneu- 
monia. Only  the  experience,  a  hundred  times  repeated,  that  extensive  capil- 
lary bronchitis  is  apt  to  lead  to  lobular  pneumonia,  permits  us  to  suspect 
the  latter,  with  considerable  certainty,  even  if  there  is  no  direct  clinical 
evidence  of  it.  The  most  important  objective  physical  sign  of  broncho- 
pneumonia is  the  not  very  loud,  medium  moist  rales,  almost  always  to  be 
heard  in  the  lower  lobes.  These  rales  are  often  high-pitched.  Dullness  of  the 
percussion  note  develops  only  when  many  lobular  nodules  coalesce  and  form 
a  more  extensive  infiltration  of  the  lung.  Then  we  also  find  bronchial  res- 
piration. 

Catarrhal  pneumonia  is  almost  always  associated  with  fever,  which  is 
moderately  high  and  generally  has  a  remitting  character.  We  must,  of 
course,  judge  of  the  fever  in  connection  with  the  primary  disease  and  any 
other  complications. 

No  general  statements  can  be  made  as  to  the  duration  of  secondary  catar- 
rhal pneumonia.  Sometimes  the  acute  symptoms  last  only  a  few  days,  in 
other  cases  they  continue  for  weeks.  Catarrhal  pneumonia  is  not  infre- 
quently followed  by  pleuritic  effusion,  when  the  lobular  infiltration  reaches 
the  pleura.  Foci  of  lobular  pneumonia  may  develop  into  abscess  or  gangrene, 
but  this  is  rare. 

3.  Catarrhal  Pneumonia  in  Childhood. — The  catarrhal  pneumonia  of 
childhood  is  very  characteristic  and  clinically  important.  It  is  observed  most 
frequently  in  measles  and  whooping  cough,  and  also  in  Aveak,  atrophic,  and 
rachitic  children.  The  increased  frequency  of  respiration  is  most  striking. 
The  breathing  is  superficial,  but  labored,  as  is  shown  by  the  contraction  of 
the  auxiliary  muscles  of  inspiration  and  the  play  of  the  nostrils.  We  also 
notice  inspiratory  retraction  of  the  lower  lateral  portions  of  the  thorax  as 
a  result  of  the  incomplete  entrance  of  air.  The  number  of  respirations  in  a 
minute  increases  in  children  to  sixty  or  eighty,  or  even  more.  In  most  cases 
the  child  has  a  frequent  and  apparently  painful  cough.  Expectoration  is 
entirely  absent  in  small  children.  When  it  is  present  it  shows  no  charac- 
teristic peculiarities  different  from  ordinary  catarrhal  sputum.  The  general 
condition  is  always  bad.  The  child  is  restless.,  apathetic,  and  more  or  less 
stupid.  Its  face  is  usually  pale,  but  often  quite  cyanotic.  The  pulse  is 
very  rapid,  and  in  small  children  may  attain  i  frequency  of  140  to  180  a 
minute.  Fever  is  almost  always  present.  It  shows  no  typical  course,  it  is 
now  remitting  and  now  intermitting,  and  toward  evening  it  perhaps  rises 
to  104°  or  105°  F.  (39.5°  to  40.5°  C).  The  occurrence  of  such  a  rise  in 
temperature  is  not  without  value  in  the  diagnosis  of  catarrhal  pneumonia. 


CIATARRfrAL   PNEUMONIA  247 

Tf  in  diffuse  capillary  bronchitis  a  high  fever  is  presenl  for  Bome  time,  we 
may  assume  with  considerable  certainty  thai  the  lobular  infiltration  haf 
already  begun. 

Physica]  examination  furnishes  dired  evidence  of  the  affection  of  the 
lungs,  but  its  results  are  for  the  most  part  to  be  referred  to  the  diffuse  bron- 
chitis and  not  to  the  lobular  infiltration.  Auscultation  gives  the  mos1  valu- 
able signs.  We  hear  over  the  lungs,  in  a  greater  or  less  extent,  numerous 
fine  and  medium  moist  rales,  often  quite  high-pitched.  From  these  signs, 
strictly  interpreted,  we  can  diagnosticate  merely  bronchitis,  bul  we  may 
suspect  pneumonia  with  the  greatest  probability.  With  very  confluent  bron- 
cho-pneumonia, auscultation  sometimes  gives  bronchial  breathing  and  bron- 
chophony, besides  the  rales. 

It  goes  without  saying  that  little  lobular  foci,  surrounded  by  normal 
lung  tissue  containing  air,  give  no  special  signs  on  percussion.  With  numer- 
ous nodules  running  into  one  another,  the  percussion  note  is  duller,  and 
there  is  sometimes  tympanitic  resonance.  The  dullness  is  often  first  to  be 
made  out  over  a  stripe  extending  along  the  vertebral  column — so-called 
"  stripe  pneumonia."  X-ray  pictures  bring  out  the  lobular  foci  very  dis- 
tinctly. 

An  attack  of  extensive  lobular  pneumonia  is  usually  quite  protracted. 
Even  in  favorable  cases  the  disease  rarely  lasts  less  than  two  or  three  weeks, 
and  it  may  persist  much  longer.  The  course  of  the  disease  is  apt  to  be  irreg- 
ular, relapses  succeeding  improvement.  The  chief  danger  of  the  disease  lies 
in  this  tendency  to  a  protracted  course,  extending  over  weeks  and  months. 
Many  children  finally  die,  not  of  the  lobrdar  pneumonia  itself,  but  from  the 
general  weakness  and  emaciation  following  the  tedious  febrile  disease.  We 
must  remember,  however,  that  complete  recovery  may  sometimes  take  place 
quite  late  in  the  disease. 

The  "  transition  of  catarrhal  pneumonia  to  caseation  and  tuberculosis " 
is  a  clinical  fact  with  which  physicians  have  long  been  conversant.  In  fact, 
we  often  find  true  tuberculous  changes  in  the  lungs  of  children  who  have  died 
after  a  tedious  illness,  as  a  result  of  measles,  whooping  cough,  etc.  There 
can,  of  course,  be  no  real  question,  however,  of  an  actual  transition  from  one 
disease  to. the  other.  In  such  cases  either  we  have  to  do  with  an  acquired 
tuberculous  infection,  which  has  found  a  favorable  soil  in  an  already  dis- 
eased lung,  or  (what  is  probably  more  frequently  the  case)  the  disease  of 
the  lung  has  promoted  the  development  of  a  previously  existing  tuberculosis. 
It  is  usually  weak  children,  with  a  hereditary  predisposition  to  tubercle, 
who  succumb  to  tuberculosis  as  a  result  of  the  above-named  diseases.  The 
diagnosis  of  a  developing  tuberculosis  is  not  always  easy,  since  it  is  only 
rarely  that  marked  phthisical  changes — like  dullness  at  the  apex,  cavities, 
etc.,  which  can  be  made  out  by  a  physical  examination — are  found  in  the 
lungs.  We  can  usually  suspect  tuberculosis  only  from  the  general  conditions 
(emaciation,  persistent  hectic  fever,  hereditary  predisposition,  or  some  sec- 
ondary tubercular  disease,  such  as  meningitis,  etc.),  especially  as  absolute 
proof,  from  the  detection  of  tubercle  bacilli  in  the  sputum,  is  only  rarely 
possible  in  children.  [Sometimes  the  physician  or  a  good  nurse  can  obtain 
sputum  on  a  stick'  wrapped  with  absorbent  cotton,  as  the  baby  coughs  it  up 
before  he  has  time  to  swallow  it.] 


248  DISEASES   OF  THE   RESPIRATORY  ORGANS 

Treatment. — Since  we  have  already  mentioned  the  proper  treatment,  in  our 
description  of  the  various  diseases  in  which  secondary  pneumonia  is  especially 
prone  to  develop,  we  can  now  be  brief.  We  have  also  laid  repeated  stress  upon 
the  possibility  and  the  great  practical  importance  of  prophylaxis,  which  is 
self-evident  from  a  just  comprehension  of  the  origin  of  lobular  pneumonia. 
Besides  keeping  the  nose,  the  mouth,  and  the  pharynx  as  clean  as  possible, 
tepid  baths,  perhaps  with  cool  douching,  are  the  best  means  of  preventing  the 
development  of  lobular  pneumonia,  or  of  checking  its  further  extension.  Wet 
cold  packs  are  often  used  with  advantage  (vide  infra).  It  is  an  advantage, 
which  is  indeed  to  be  considered  in  the  second  rank  in  comparison  with  the 
improvement  in  respiration,  that  by  both  the  bath  and  the  pack  the  febrile 
temperature  is  at  the  same  time  reduced. 

In  the  treatment  of  the  lobular  pneumonia  of  children  a  wet  pack  includ- 
ing the  whole  body  is  the  best  remedy.  A  sheet  is  dipped  in  water,  wrung 
out,  and  wrapped  around  the  whole  of  the  patient  except  his  head  and  arms. 
Outside  of  this  is  to  be  placed  a  dry  woolen  blanket  or  a  layer  of  oiled  muslin. 
The  temperature  of  the  water  employed  should  be  68°  to  75.2°  F.  (20°  to 
24°  C).  The  higher  the  fever  the  colder  should  the  water  be,  and  the  oftener, 
say  every  hour  or  two,  must  the  pack  be  renewed.  In  milder  cases  and  at 
night  it  may  be  allowed  to  remain  for  three  or  four  hours.  The  beneficial 
influence  of  the  pack  is  shown  not  only  by  the  temperature,  but  still  more 
by  the  respiration.  It  is  often  striking  to  see  how  much  quieter  the  child 
becomes  in  the  pack.  If  the  breathing,  despite  this  remedy,  remains  unsatis- 
factory, and  the  patient  becomes  more  and  more  stuporous,  the  treatment  must 
be  changed  to  lukewarm  baths  of  a  temperature  of  77°  to  86°  F.  (25°  to  30° 
C),  with  douchings  of  colder  water.  It  is  sometimes  advisable  in  severe  cases 
to  add  to  the  water  employed  for  bathing  or  for  the  wet  pack  a  few  handfuls  of 
mustard.     The  stimulation  thus  exerted  upon  the  skin  is  quite  marked. 

Among  external  applications  to  the  chest,  besides  mustard  plasters  and 
poultices,  dry  cups  are  to  be  mentioned,  which  often  do  very  good  service  in 
strong,  older  children,  and  especially  in  adults.  We  never  need  to  use  local 
blood  lettings,  however,  in  catarrhal  pneumonia. 

Of  internal  remedies,  expectorants  are  most  used.  Chief  among  these  are 
ipecac,  apomorphin,  senega,  and  benzoic  acid.  This  last  is  particularly  useful 
in  the  lobular  pneumonia  of  children.  In  strong  children  the  abundant 
collection  of  mucus  in  the  bronchi  may  sometimes  be  relieved  by  the  admin- 
istration of  an  emetic,  but  we  seldom  need  to  resort  to  this.  We  should  also 
be  cautious  in  the  use  of  narcotics.  Stimulants  (camphor,  caffein)  must  be 
used  in  severe  cases.  Antipyretics  may  be  given  to  reduce  the  temperature, 
but  if  cool  packs  be  used,  antipyretics  can  be  wholly  dispensed  with.  Inha- 
lations or  sprays  are  quite  valueless  in  lobular  pneumonia,  yet  it  is  recom- 
mended to  keep  the  air  in  the  sick-chamber  constantly  moist  by  hanging  up 
wet  towels,  or  by  sprinkling  with  water.  The  room  should  also  be  as  large 
and  as  well  ventilated  as  possible.  [Inhalations  of  oxygen  may  do  much 
good.]  The  general  hygienic  treatment  is  of  the  greatest  importance.  One 
of  the  most  important  duties,  of  which  the  physician  must  always  be  mind- 
ful, is  to  keep  up  the  patient's  strength  by  sufficient  and  proper  food.  When 
convalescence  sets  in,  complete  restoration  to  health  may  be  materially  fur- 
thered by  going  to  a  suitable  place  in  the  country. 


cnoi  j'Ois  I'.nki  aioma  249 


CHAPTER    V 

CROUPOUS    PNEUMONIA 

(Lung  Fever.     Lobar  Pneumonia.     Fibrinous  Pneumonia.     Pleuropneumonia) 

Croupous  pneumonia  is  a  sharply  defined  febrile  disease  of  the  lungs, 
which,  in  the  great  majority  of  cases,  displays  a  distinct  individuality  in  its 
clinical,  anatomical,  and  usually,  also,  its  etiological  relations.  Among  the 
severe  acute  diseases  it  is  decidedly  one  of  the  most  important  and  frequent, 
and  it  is  universally  familiar  even  to  the  laity  under  the  names  of  pneumonia 
or  inflammation  of  the  lungs.  In  most  cases  this  disease  appears  quite  sud- 
denly, and  often,  apparently  without  any  special  cause,  in  persons  up  to  that 
time  in  perfect  health.  Such  cases  are  described  as  primary,  genuine,  or  frank 
pneumonia.  On  the  other  hand,  a  case  of  croupous  pneumonia  will  sometimes 
occur  as  a  complication  of  all  sorts  of  other  diseased  conditions  (secondary 
pneumonia).  The  clinical  picture  of  pneumonia  in  these  latter  cases,  how- 
ever, is  usually  obscure  and  not  well  characterized,  and  consequently  the  fol- 
lowing description  is  especially  applicable  to  the  primary  form  of  the  disease. 

.ZEtiology. — The  thought  that  croupous  pneumonia  might  be  an  acute  in- 
fectious disease  had  impressed  the  majority  of  physicians  for  a  considerable 
length  of  time,  but  this  suspicion  did  not  receive  satisfactory  substantiation 
until  the  more  recent  investigations  in  bacteriology  had  been  made.  For 
instance,  Friedlander  demonstrated  a  special  form  of  bacillus  in  lungs  affected 
with  pneumonia.  Then,  later,  A.  Frankel,  and,  soon  after  him,  Weichselbaum, 
proved  that  while  this  "  pneumonia  bacillus  of  Friedlander  "  is  to  be  regarded 
as  the  cause  of  croupous  inflammation  of  the  lungs  in  a  few  cases  (just  as  we 
have  a  peculiarly  malignant  form  of  streptococcus  pneumonia),  yet  in  the 
overwhelming  majority  of  instances  the  particular  etiological  factor  is  the 
so-called  Diplococcus  pneumonice  (pneumococcus). 

The  pneumonia  diplococcus  is  characterized  by  its  lancet-shaped  outline 
("like  the  flame  of  a  candle  "),  and  its  frequent  arrangement  in  pairs,  the 
individuals  of  each  pair  having  usually  their  broad  ends  apposed.  Very  often 
there  are  short  chain  forms.  The  pairs  of  diplococci  are  usually  surrounded 
by  a  delicate  capsule.  This  is  especially  easy  to  see  in  preparations  of  the 
sputum.  We  have  not  space  to  describe  particulars  as  to  the  pure  cultures  of 
the  pneumococci  upon  agar  and  similar  media. 

The  pneumococcus  is  very  virulent  for  mice,  guinea  pigs,  and  rabbits, 
and,  when  injected,  causes  a  rapidly  fatal  pneumococcus  sepsis. 

Pneumonia  diplococci  are  among  the  most  widely  distributed  of  pathogenic 
organisms.  They  produce  severe  disease  not  only  in  the  lungs,  but  in  many 
other  organs.  With  regard  to  the  development  of  the  pneumonic  infection, 
it  is  a  particularly  interesting  fact  that  these  diplococci  have  been  not  infre- 
quently found  in  the  mouths  of  healthy  persons.  This  suggests  the  thought 
that  the  germs  are  drawn  into  the  lungs  with  the  inspired  air,  and  there 
settle  and  proliferate  when  the  conditions  are  especially  favorable — for  in- 
stance, if  the  resisting  powers  of  the  organism  have  been  impaired,  or  perhaps 
if  the. diplococci  are  especially  virulent.     In  animals  the  injection  of  diplo- 


250  DISEASES   OF  THE   RESPIRATORY   ORGANS 

cocci  into  the  lungs  almost  always  excites  pneumonia,  but  yet  it  is  doubtful 

whether  the  incidence  of  the  disease  in  man  always  bears  out  the  surmise 

above  mentioned.     The  severity  of  the  constitutional  disturbance  at  the  very 

onset  of  many  cases  certainly  justifies  the  supposition  that  at  least  often  the 

infection  takes  place  through  the  blood,  and  that  the  pathogenic  organisms 

are  carried  to  the  lungs  by  way  of  the  blood  vessels.     Diplococci  are  often  to 

be  found  in  the  blood  of  pneumonia  patients   (vide  infra).     Certain  clinical 

facts  suggest  that  perhaps  in  individual  cases  there  may  be  other  modes  of 

infection;  for  instance,  by  way  of  the  intestine 

%  in  cases  with  well-marked  intestinal  symptoms. 

Starting   from   the   lungs,   the   diplococci   may 

«  invade  the  pleura,  less  often  the  pericardium, 

the  meninges,  and  other  organs,  so  that  they 

are  invariably  demonstrable  in  the  pus  of  cases 

of  metapneumonic  empyema,  pericarditis,  and 

meningitis.     From  a  clinical  point  of  view  their 

almost   invariable    presence   in   pneumonic    ex- 

■p       .,       T,  •     j-  i         •    pectoration  (Fig.  45)  is  of  the  greatest  impor- 

i*iG.    45.  —  Pneumonia    diplococci     x  \      o  /  t>  r 

from  a  pneumonic  sputum.  tance.     They  can  be  easily  demonstrated  by  the 

staining  of  a  dried  preparation  with  gentian- 
violet,  although  for  absolute  certainty  of  diagnosis  further  investigation  is 
required. 

With  the  infectious  nature  of  pneumonia  established,  all  the  other  alleged 
causes  may,  of  course,  be  regarded  as  at  most  "  predisposing  causes."  The  old 
opinion,  which  is  yet  current,  that  pneumonia  is  due  to  catching  cold,  is  to  be 
received  with  great  limitations,  for  croupous  pneumonia  is  very  frequently 
seen  independently  of  any  such  influence.  In  many  cases  it  will  be  found  that 
an  exposure  to  cold  immediately  preceded  the  commencement  of  the  disease; 
but  in  these  instances  the  cold  is  probably  to  be  regarded  merely  as  that  cir- 
cumstance which  promoted  the  occurrence  of  the  infection,  possibly  because  of 
the  resultant  injury  to  the  bronchial  and  pulmonary  epithelium.  This  explains 
the  fact  that  pneumonia  is  especially  frequent  in  certain  classes,  for  instance, 
among  clay  laborers  and  soldiers.  With  regard  to  the  so-called  "  traumatic 
pneumonia,"  the  state  of  the  case  is  similar  to  that  of  pneumonia  due  to  cold. 
Patients  from  the  laboring  classes  sometimes  assert  that  they  were  taken  ill 
as  a  result  of  heavy  lifting  or  of  a  blow  on  the  chest,  but  in  such  cases  the  sub- 
sequent stitch  in  the  side  was  probably  not  the  result  of  the  injury,  but  a 
symptom  of  the  disease  which  had  previously  begun  to  develop.  But  still,  in 
some  few  cases  it  may  be  that  a  preceding  trauma  injures  the  pulmonary  tissue 
in  such  a  way  as  to  promote  the  occurrence  of  the  infection. 

It  is  a  strong  argument  in  favor  of  our  conception  of  pneumonia  as  an  acute 
infectious  disease  that  it  may  rarely  be  endemic.  Extensive  endemics  of  pneu- 
monia, usually  of  quite  a  malignant  character,  have  been  repeatedly  observed  in 
single  buildings,  especially  in  barracks  or  prisons,  as  well  as  in  tenement  houses 
and  other  localities.  It  is  possible  that  precisely  these  severe  cases  of  endemic 
pneumonia  are  aetiologically  different  from  the  ordinary  croupous  form  and 
occasioned  by  some  other  pathogenic  organism;  but  it  is  also  true  that  the 
diplococcus  of  pneumonia  itself  appears  to  vary  greatly  in  its  virulence. 

Pneumonia  does  not,  as  a  rule,  show  a  decided  epidemic  character.     In  a 


CROUPOUS   PNEUMONIA  L\"jl 

large  population  sporadic  cases  "c  eur  at  any  season.    Ii  has  hci  od,  how- 

ever, that  the  disease  may  become  yery  frequeni  or  almosl  completely  disap- 
pear, and  then  again  for  a  time  be  decidedly  prevalent.  In  a  limited  way,  there- 
fore, it  is  quite  proper  to  say  that  there  are  actual  epidemics  of  pneumonia, 
and  these,  again,  differ  from  one  another  in  special  peculiarities,  particularly 
in  their  comparatively  benign  or  malignant  character.  Mosi  attacks  occur  in 
the  winter  or  spring  months,  without  any  necessary  relation,  however,  between 
the  frequency  of  pneumonia  and  the  occurrence  of  especially  had,  wet,  or  cold 
weather. 

Individual  predisposition  plays  an  unmistakable  part  in  the  disease,  as  we 
must  suppose  that  it  does  in  all  infectious  diseases.  Like  facial  erysipelas  and 
acute  articular  rheumatism,  pneumonia  is  one  of  those  diseases  which  is  prone 
to  attack  the  same  individual  several  times.  There  are  persons  who  have  had 
acute  pneumonia  four  or  five  or  even  more  times. 

"We  cannot  affirm  with  certainty  that  the  liability  to  pneumonia  is  due  to  a 
special  bodily  constitution.  The  strongest  and  most  robust  often  fall  ill  with 
it,  and,  on  the  other  hand,  weak  and  delicate  people,  with  a  tendency  to 
phthisis,  are  frequently  attacked.  Drunkards  seem  to  have  a  special  predis- 
position to  the  disease,  but  of  course  it  is  exceedingly  hard  to  give  any  definite 
statistics  upon  this  point. 

Pneumonia  occurs  at  any  time  of  life,  most  frequently  in  youth  or  middle 
age ;  but  it  is  by  no  means  rare  in  early  childhood,  and  also  in  more  advanced 
years  up  to  sixty  or  seventy.  In  general  it  is  observed  rather  more  often  in 
men  than  in  women. 

[Defective  house  drainage  seems  to  be  a  predisposing  cause  of  pneumonia 
in  some  cases.  A  careful  inspection  of  the  local  sanitary  conditions  is  desir- 
able, especially  where  more  than  one  case  occurs  in  a  house.] 

Pathological  Anatomy. — The  anatomical  process  in  croupous  pneumonia 
consists  in  the  formation  of  a  hemorrhagic,  coagulable  "  fibrinous  "  or  "  croup- 
ous "  exudation  into  the  pulmonary  alveoli  and  the  smallest  bronchi.  The 
development  of  the  exudation  usually  extends  over  one  or  more  lobes  to  their 
whole  extent,  and,  as  the  alveoli  and  finer  bronchi  are  completely  filled  by  the 
tough  exudation,  the  spongy  lung,  filled  with  air,  is  changed  to  a  firm  tissue, 
devoid  of  air,  except  as  it  is  penetrated  by  the  large  bronchi. 

Since  Laennec's  day  we  distinguish  three  stages  in  the  development  of  the 
process.  In  the  first  stage  (stage  of  inflammatory  engorgement,  engouement) 
the  lung  is  very  hypergemic,  dark  red,  and  the  air  contained  in  it  is  even  now 
much  diminished,  but  not  entirely  absent.  The  alveoli  are  filled  with  an 
abundant  exudation,  already  hemorrhagic,  but  still  fluid  and  not  coagulated. 

In  the  second  stage  (stage  of  red  hepatization)  the  coagulation  of  the  exu- 
dation is  complete,  and  the  lung  has  become  throughout  of  the  consistence  of 
liver.  The  hepatized  lung  shows  a  somewhat  increased  volume,  and  is  strik- 
ingly hard.  The  surface  of  the  section  has  a  red  and  manifestly  granular 
appearance,  which  is  due  to  the  projection  of  the  numerous  little  fibrinous 
plugs  situated  in  the  alveoli.  With  the  knife  we  can  scrape  off  a  tenacious, 
creamy,  grayish-red  fluid  from  the  surface  of  the  section.  In  the  small  bronchi, 
divided  by  the  knife,  we  find  characteristic  tubular  bronchial  casts. 

In  the  third  stage  (stage  of  yellow  or  gray  hepatization),  which  gradually 
develops  from  the  second,  the  red  surface  of  the  section  changes  to  a  yellowish- 


252  DISEASES   OF  THE   RESPIRATORY   ORGANS 

gray  color,  often  mottled,  while  the  lung  grows  anaemic  and  the  exudation 
poor  in  red  but  rich  in  white  blood  corpuscles.  The  consistence  of  the  lung 
is  still  dense  but  more  friable.  The  fluid  scraped  from  the  surface  of  the 
section  is  more  abundant,  milky,  and  puriform. 

The  recovery  from  the  process  begins  as  the  exudation  becomes  fluid.  The 
fluid  is  in  part  absorbed  and  in  part  coughed  up. 

It  is  not  necessary  for  every  pneumonia  to  go  through  all  three  stages  com- 
pletely.   In  mild  cases  the  process  may  stop  sooner  and  recovery  begin. 

Concerning  the  finer  histological  processes  in  croupous  pneumonia,  the  pri- 
mary change  is  probably  to  be  found  in  the  injury  and  partial  destruction  of 
the  epithelium  in  the  alveoli  and  smallest  bronchi,  produced  by  inflammation 
due  to  the  specific  causes  of  the  disease.  As  in  every  croupous  inflammation 
of  a  mucous  membrane  (see  the  chapter  on  Diphtheria),  a  coagulable  exuda- 
tion is  formed  on  the  surface  of  the  alveoli  and  smaller  bronchi  after  the  de- 
struction of  the  epithelium.  With  the  microscope  we  see  the  fibrinous  net- 
work of  the  exudation  filling  the  alveoli.  Between  its  meshes  lie  numerous 
red  blood  corpuscles — red  hepatization.  Where  there  is  any  of  the  alveolar 
epithelium  left,  we  often  notice  active  proliferation — increase  and  growth  of 
cells.  Later  on  the  white  blood  corpuscles  increase,  migrating  from  the  ves- 
sels into  the  exudation — yellow  hepatization.  The  red  blood  corpuscles  are 
dissolved  unless  they  are  removed  by  expectoration. 

The  fibrinous  exudation  is  also  gradually  dissolved,  and  this,  as  Fr.  Miiller 
has  shown,  results  from  chemical  changes  which  are  very  similar  in  many 
respects  to  the  digestive  changes  that  albuminous  substances  undergo  in  the 
stomach  and  intestines.  The  coagulated  albumen  is  broken  up  into  soluble 
albuminoids  and  further  decomposition  products  through  the  action  of  a  fer- 
ment that  is  probably  given  off  by  the  leucoc}rtes.  In  addition  to  phosphoric 
acid,  considerable  quantities  of  the  xanthin  bases  (xanthin  and  hypoxanthin) 
are  formed  from  the  disintegrated  nuclei  of  the  dying  cells.  All  these  proc- 
esses facilitate  the  rapid  absorption  of  the  pneumonic  exudation.  The  regen- 
eration of  the  missing  epithelium  comes  from  the  epithelium  that  has  remained 
intact,  and  with  that  follows  a  gradual  and  complete  restitutio  ad  integrum. 

The  whole  process  is  comparatively  brief,  usually  running  its  course  in  a 
week  or  ten  days.  The  most  frequent  termination  is  in  complete  recovery. 
The  other  methods  of  termination,  as  well  as  the  complications  in  other 
organs,  will  be  spoken  of  in  connection  with  the  clinical  symptoms.  We  may 
here  mention  simply  that  the  pleura  over  the  affected  portion  of  the  lung 
takes  part  in  the  inflammation,  without  exception,  as  soon  as  the  disease 
reaches  the  periphery,  and  a  fibrinous  pleurisy,  which  is  more  or  less  intense, 
may  then  be  recognized ;  hence  the  former  use  of  the  terms  "  pleuropneu- 
monia "  and  "  peripneumonia." 

Croupous  pneumonia  usually  spreads  rapidly  over  a  great  part  of  the  lung. 
It  is  very  often  quite  sharply  limited  to  a  single  lobe — "  lobar  pneumonia  " — 
so  that  the  septum  of  connective  tissue  between  two  lobes  also  forms  a  strict 
boundary  between  pneumonic  infiltration  and  healthy  lung  tissue;  but  this 
boundary  is  by  no  means  insurmountable,  and  quite  frequently  several  lobes 
are  wholly  or  in  part  attacked  by  pneumonia.  According  to  all  statistics,  the 
lower  lobes  are  more  frequently  affected  than  the  upper.  Isolated  disease  of 
the  right  middle  lobe  may  occur,  but  it  is  much  rarer  than  pneumonia  of  the 


CROUPOUS  PNEUMONIA  253 

upper  lobes.  Of  the  two  lungs,  the  right  is  attacked  with  decidedly  greater 
frequency  than  the  left.  We  have  ourselves  seen,  in  ~i\\  cases,  13*3  on  the 
right,  86  on  the  left,  and  21  in  which  both  Lungs  were  attacked  to  a  great  ex- 
tent. Simultaneous  affection  of  the  lower  lobe  on  one  side  and  the  upper  lobe 
on  the  other — quite  a  rare  occurrence — is  termed  "  crossed  pneumonia/' 

General  Course  of  the  Disease. — In  spite  of  the  numerous  modifications 
which  the  course  of  pneumonia  may  undergo  in  individual  instances,  we  can 
still  call  pneumonia  a  typical  disease,  considering  the  great  majority  of  cases. 
The  subjective  and  objective  symptoms  dependent  upon  the  local  affection  of 
the  lung  usually,  but  not  always,  take  the  chief  place  among  the  clinical  phe- 
nomena. In  this  pneumonia  differs  from  many  other  infectious  diseases,  such 
as  typhoid,  in  which  the  local  organic  disease  is  subordinated  to  the  general 
infection. 

Pneumonia  usually  begins  quite  suddenly.  In  the  majority  of  cases  it 
starts  with  a  pronounced  chill  of  half  an  hour  to  an  hour's  duration,  or  at 
least  with  a  marked  and  prolonged  chilliness.  The  initial  chill  may  attack 
the  jDatient  while  in  the  best  of  health.  Many  patients  are  able  to  tell  almost 
the  very  hour  when,  having  been  previously  in  perfect  health,  they  were  at- 
tacked by  the  disease.  The  chill  comes  on  in  the  daytime,  in  the  evening,  or 
even  in  the  middle  of  the  night,  after  a  previously  quiet  sleep.  At  the  same 
time  the  patient  almost  always  feels  as  if  a  severe  illness  were  beginning. 
Almost  at  once  he  is  obliged  to  give  up  work,  has  violent  headache,  and  loss 
of  appetite.  Not  infrequently  there  is  a  single  initial  act  of  vomiting.  Some- 
times there  are  at  once  pulmonary  symptoms,  such  as  a  stitch  in  the  side  and 
cough.  Usually,  however,  these  phenomena  do  not  develop  until  later  (vide 
infra). 

In  other  and  somewhat  rarer  cases  the  beginning  of  pneumonia  is  more 
gradual.  A  prodromal  stage  of  a  few  days,  or  even  longer,  precedes  the  severe 
illness.  The  symptoms  are  either  of  quite  a  general  and  indefinite  nature, 
consisting  of  malaise,  dullness,  loss  of  appetite,  and  headache,  or  the  prodromal 
symptoms  point  more  strongly  to  a  pulmonary  affection.  The  patient  com- 
plains several  days,  or  even  weeks,  before  the  onset  of  the  severe  disease,  of 
cough,  thoracic  discomfort,  slight  dyspnoea,  and  similar  symptoms.  At  the 
same  time  it  is  not  possible  to  determine  certainly  whether  these  prodromata 
are  caused  by  an  already  existing  pneumonia  or  not.  It  is  undoubtedly  true 
that  in  most  cases  we  have  merely  a  simple  bronchitis  which  furnishes  a  favor- 
able soil  for  the  development  of  pneumonia;  but  perhaps  the  initiatory  bron- 
chitis may,  in  some  cases,  itself  be  an  effect  of  the  diplococcus  infection,  already 
begun,  but  not  yet  completely  developed. 

The  subjective  symptoms  in  the  chest  begin  shortly  after  the  onset  of  the 
disease,  often  on  the  very  first  day,  but  in  other  cases  later.  The  patient  has 
a  stabbing  pain  in  the  side  whenever  he  draws  a  deep  breath;  the  respiration, 
therefore,  becomes  superficial  and  accelerated,  and  often  somewhat  irregular; 
his  speech  is  interrupted  by  frequent  pauses.  In  the  further  progress  of  a 
severe  case  the  dyspnoea  becomes  extreme  and  the  respirations  very  frequent. 
With  the  stitch  in  the  side  is  associated  a  desire  to  cough.  The  cough  is  pain- 
ful, and  hence  short,  half  suppressed,  and  quite  frequent  and  troublesome. 
From  the  second  day  the  expectoration  may  assume  its  characteristic  viscid, 
rusty,  hemorrhagic  appearance.    Physical  examination  gives  on  percussion  and 


254  DISEASES   OF  THE   RESPIRATORY   ORGANS 

auscultation  the  signs  to  be  described  more  fully  below.  These  are  rarely  to 
be  found  on  the  first  day,  but  more  frequently  on  the  second,  and  sometimes 
not  till  later. 

In  well-marked  cases  the  severe  constitutional  symptoms  persist  or  grow 
worse.  We  observe  general  weakness,  headache,  complete  loss  of  appetite,  rest- 
lessness, stupor,  and  delirium.  Herpes  appears  on  the  lips  or  nose ;  the  bowels 
are  sluggish,  or,  again,  they  may  be  loose ;  the  urine  is  concentrated,  and  very 
often  it  contains  a  small  amount  of  albumen, 

Almost  always  the  pneumonia  is  associated  with  high  fever.  The  typical 
character  of  the  disease  and  the  peculiarities  of  the  individual  case  are  always 
well  shown  by  the  temperature  chart.  As  the  bodily  temperature  rises  there  is 
a- corresponding  increase  in  the  frequency  of  the  pulse. 

The  course  varies  greatly  according  to  the  previous  individual  circum- 
stances, the  severity  of  the  disease,  and  the  existence  of  complications.  In  the 
majority  of  cases,  after  a  comparatively  short  duration,  the  disease  takes  a 
favorable  turn.  The  beginning  of  improvement  is  often  sudden,  like  the  onset 
of  the  disease.  After  the  symptoms  have  lasted  for  some  five  to  seven  days, 
or  in  rarer  cases  a  shorter  or  a  longer  time,  at  a  constant  height  or  with  in- 
creasing intensity,  there  occurs  in  the  regular  course  of  the  disease  a  critical 
decline  of  the  fever — frequently  associated  with  quite  a  copious  perspiration 
— and  with  that  a  very  rapid  improvement  of  all  the  other  symptoms.  In  a 
short  time  complete  recovery  follows. 

In  other  cases,  however,  the  course  is  not  so  favorable.  The  disease  may 
have  a  fatal  termination.  In  a  third  small  class  of  cases  the  disease  finally 
takes  a  protracted  course,  which  is  usually  due  to  the  occurrence  of  sequelae 
in  the  lungs  or  pleura. 

To  this  brief  sketch  of  the  disease  we  must  append  a  description  of  the 
special  symptoms. 

1.  Lung  Symptoms. — First  among  the  subjective  symptoms  comes  the  char- 
acteristic painful  feeling  or  "  stitch  "  in  the  side.  This  probably  always  has  its 
origin  in  the  dry  pleurisy  which  accompanies  the  pneumonia.  It  is  therefore 
absent  in  the  cases  of  central  pneumonia  (vide  infra).  In  pneumonia  of  the 
lower  and  right  middle  lobes  the  pain  is  usually  more  severe  than  in  pneu- 
monia of  the  upper  lobes.  One  result  of  the  stitch  in  the  side  is  the  difficulty, 
or  even  the  impossibility,  of  deep  inspiration.  Hence  the  patient's  dyspnoea 
is  considerably  increased,  and  this  explains  the  incongruity  between  the  short- 
ness of  breath  and  the  relatively  slight  extent  of  the  pneumonia  in  many  cases. 
If  the  pneumonic  infiltration  of  the  lung  is  extensive,  of  course  the  dyspnoea 
of  the  patient  is  also  referable  in  part  to  the  diminution  of  the  respiratory 
surface.  The  subjective  feeling  of  difficulty  of  breathing  is  prominent  in  the 
majority  of  cases,  and  it  may  become  most  distressing. 

Cough  is  one  of  the  most  constant  symptoms  in  pneumonia,  and  is  usually 
very  painful ;  hence  the  patient  often  tries  to  suppress  it.  Expectoration  is  apt 
to  be  very  difficult  at  the  onset  of  the  disease,  from  the  viscidity  and  scanty 
amount  of  the  sputum;  hence  severe  and  distressing  paroxysms  of  coughing 
are  sometimes  observed.  The  cause  of  the  cough  is  j)robably  not  to  be  found 
in  the  affection  of  the  alveoli,  but  in  the  coexisting  bronchitis.  The  irritation 
of  the  pleura  may  also  set  up  a  reflex  cough.    In  rare  cases  cough  is  entirely 


CROUPOUS    PNEUMONIA 


2:,:, 


absent  in  pneumonia.  Except  in  the  cases  of  limited  or  late  localization  (vide 
infra),  we  observe  this  ahsence  of  cough  chiefly  in  the  pneumonia  of  <>hl  or 
very  weak  people,  and  also,  what  is  of  practical  importance,  in  the  drunkard's 
pneumonia  associated  with  delirium  tremens. 

The  pneumonic  expectoration  is  so  characteristic  that  we  can  often  make 
the  diagnosis  of  croupous  pneumonia  from  this  alone.  It  consists  of  a  very 
tough  viscid  mucus,  which  sticks  fast  to  the  bottom  of  the  cup  even  when 
inverted,  and  contains  an  intimate  admixture  of  blood,  which  gives  it  a  more 
or  less  pronounced  red  or  yellow  hemorrhagic  color.  In  individual  cases  there 
are  numerous  gradations.  We  usually  call  the  pneumonic  sputum  "  rusty," 
or  "brick-red,"  or  of  a  "prune-juice  color,"  etc.  Sometimes  it  has  only  a  slight 
reddish  or  yellowish  tint,  and  sometimes  it  consists  almost  entirely  of  blood. 
Often  the  sputum  is  very  frothy.  In  some  cases  it  assumes  a  peculiar  grass- 
green  ["greengage"]  color,  which  is  due  to  a  change  in  the  blood  coloring 
matter,  or  to  a  mixture  with  bile  pigment  in  "  bilious  pneumonia." 

The  red  color  of  the  sputum,  as  microscopic  examination  shows,  is  due  to 
numerous  red  blood  corpuscles,  many  of  them  still  well  preserved,  mixed  with 
it.  They  are,  however,  in 
part  dissolved,  and  hence 
the  uniform  red  color  of 
the  sputum.  Separate  spots 
containing  much  blood  are 
often  seen  in  it.  Besides 
the  red  blood  corpuscles, 
the  microscope  shows  nu- 
merous partly  swollen  or 
fatty-degenerated  pus  cor- 
puscles. We  also  see  long 
threads  of  mucus;  some- 
times large,  round,  pig- 
mented cells  (alveolar  epi- 
thelium?); and  finally,  in 
rare  cases,  ciliated  epi- 
thelium and  crystals  of 
hematoidin. 

Frankel's  diplococci  are, 
as  we  have  said,  almost  al- 
ways easily  demonstrable  in 
the  expectoration,  and  of 
course  numerous  other  bac- 
teria besides. 

We  have  still  to  men- 
tion the  bronchial  casts  as 
important  constituents  of 
pneumonic  sputum.     Since 

they  are  usually  rolled  up  together,  we  may  not  find  them  except  by  spread- 
ing out  the  sputum  in  water.  They  consist  of  the  most  beautiful  casts  of 
the  small  bronchi,  with  many  diehotomous  divisions,  and  are  a  product  of  the 
croupous  inflammation  extending  into  the  bronchi.    The  casts  of  the  smallest 


/    ffl 


I      I  ...IV* 


H       I  P 

A  I 


/   .  1  \ 


\  \\ 


Fig.  46. — Bronchial  cast,  %  natural  size. 


256  DISEASES  OF  THE  RESPIRATORY  ORGANS 

bronchi  are  sometimes  found  in  the  form  of  "  spirals,"  like  those  in  asthmatic 
bronchitis  (see  page  224). 

The  amount  of  the  pneumonic  sputum  is,  as  a  rule,  not  very  considerable, 
but  it  differs  a  good  deal  in  different  cases.  The  chemical  examination  of  the 
sputum  has  so  far  given  no  remarkable  results.  The  amount  of  common  salt 
contained  in  it  is  quite  considerable. 

In  many  cases  the  pneumonic  expectoration  is  absent,  either  because  there 
is  no  cough  or  because  the  exudation  is  firmly  coagulated  and  is  absorbed  with- 
out ever  liquefying.  Sometimes  it  is  very  tough  and  slimy,  but  without  any 
admixture  of  blood ;  in  other  cases  the  sputum  is  simply  catarrhal,  when  pres- 
ent at  all,  and  then,  of  course,  it  comes  not  from  the  parts  infiltrated  with 
pneuj£2onia,  but  from  the  catarrh  of  the  larger  bronchi.  In  many  severe  cases 
the  hemorrhagic  expectoration  soon  assumes  more  of  a  purulent  character. 
We  often  find  simple  catarrhal  sputum,  too,  besides  the  characteristic  pneu- 
monic sputum. 

The  pneumonic  sputum  is  sometimes  seen  in  the  first  or  second  day  of 
pneumonia,  but  it  may  not  appear  until  later.  With  the  beginning  of  resolu- 
tion it  gradually  loses  its  characteristic  appearance.  The  expectoration  then 
becomes  less  tenacious  and  simply  mucopurulent,  and  finally  disappears 
entirely. 

Physical  Examination. — Inspection  shows  no  especial  anomaly  in  the  gen- 
eral contour  of  the  thorax.  A  marked  bulging  of  the  affected  side  occurs  only 
when  there  is  also  abundant  effusion  into  the  pleural  cavity.  The  action  of 
the  thorax  in  respiration  is  very  important.  Even  with  a  limited  pneumonia 
we  often  notice  a  very  marked  delay  and  limitation  of  motion  of  the  affected 
side  on  inspiration.  This  is  due  in  part  to  the  pain  in  the  side,  which  comes 
on  with  every  deep  inspiration,  and  also,  in  extensive  pneumonia,  of  course, 
to  the  physical  conditions  resulting  from  the  anatomical  changes.  The  un- 
affected portions  of  the  lung  act  all  the  more  forcibly. 

The  acceleration  of  respiration  is  very  striking,  its  frequency  increasing  to 
thirty  or  forty,  or  even  more,  a  minute.  We  have  repeatedly  counted  sixty  res- 
pirations in  adults,  even  in  cases  that  finally  resulted  favorably.  The  breath- 
ing is  shallow,  but  yet,  in  all  severe  cases,  labored,  and  often  also  irregular,  as 
a  result  of  pleuritic  pain  or  cough.  We  see  the  inspiratory  contraction  of  the 
sterno-cleido-mastoids  and  scaleni  in  the  neck,  and  often  in  the  face  a  marked 
dilatation  of  the  nostrils  on  inspiration.  If  there  is  marked  dyspnoea  the  pa- 
tient sometimes  reclines  in  bed  with  the  upper  half  of  the  body  raised.  The 
cheeks  and  lips  are  cyanotic.  There  is  often  a  sharp  contrast  between  the  pale 
portions  of  the  face  near  the  corners  of  the  mouth  and  the  striking  feverish 
and  slightly  cyanotic  flush  of  the  cheeks. 

The  results  of  percussion  are  directly  dependent  upon  the  changed  physical 
condition  in  the  lung,  due  to  the  anatomical  processes.  In  the  beginning  of 
pneumonia,  so  long  as  the  total  amount  of  air  in  the  lung  remains  but  little 
altered,  the  percussion  note  is  clear,  but  when  the  elasticity  and  tension  of  the 
tissue  in  the  diseased  portion  of  the  lung  diminish,  the  resonance  often  be- 
comes quite  tympanitic.  With  increased  exudation  into  the  alveoli  and  small- 
est bronchi  the  amount  of  air  in  the  lung  constantly  grows  less,  and  therefore 
the  percussion  resonance  becomes  very  dull,  but  it  usually  retains  its  tym- 
panitic timbre.    Since  the  pneumonic  lung  is  rarely  absolutely  deprived  of  air 


CROUPOUS   PNEUMONIA  257 

— for  a  certain  amount  is  always  left  in  the  larger  bronchi — the  percussion 
resonance  seldom  becomes  so  completely  dull  or  flat,  as  it  does,  for  example, 
with  a  large  pleuritic  effusion.  The  sensation  of  resistance  upon  the  percus- 
sion of  a  pneumonic  lung  is  likewise  much  less  marked  than  over  a  pleuritic 
exudation.  A  marked  sense  of  resistance  implies,  therefore,  an  unusual  degree 
of  involvement  of  the  pleura  in  the  inflammation.  As  soon  as  the  absorption 
of  the  exudation  begins,  the  volume  of  air  in  the  lung  increases,  and  the  per- 
cussion note  becomes  clearer,  but  remains  for  some  time  still  markedly  tym- 
panitic, until  the  lung  has  regained  its  normal  tension  and  elasticity.  We 
have  also  to  note  that  the  intensity  of  the  dullness  in  croupous  pneumonia  is 
sometimes  subject  to  quite  marked  variations,  since  the  secretion  retained  in 
the  bronchi  is  at  one  time  abundant  and  at  another,  after  expectoration, 
scanty. 

The  extent  of  the  dullness  or  of  the  tympanitic  resonance  is  naturally  de- 
pendent upon  the  extent  of  the  anatomical  process.  Small  and  central  infil- 
trations may  entirely  escape  detection  by  percussion. 

Auscultation  is  of  almost  greater  importance  than  percussion  in  the  detec- 
tion of  a  beginning  or  limited  pneumonic  infiltration.  The  auscultatory  signs 
depend  upon  the  presence  of  the  pneumonic  exudation,  and  upon  the  conse- 
quent transformation  of  the  lung  into  a  firm  tissue  devoid  of  air  except  in 
the  larger  bronchi.  In  the  beginning  of  the  disease  we  hear  over  the  affected 
portions  coarse  or  fine  rales,  and  very  often,  too,  the  characteristic  crepitant 
rale  on  insj)iration  discovered  by  Laennec.  This  arises  because  the  walls  of  the 
alveoli  and  smallest  bronchi,  which  are  glued  together  by  the  viscid  exudation, 
are  torn  apart  at  each  inspiration.  The  crepitation,  however,  is  neither  pathog- 
nomonic of  pneumonia,  nor  heard  in  every  case  of  pneumonia.  With  increas- 
ing infiltration,  bronchial  breathing  replaces  the  vesicular.  The  bronchial 
breathing  in  pneumonia  is  usually  very  loud,  sharp,  and  close  to  the  ear. 
When  the  infiltration  is  very  complete  there  is  often  to  be  heard  a  pure  and 
loud  bronchial  respiration,  without  any  adventitious  sounds;  but  of  course 
there  are  often  heard,  besides  the  bronchial  breathing,  high-pitched,  moist  rales 
in  greater  or  less  abundance.  It  is  especially  true  that  with  the  commence- 
ment of  "  resolution  " — that  is,  as  soon  as  the  exudation  becomes  more  fluid, 
abundant  moist  rales  reappear,  enough  to  obscure  more  or  less  the  bronchial 
respiration.  These  rales  are,  for  the  most  part,  rather  coarse,  moist,  and  have 
a  musical  character.  Often  we  hear  at  this  time  the  characteristic  crepitant 
rale  again  (crepitus  redux).  The  rales  gradually  disappear,  the  respiratory 
murmur  loses  its  bronchial  character,  becomes  harsh  and  indefinite,  and  finally 
is  normally  vesicular  once  more. 

We  often  hear  a  few  rhonchi  over  the  unaffected  portions  of  the  lungs.  On 
the  diseased  side,  the  respiratory  murmur  is  often  more  or  less  diminished 
because  of  the  diminished  respiratory  movement.  Otherwise  respiration  in  the 
unaffected  portions  of  the  lungs  is  usually  completely  normal. 

The  auscultatory  signs  just  described  undergo  an  important  change  if  the 
larger  bronchi  leading  to  the  affected  portion  of  the  lung  are  completely 
plugged  by  the  secretion,  as  they  are  quite  liable  to  be.  The  respiratory  mur- 
mur may  then  almost  entirely  disappear,  and  we  hear,  perhaps,  only  here  and 
there  a  few  obscure  rales.  Since  such  a  plugging  may  be  very  transitory,  we 
understand  why  in  one  day,  over  the  same  portion  of  the  lung,  we  hear  first 


258  DISEASES   OF  THE   RESPIRATORY   ORGANS 

loud  bronchial  breathing  and  rales,  and  then  quite  obscure  and  diminished 
breathing. 

Wherever  there  is  bronchial  breathing,  we  hear  marked  bronchophony. 
Sometimes  one  can  discover  a  beginning  pneumonic  infiltration  by  bron- 
chophony sooner  than  by  any  other  physical  sign.  The  vocal  fremitus  persists 
or  is  somewhat  increased  over  a  pneumonic  lung  so  long  as  the  large  bronchi 
are  open;  but  when  they  become  plugged,  as  they  are  quite  liable  to  be,  the 
vocal  fremitus  is  weakened  or  wholly  abolished;  and  again,  the  voice  sounds 
are  weakened  whenever  there  is  a  considerable  amount  of  pleurisy  accompany- 
ing the  pneumonia. 

We  have  yet  to  add  a  few  remarks  about  the  parts  of  the  lung  in  which  we 
may  expect  first  to  perceive  the  physical  signs  of  pneumonia,  especially  the 
auscultatory  signs. 

In  the  first  place,  we  should  never  neglect  to  examine  carefully  the  lateral 
portions  of  the  thorax  and  the  axillary  region  when  we  suspect  a  developing 
pneumonia.  We  often  find  the  first  rales  here  in  pneumonia  of  the  lower  lobes. 
The  first  signs  of  infiltration  may  be  found  in  the  posterior  middle  portion  of 
the  thorax — that  is,  in  the  upper  part  of  the  lower  pulmonary  lobes — and 
thence  they  extend  downward.  Pneumonia  of  the  upper  lobes  begins  just  as 
frequently  behind  in  the  apices  as  in  front  in  the  infraclavicular  fossae.  Iso- 
lated pneumonia  of  the  right  middle  lobe  also  occurs,  to  be  made  out  in  front, 
on  the  right,  between  the  fourth  and  sixth  ribs.  This  may  remain  confined 
to  the  middle  lobe,  or  extend  to  the  neighboring  lobes. 

Few  general  statements  can  be  made  about  the  mode  or  the  rapidity  of  the 
extension  of  pneumonia,  since  in  these  respects  the  greatest  differences  are 
observed.  The  infiltration  may  remain  confined  to  a  small  portion  of  the  lung, 
or  again  it  may  spread  over  a  whole  lobe  or  more  in  a  short  time,  even  in  one 
or  two  days.  We  call  the  pneumonia  whose  constant  extension  by  contiguity 
we  can  follow  from  day  to  day  wandering  pneumonia  (pneumonia  migrans), 
or,  from  a  purely  superficial  resemblance,  which  has  given  rise  to  many  wrong 
ideas,  "  erysipelatous  pneumonia."  In  these  cases  all  the  signs  of  resolution 
are  present  in  the  parts  first  attacked,  while  the  parts  affected  later  are  found 
still  at  the  height  of  the  disease,  or  in  the  beginning  of  infiltration;  but  we 
may  also  find  in  the  autopsies  of  wandering  pneumonia  the  parts  of  the  lung 
affected  later  in  a  more  advanced  stage  (gray  hepatization)  than  the  parts  first 
attacked,  which  are  still  in  the  stage  of  red  hepatization — that  is,  the  inflam- 
matory process  in  such  cases  seems  to  go  through  a  more  rapid  evolution  in 
the  portions  of  lung  later  affected.  Wandering  pneumonia  is  almost  always 
severe  and  quite  protracted. 

Pneumonia  in  rare  cases  progresses  by  leaps.  Such  cases  have  been  termed 
erratic  pneumonia.  In  severe  cases  it  is  not  unusual  for  both  lungs  to  be 
affected.  We  then  find  the  pneumonia  either  in  both  lower  lobes,  or  in  the 
lower  lobe  on  one  side  and  the  upper  lobe  on  the  other  side. 

2.  Pleura  Symptoms. — As  we  have  already  mentioned,  every  case  of  pneu- 
monia which  reaches  to  the  surface  of  the  lung  is  associated  with  a  fibrinous 
pleurisy,  and,  furthermore,  it  is  not  impossible  that  there  should  be  an  infec- 
tion of  the  pleura  without  any  direct  extension  from  the  neighboring  pulmo- 
nary tissue.  In  many  instances,  the  mild  pleurisy  which  attends  a  pneumonia 
causes  no  physical  signs.     On  the  other  hand,  the  pain  in  the  side  in  pneu- 


CROUPOUS   PNEUMONIA  259 

riionia  is  probably  always  referable  to  the  involvement  of  the  pleura,  [n 
other  cases  the  dry  pleurisy  attracts  attention  by  the  clearly  audible  friction, 
which  may  often  be  very  loud,  ami  is  sometimes  appreciable  to  the  touch,  if 
the  hand  is  laid  upon  the  side.  We  rarely  hear  the  pleuritic  friction  Bound  in 
the  beginning  of  pneumonia,  but  more  frequently  in  the  later  stages,  and  per- 
haps not  till  many  days  after  the  crisis  has  taken  place. 

The  cases  in  which  pleurisy  with  effusion  complicates  pneumonia  are  more 
important.  This  may  occur  quite  early.  The  abnormality  of  the  clinical 
course  is  shown  in  these  cases,  as  a  rule,  by  the  irregular  behavior  of  the  fever. 
There  will  be  no  typical  crisis,  but  instead  a  slow  lysis;  or  after  the  cri.-is 
occurs,  the  temperature  will  rise  again.  In  most  instances  the  exudation  is 
serous,  but  it  may  be  purulent  (metapneumonic  empyema).  Long-continued 
fever  should  arouse  suspicion  of  an  empyema.  In  the  pus  of  such  cases  of 
empyema  the  pneumonic  diplococcus  above  mentioned  (see  page  24!))  has  been 
repeatedly  found.  In  two  fatal  cases  the  author  has  seen  a  hemorrhagic  pleu- 
risy with  a  large  amount  of  coagulated  blood  in  the  pleural  cavity. 

The  diagnosis  of  pleurisy  with  effusion  complicating  pneumonia  is  seldom 
difficult.  The  percussion  resonance  is  duller,  and  the  sense  of  resistance  is 
more  marked  than  in  pure  pneumonia  (vide  supra).  The  respiratory  murmur 
and  the  vocal  fremitus  are  constantly  diminished  and  finally  entirely  absent. 
The  symptoms  of  pressure  on  the  neighboring  organs  and  cavities,  the  heart, 
the  liver,  and  the  semilunar  space  (see  page  350),  are  especially  important 
because  they  are  most  unequivocal.  An  exploratory  puncture  with  a  Pravaz's 
[hypodermic]  syringe,  that  has  been  carefully  cleansed  and  disinfected,  gives 
a  certain  and  safe  method  of  recognizing  pleurisy  in  doubtful  cases.  When 
there  is  suspicion  that  an  empyema  has  begun,  an  exploratory  puncture  is 
imperative. 

A  moderate  degree  of  pleurisy  may  somewhat  delay  the  course  of  the  dis- 
ease, but  it  has  no  special  significance.  Large  effusions,  however,  may  decidedly 
increase  the  difficulty  in  respiration  and  the  duration  of  the  illness.  Again, 
the  pneumonia  may  recover,  leaving  the  pleuritic  effusion  quite  undisturbed. 
In  pneumonia  of  an  upper  lobe,  too,  the  pleurisy  may  develop  below  and  lead 
to  an  effusion  there,  while  the  lower  lobe  itself  remains  quite  free  from  pneu- 
monia. Metapneumonic  empyema  invariably  requires  surgical  intervention, 
but  after  operation  it  almost  always  pursues  a  rapid,  course  to  recovery. 

3.  Circulatory  Apparatus.  Blood. — The  pulse  is  accelerated  from  the  be- 
ginning of  the  disease.  In  cases  of  moderate  severity  its  frequency  reaches  100 
or  120;  and,  in  very  severe  cases,  a  still  higher  rate  up  to  140  or  160  is  seen, 
and  is  always  a  dangerous  symptom.  This  high  rate  of  the  pulse  does  not  have 
as  bad  a  significance  in  children  as  it  does  in  adults.  The  consideration  of 
the  quality  of  the  pulse  is  important.  Smallness,  weakness,  and  irregularity 
of  the  pulse  are  of  bad  omen  as  symptoms  of  the  onset  of  cardiac  weakness. 
The  attacks  of  collapse,  which  sometimes  come  on  quite  suddenly  in  severe  cases 
of  pneumonia  as  in  other  acute  diseases,  are  especially  dangerous.  They  oc- 
casion sudden  weakness  of  the  heart  with  a  very  small  and  frequent  pulse.  The 
temperature  sinks  to  subnormal,  95°  to  93°  F.  (35°  to  34°  C).  The  periph- 
eral parts,  the  nose  and  extremities,  become  cool,  pale,  and  somewhat  cyanotic. 
The  general  weakness  and  prostration  become  extreme.  The  collapse  may  be 
recovered  from,  especially  with  timely  assistance,  but  patients  may  die  in  it. 


260  DISEASES   OF  THE   RESPIRATORY   ORGANS 

Pericarditis  with  fibrinous  or  serofibrinous  exudation  is  one  of  the  most 
serious  cardiac  complications.  This  can  always  be  explained  by  a  direct  con- 
duction of  the  inflammatory  process  from  the  neighboring  pleura,  and  is  there- 
fore somewhat  more  frequent  in  left-sided  pneumonia  than  in  right.  It  is  a 
serious  matter.  Its  diagnosis  is  seldom  difficult  if  we  make  a  careful  physical 
examination  of  the  heart,  but  with  very  severe  and  extensive  symptoms  in  the 
lungs  a  complicating  pericarditis  may  be  overlooked. 

A  slight  fresh  endocarditis  is  sometimes  found  at  the  autopsy,  but  it  has  no 
clinical  significance.  Diseases  of  the  cardiac  muscle,  especially  fatty  and  paren- 
chymatous degeneration,  may  be  discovered  postmortem,  but  they  are  by  no 
means  frequent.  In  very  weak  persons,  drunkards,  etc.,  who  die  of  pneumonia, 
we  sometimes,  indeed,  find  the  heart  remarkably  flabby,  with  the  right  ventricle 
dilated,  but  in  many  cases  of  pneumonia  we  find  the  muscle  of  the  heart  at  the 
autopsy  perfectly  normal.  Here  we  almost  always  have  to  do  with  conditions 
of  the  heart  which  existed  previously  to  the  pneumonia,  and  merely  became 
prominent  during  its  course.  When  persons  of  vigorous  and  healthy  consti- 
tution die  of  pneumonia,  as,  indeed,  seldom  occurs,  the  myocardium  is  found 
at  the  autopsy  essentially  healthy.  It  must  be  emphatically  stated  that  our 
present  knowledge  does  not  enable  us  to  establish  before  death  any  positive 
relation  between  the  histological  condition  of  the  cardiac  muscle  and  its  func- 
tional ability.     Frequent  experience  has  made  us  certain  of  this  fact. 

With  regard  to  the  blood,  there  is  usually  a  well-marked  leucocytosis  in 
pneumonia.  The  exact  count  shows,  not  infrequently,  twenty  to  twenty-five 
thousand  or  more  of  leucocytes  in  a  cubic  millimeter.  With  the  crisis  of  the 
fever  the  number  of  leucocytes  also  falls  abruptly,  while  in  case  of  a  pseudo- 
crisis  their  number  remains  high.  After  the  crisis,  the  lymphocytes,  whose 
number  is  greatly  diminished  during  the  course  of  the  disease,  show  a  decided 
increase  ("  post-  infectious  lymphocytosis").  In  some  instances  the  leucocy- 
tosis is  not  marked.  This  is  particularly  frequent  in  severe  and  fatal  cases, 
so  that  the  absence  of  leucocytosis  is  regarded  with  some  justice  as  an  unfa- 
vorable element  in  prognosis.  Pneumococci  can  often  be  found  in  the  blood. 
Their  presence  in  large  numbers  indicates  a  severe  infection.  Accordingly,  we 
find  a  bacterisemia  more  especially  in  cases  that  have  no  marked  leucocytosis. 

4.  Digestive  Apparatus. — In  severe  cases  of  pneumonia  the  tongue  is  dry, 
coated,  and  quite  like  the  tongue  in  typhoid.  The  appetite  is  also  almost 
wholly  lost  from  the  beginning.  Vomiting  is  not  infrequent,  especially  in 
the  beginning  of  pneumonia,  and  it  also  occurs  later.  It  is  observed  with 
especial  frequency  in  the  pneumonia  of  children.  Severe  symptoms  on  the 
part  of  the  intestinal  canal  are  rare.  As  a  rule,  the  bowels  are  constipated, 
but  there  are  also  cases  in  which  diarrhea  is  so  troublesome  that  we  must 
believe  that  the  mucous  membrane  of  the  intestine  is  considerably  involved 
in  the  morbid  process   (vide  infra). 

The  complication  of  pneumonia  with  jaundice  has  a  certain  significance, 
but  its  causes  are  not  always  very  clear.  It  is  apparently  sometimes  due  to 
an  accompanying  catarrh  of  the  duodenum.  In  other  cases  the  veins  of  the 
liver,  dilated  from  stasis,  may  exert  a  pressure  on  the  bile  ducts.  Slight 
jaundice  has  no  special  significance,  and  is  frequent,  even  in  mild  cases;  a 
marked  jaundice,  however,  is  seen  only  in  severe  cases,  especially  in  drunk- 
ard's  pneumonia.      We   call   such   cases,   associated   with   jaundice,   "  bilious 


CROUPOUS  PNEUMONIA  201 

pneumonia."  They  have  often  other  Bevere  gastro-intestinal  symptoms,  such 
as  vomiting,  diarrhea,  and  meteorism,  and  severe  nervous  symptoms,  such  as 
stupor  and  delirium. 

The  liver  may  be  somewhat  enlarged,  usually  because  of  passive  congestion. 
The  spleen  is  often  moderately  swollen,  particularly  in  severe  cases,  just  as 
in  other  infectious  diseases  (acute  splenic  tumor). 

5.  Kidneys  and  Urine. — The  infectious  character  of  pneumonia  is  also 
shown  by  frequent  involvement  of  the  kidneys.  Careful  examination  of  the 
urine  almost  always  shows  a  trace,  or  even  a  considerable  amount,  of  albumen. 
However,  this  is  very  seldom  of  serious  import,  and  vanishes  promptly  after 
the  crisis.  In  many  instances  the  changes  in  the  urine  are  so  considerable 
as  to  show  an  acute  nephritis.  There  is  a  large  amount  of  albumen,  with 
casts,  epithelium,  and  blood,  in  the  urine.  But  even  these  cases  of  genuine 
pneumonic  nephritis,  which  usually  develop  about  the  third  to  the  sixth  day 
of  the  illness,  seldom  prove  to  be  serious,  and  scarcely  ever  result  in  oedema, 
uremia,  or  other  complications.  Usually  they  get  well  rapidly.  In  one 
single  case  the  author  has  observed  a  transition  into  chronic  nephritis.  The 
way  in  which  pneumonia  causes  albuminuria  and  nephritis — between  which 
no  sharp  dividing  line  can  be  drawn — is  probably  by  the  production  and 
excretion  of  toxins. 

Great  weight  was  formerly  laid  upon  the  diminution  of  the  chlorids  in 
the  urine  of  pneumonia.  In  fact,  the  precipitate  of  chlorid  of  silver,  when 
we  put  a  drop  of  solution  of  nitrate  of  silver  into  the  urine,  may  be  very 
slight  or  entirely  absent.  The  chief  cause  of  this  diminution  of  the  chlorids 
is  the  small  amount  of  nourishment  taken  by  the  patient,  but  we  must  also 
bear  in  mind  the  large  amount  of  chlorid  of  sodium  contained  in  the  pneu- 
monic exudation,  and  the  retention  of  the  chlorids  in  the  body. 

Great  significance  was  also  formerly  ascribed  to  the  abundant  sediment  of 
sodium  urate  (exceptionally,  uric  acid)  which  is  often  noticed  on  the  day  of 
the  crisis.  This  is  known  as  brick-dust  sediment  (sedimentum  lateritium), 
and  is  perhaps  due  in  part  to  a  material  increase  in  uric  acid  from  the  break- 
ing down  of  the  increased  number  of  leucocytes  in  the  blood,  or  it  may  be 
derived  from  the  degenerated  nuclei  of  the  cellular  pneumonic  exudate.  On 
the  other  hand,  it  should  be  borne  in  mind  that  the  conditions  for  the  depo- 
sition of  sediment  are  especially  favorable  on  the  day  of  the  crisis.  The 
urine  is  scanty  in  amount  because  perspiration  is  so  excessive,  and  hence  it 
is  concentrated  and  relatively  very  acid.  It  is,  therefore,  natural  for  the 
urates  contained  in  it  to  be  deposited  in  the  form  of  a  sediment. 

Pneumonia,  in  common  with  most  of  the  other  acute  febrile  diseases,  is 
attended  with  an  increased  secretion  of  urea  during  the  disease.  The  greatly 
increased  excretion  of  urea  in  the  days  following  the  crisis  is  due  in  great 
part  to  the  absorption  of  the  pneumonic  exudate  (vide  supra,  page  252). 
The  fact  is  of  theoretic  interest  that  during  the  resolution  of  pneumonia  the 
urine  often  contains  a  demonstrable  quantity  of  peptone,  which  is,  in  all 
probability,  due  to  the  destruction  of  the  cells  in  the  pneumonic  exudation 
and  their  absorption  into  the  blood. 

6.  Nervous  System. — As  in  every  severe  febrile  disease,  nervous  symptoms 
of  a  mild  type  are  very  rarely  absent  in  pneumonia.  Among  the  nervous 
symptoms  are  general  weakness  and  dullness,  and  especially  headache,  which 
17 


262  DISEASES  OF  THE  RESPIRATORY  ORGANS 

is  often  very  intense,  and  is  usually  increased  by  coughing.  The  onset  of 
more  severe  cerebral  symptoms,  particularly  delirium,  is  of  great  importance. 
Delirium  may  appear  in  any  case  of  severe  pneumonia,  but  it  is  most  marked 
and  has  peculiar  characteristics  in  alcoholic  subjects.  This  delirium  gives 
the  pneumonia  of  drunkards   (vide  infra)  its  characteristic  stamp. 

The  usual  cerebral  symptoms  in  pneumonia  do  not  correspond  with  macro- 
scopic changes  in  the  brain,  but  result  from  the  poisoning  of  the  body  with 
the  toxins  of  the  pneumonia  diplococcus;  and  yet  there  is  also  a  true  cere- 
bral disease  which  has  beyond  a  doubt  a  special  relation  to  pneumonia, 
although  it  is  an  infrequent  complication.  We  refer  to  purulent  cerebro- 
spinal meningitis.  This  complication  is  particularly  apt  to  appear  at  times 
when  an  epidemic  of  cerebro-spinal  meningitis  prevails,  but  it  has  been 
repeatedly  observed  at  other  times.  The  diagnosis  of  pneumonic  meningitis 
may  be  obscured  by  the  severe  constitutional  disturbances.  Factors  of  im- 
portance are :  the  stiffness  of  the  back  and  the  neck ;  the  pain  in  the  head  and 
in  the  nape  of  the  neck;  the  stupor,  changing  to  deep  coma;  and,  in  many 
cases,  optic  neuritis,  demonstrable  by  the  ophthalmoscope.  The  termination 
of  a  well-marked  case  of  meningitis  is  probably  invariably  fatal,  but  we  may 
have  milder  meningeal  symptoms  in  pneumonia,  such  as  pain  and  stiffness 
in  the  neck,  followed  by  complete  recovery.  With  regard  to  the  development 
of  this  meningitis,  it  is  probably  to  be  regarded  as  a  true  metastatic  inflam- 
mation, inasmuch  as  the  pneumonia  diplococci  have  been  repeatedly  found 
in  the  pus  of  the  meningitis.  As  to  the  path  which  the  pathogenic  germs 
take  to  reach  the  meninges,  we  are  not  yet  certain,  but  suppose  that  they 
travel  along  the  lymph  channels  of  the  intercostal  nerves  into  the  meninges 
surrounding  the  spinal  cord,  and  thence  farther  to  the  membranes  of  the  brain. 

7.  Skin. — The  frequent  appearance  of  herpes  in  the  course  of  pneumonia  is 
characteristic,  and  is  of  diagnostic  importance.  It  appears  from  the  second 
to  the  fourth  day  of  the  disease,  or  sometimes  later.  Its  ordinary  seat  is  on 
the  lips,  especially  at  the  corners  of  the  mouth,  also  on  the  alse  of  the  nose, 
and  more  rarely  on  the  cheeks  or  the  ear  (herpes  labialis,  nasalis,  etc.).  It 
has  been  seen  only  very  rarely  on  other  portions  of  the  body  besides  the  face, 
for  example,  on  the  forearm  and  the  buttock,  and  in  some  cases  on  the  cornea 
and  on  the  mucous  membrane  of  the  tongue  or  gums.  The  herpes  does  not 
always  come  out  all  at  once,  but  in  fresh  crops  on  successive  days.  We  have 
several  times  seen  two  eruptions  of  herpes  separated  by  an  interval  of  sev- 
eral days.  In  repeated  instances,  under  our  own  observation,  herpes  labialis, 
with  a  fresh  rise  of  temperature,  appeared  some  days  after  the  crisis  had 
taken  place.  Herpes  may  be  extensive  in  the  mildest  cases,  while  it  is  par- 
ticularly apt  to  be  scanty  or  absent  in  severe  cases.  We  are,  therefore,  on 
the  whole,  inclined  to  regard  a  well-marked  eruption  of  herpes  as  of  favor- 
able prognosis.  The  true  cause  of  the  herpetic  eruption  is  unknown.  One 
might  think  of  referring  it  to  the  action  of  toxins,  just  as  in  the  herpes  of 
other  infectious  diseases,  such  as  intermittent  and  relapsing  fevers,  and  epi- 
demic meningitis.  Other  affections  of  the  skin  are  of  rare  occurrenec.  We 
have  seen  urticaria  in  some  cases.  The  jaundice  occurring  in  pneumonia 
has  already  been  described. 

8.  Course  of  the  Fever  (see  Figs.  47  and  48). — Pneumonia  is,  almost  with- 
out exception,  accompanied  by  a  more  or  less  high  fever  with  a  very  typical 


CROUPOUS   IWKi'MONIA 


203 


40.0° 


39.0° 


38.0C 


37.0° 


36.0C 


liiiiiiisiiiiiliiiiii! 

■■■  mum  ihih 

!iS  warn  !■■ 

iiiiiisssssiiSiiiiSS 

flilllliiiiiiillilii 


Fig.  47. 


Pseudo-crises 
-Example  of  the  temperature-curve  in  croupous 
pneumonia.     (Personal  observation.) 


course.  In  the  beginning  of  the  fever  the  temperature  rises  very  rapidly  to 
a  high  point.  Even  during  the  initial  chill  the  bodily  beai  increases  from 
normal  to  about  104°  F.  (40°  C.)  and  over.  There  are  a1  present  do  obser- 
vations to  show  whether,  in 
the  cases  of  pneumonia  that 
begin  gradually,  there  is  also 
a  gradual  increase  of  the 
fever.  During  the  course  of 
the  disease  the  fever  shows  on 
the  whole  a  continuous  or  re- 
mitting character,  but  there 
is  with  this  a  decided  tend- 
ency to  single  deep  falls  of 
temperature.  Since  these  at 
first  may  easily  be  taken  for 
the  actual  occurrence  of 
crises,  although  later  they  are 
proved  by  the  renewed  rise  in 
temperature  to  be  a  mere  tem- 
porary decline  in  the  bodily 
heat,  they  are  termed  pseudo- 
crises.  Pseudo-crises  are  usu- 
ally seen  in  the  first  days  of 
the  disease,  but  in  some  cases  they  appear  later  and,  what  is  remarkable,  they 
are  more  apt  to  appear  on  those  days,  such  as  the  fifth  or  "seventh,  on  which 
the  true  crisis  is  apt  to  occur.     They  may  be  repeated  one  or  more  times, 

giving  the  fever  a  decided- 
ly intermitting  character. 
These  intermitting  pneu- 
monias, so  called  from  the 
course  of  the  fever,  have 
nothing  at  all  to  do  with 
malaria,  which  fact  must 
be  especially  noted  because 
of  the  frequency  of  errone- 
ous statements. 

The  fever  may  be  de- 
cidedly high  in  pneu- 
monia, often  reaching  104° 
or  106°  F.  (40°  to  41°  C). 
The  highest  temperature 
observed  by  us  was  107.8° 
F.  (42.1°  C).  This  was 
temporary.  There  is  a  cer- 
tain parallelism  between 
the  height  of  the  fever  and 
its  severity  to  this  extent,  that  severe  cases  are  often  associated  with  persistent 
and  especially  high  fever.  But  sometimes  the  most  severe  and  even  fatal  cases 
have  a  comparatively  low  temperature — between  101°  and  103°  F.   (38.5°  to 


11      12 


41.0' 


40.0° 


39.0' 


38.0C 


37.0° 


36.0= 


ffiSSi' 


saHssBSBSfssssaiBaasra 

■iinilsu  isii&ssKHiHH  «■■■»■  Mi  ran 

■Hflna'HIIISflHHraiBieaUMHBH        _ 


Mil 

IfllHI 
HI- 

■MIL 

9H1IHEI 


IIIKilH 
1IMIB 
IIMII 

■nil 


HIHB1NHHI 
miHBWilgggSE 


BSHSSSSZiSSSSginSjSg 

BSBSIiSSSi«SS™SSSiflii 


M 

ihbbhh  imwimmmmm 


1MB 
!■■■ 


IW 


Fig.  48. — Example  of  the  temperature-curve  in  "intermit- 
ting pneumonia."      (Personal  observation.) 


264  DISEASES   OF  THE   RESPIRATORY   ORGANS 

39.5°  C).  The  highest  temperatures  are  especially  common  in  the  first  days  of 
the  illness,  and  yet,  in  spite  of  very  high  fever  at  the  onset,  the  general  course 
of  the  disease  may  turn  out  to  be  favorable,  for  the  crisis  may  occur  on  the  sec- 
ond or  third  day  (vide  infra,  rudimentary  and  abortive  pneumonia) .  In  severe 
cases  the  progress  of  the  disease  often  stamps  itself  plainly  on  the  temperature. 
The  pseudo-crises  correspond  to  temporary  improvements,  and  the  fresh  ex- 
acerbations of  temperature  to  the  invasion  of  a  fresh  lobe  of  the  lung.  We  have 
certainly  not  seen  a  special  rise  immediately  before  the  crisis — the  so-called 
perturb atio  critica — so  often  as  many  statements  would  lead  us  to  expect. 
We  have  seen  a  gradual  decline  in  temperature  quite  frequently  in  the  closing 
days  in  fatal  cases,  but  the  opposite  condition  also  obtains.  A  marked  rise 
before  death  is  not  peculiar  to  pneumonia,  but  it  does  occur  when  there  is  a 
complicating  meningitis. 

The  decline  of  the  fever  is  the  most  characteristic  portion  of  the  pneu- 
monia curve.  The  fall  in  temperature  usually  comes  on  in  the  form  of  a 
decided  crisis.  Generally  in  the  night  there  is  a  sinking  of  the  temperature 
with  a  more  or  less  abundant  perspiration,  in  which,  as  a  rule,  the  tempera- 
ture may  reach  a  subnormal  point— 96°  to  95°  P.  (3G°  to  35°  C.)..  The 
critical  decline  is  often  broken  by  new  and  slight  elevations  of  temperature, 
so  that  on  the  morning  of  the  next  day  there  may  be  a  definite  increase  of 
fever,  the  so-called  protracted  crisis.  Only  in  a  comparatively  small  number 
of  cases  does  the  fever  end  by  lysis,  in  which  the  temperature  goes  down 
like  steps.  The  duration  of  lysis  is  seldom  more  than  three  or  four  days  at 
most.  A  decline  of  temperature  by  lysis  is  most  frequent  in  severe  and  pro- 
tracted cases,  in  so-called  typhoid  pneumonia  (vide  infra),  and  also  particu- 
larly in  pneumonia  migrans. 

After  the  final  crisis  has  occurred,  the  active  pneumonic  process  ceases. 
The  day  of  the  crisis  is  therefore  reckoned  as  the  last  day  of  actual  illness. 
The  pneumonia  makes  no  advance  after  that,  but  resolution  and  absorption 
of  the  exudation  and  the  restoration  of  the  patient's  strength  still  take  time. 
Hippocrates  knew  when  the  time  of  the  crisis  occurs,  and  that  the  odd  days, 
especially  the  fifth  and  the  seventh,  have  a  special  significance  in  regard  to  it. 
In  an  infectious  disease  that  has  a  typical  course  there  can  be  nothing  strange 
in  the  fact  that  the  cessation  of  fever,  to  a  certain  degree,  is  associated  with 
a  definite  period  of  time;  but  Hippocrates'  rule  has  frequent  exceptions. 
The  crisis  sometimes  occurs  on  the  ninth,  the  twelfth,  or  the  thirteenth  day, 
and  even  later,  and,  on  the  other  hand,  there  are  quite  short  pneumonias  of 
but  one  or  two  days'  duration  (vide  infra). 

In  the  days  following  the  crisis  the  temperature,  which,  as  we  have  said, 
falls  to  subnormal,  regains  its  normal  height.  The  pulse,  which  usually 
sinks  to  fifty  or  sixty  during  the  crisis,  when  it  often  shows  a  slight  irregu- 
larity, reaches  its  normal  frequency  again  in  a  few  days.  We  are  quite  apt 
to  see,  in  the  days  immediately  following  the  crisis,  a  slight  temporary 
increase  of  temperature  again,  100°  to  102°  F.  at  most  (38°  to  39°  C),  but 
this  has  no  special  significance. 

In  cases  which  run  their  course  regularly,  the  signs  in  the  lungs  upon 
auscultation  and  percussion  become  normal  again  in  about  six  or  eight  days 
after  the  crisis.  Often  the  time  is  even  shorter  than  this,  or  it  may  be  longer. 
Abnormally  delayed  resolution  will  be  mentioned  below. 


CROUPOUS   PNEUMONIA  265 

Special  Peculiarities  and  Anomalies  in  the  Course  of  Pneumonia. — 1.  Pneu- 
monia in  Children. — Besides  the  common  lobular  pneumonia  there  is  also  a 
genuine,  lobar,  croupous  pneumonia  in  children,  which  is  by  uo  means  so 
rare  as  some  authors  formerly  supposed.  An  initial  chill  is  seen  only  in 
older  children;  initial  vomiting,  however,  is  very  common  in  children.  In 
many  cases  severe  cerebral  symptoms,  like  convulsions,  drowsiness,  or  delir- 
ium, obscure  the  pulmonary  symptoms  at  first.  The  further  course,  the 
development  of  physical  signs,  the  fever,  and  the  complications,  an-  quite 
analogous  to  the  appearances  in  adults.  The  pneumonic  sputum  is  only 
exceptionally  obtained  for  observation  in  children  under  eight  years  of  age. 
In  previously  healthy  children  the  prognosis  of  croupous  pneumonia  is  almosl 
invariably  favorable. 

2.  Pneumonia  in  old  people  is,  on  the  other  hand,  always  dangerous.  It 
may  begin  suddenly,  as  in  people  of  middle  age,  but  often  it  begins  more 
slowly  and  insidiously.  Its  course  is  marked  by  the  speedy  onset  of  great 
weakness  and  debility.  Nervous  symptoms,  like  delirium,  are  not  infre- 
quent.    Often  there  is  fatal  weakness  of  the  heart. 

3.  Drunkard's  Pneumonia. — We  see  croupous  pneumonia  in  drunkards 
with  remarkable  frequency.  The  usually  severe  and  dangerous  course  of  the 
disease  is  due  to  the  feeble  resisting  powers  of  their  impaired  organs.  It  is 
characterized  by  delirium  tremens,  which  usually  develops  in  the  first  days 
of  the  disease.  The  patient's  mind  is  disturbed,  he  is  very  restless,  constantly 
tries  to  get  out  of  bed,  and  he  fumbles  night  and  day  with  his  bedclothes  or 
nightgown.  The  alcoholic  character  of  the  delirium  is  shown  by  the  patient's 
whole  manner,  the  tremor  of  the  hands  and  tongue,  and  the  cast  of  his 
thoughts,  which .  are  usually  happy  but  exceptionally  anxious  and  terrified. 
His  mind  wanders  to  his  former  occupation  or  his  usual  boon  companions, 
and  the  like.  In  some  cases  the  patients  are  noisy  and  very  violent,  strike 
out,  destroy  surrounding  objects,  etc.  Under  these  circumstances  they  often 
believe  themselves  involved  in  tavern  brawls.  The  alcoholic  delirium  is 
almost  always  associated  with  hallucinations.  The  hallucinations  of  little 
moving  black  figures  are  especially  characteristic.  They  are  either  animals, 
rats  or  beetles,  or  little  black  men  and  similar  weird  shapes,  and  they  give 
him  much  trouble.  The  subjective  symptoms  of  pneumonia  are  wholly  in 
the  background.  No  delirious  patient  with  pneumonia  complains  of  cough, 
pain  in  the  chest,  or  dyspnoea.  Careful  objective  examination  is  the  only 
thing  that  confirms  the  diagnosis.  Very  often  patients  with  a  happy  delirium 
serve  to  entertain  those  about  them,  until  suddenly  very  severe  symptoms 
arise,  and  they  become  somnolent  and  succumb,  with  the  symptoms  of  pul- 
monary oedema.  The  prognosis  of  drunkard's  pneumonia,  therefore,  is  always 
to  be  regarded  as  very  unfavorable. 

4.  Pneumonia  in  Preexisting  Chronic  Diseases. — Croupous  pneumonia  is 
occasionally  seen  in  all  forms  of  chronic  disease.  It  is  especially  dangerous 
in  persons  who  are  already  enfeebled,  or  afflicted  with  chronic  cardiac  or 
pulmonary  disease,  such  as  phthisis  or  emphysema.  The  pneumonia  which 
often  attacks  patients  with  emphysema  is  clinically  important,  since  emphy- 
sema may  render  the  objective  evidence  of  pneumonia  very  obscure.  The 
croupous  exudation  does  not  completely  fill  the  dilated  alveoli;  hence  decided 
dullness  and  bronchial  breathing  are  absent. 


266  DISEASES  OF  THE  RESPIRATORY  ORGANS 

5.  Pneumonia  with  Late  Localization — Central  Pneumonia. — Cases  are 
quite  often  seen  whose  beginning,  course,  and  subjective  symptoms  corre- 
spond throughout  to  a  croupous  pneumonia,  but  in  which  the  objective  evi- 
dence of  pneumonic  infiltration  evades  the  most  careful  examination.  The 
disease  begins  with  a  chill,  the  fever  is  high,  the  patient  complains  of  pain 
in  the  chest,  which  is  usually  slight,  there  is,  perhaps,  herpes,  but  not  till  the 
fourth,  fifth,  or  sixth  day  can  we  make  out  anywhere  any  bronchial  breathing 
or  crepitant  rales.  In  other  cases  even  the  crisis  may  set  in  before  we  are 
able  to  localize  the  pneumonia  with  certainty.  In  most  of  these  cases  we  prob- 
ably have  to  do  less  with  an  actual  late  localization  than  with  a  central  infil- 
tration which  nowhere  approaches  the  periphery,  and  hence  is  made  out  objec- 
tively only  late  or  not  at  all.  A  careful  examination  of  the  sputum  is  of 
the  greatest  diagnostic  importance,  since  it  sometimes  has  a  perfectly  char- 
acteristic appearance  in  spite  of  the  absence  or  the  indefinite  character  of  the 
physical  signs.  If  there  is  no  sputum,  the  diagnosis  may,  of  course,  remain 
very  uncertain.  The  appearance  of  herpes  and  a  critical  fall  in  the  tempera- 
ture make  the  diagnosis  of  a  pneumonic  infection  probable  even  in  these 
cases.  In  one  such  case  the  author  observed  the  development  of  a  pleuritic 
friction  rub  upon  the  first  day  after  the  crisis,  confirming  the  diagnosis  of 
pneumonia  after  the  disease  had  run  its  course.  An  X-ray  examination  is 
of  great  value  in  such  cases. 

6.  Rudimentary  and  Abortive  Forms  of  Pneumonia — Unusual  Localiza- 
tions of  the  Pneumonic  Infection. — Particularly  at  times  of  a  pneumonic  epi- 
demic, but  also  at  other  times,  the  author  has  observed  illnesses  of  short 
duration  but  often  with  high  temperature  which  did  not  seem  like  clear 
cases  of  pneumonia,  although  they  still  were,  in  all  probability,  to  be  regarded 
as  pneumonic — i.  e.,  due  to  infection  with  the  specific  diplococci.  Cases  of 
this  sort  usually  begin  suddenly  with  a  chill,  headache,  and  high  temperature. 
Generally  there  is  a  cough  and  pain  in  the  chest.  Sometimes,  however,  there 
are  no  thoracic  symptoms  at  all.  The  physician  expects  pneumonia  to  de- 
velop, but  instead,  on  the  first,  second,  or  third  day,  the  fever  ceases  abruptly, 
no  changes  in  the  lung  having  been  discovered.  Very  often  there  will  be  a 
herpes  facialis  in  such  cases,  and  we  doubt  not  that  many  instances  of  so- 
called  herpes  febrilis,  or  febris  herpetica,  are  really  cases  of  pneumonic  infec- 
tion, without  any  other  localization  than  the  herpes.  In  other  instances,  upon 
careful  examination  there  will  be  found,  at  some  place  in  the  lungs,  a  slight 
crepitation,  or  limited  bronchial  breathing;  but  the  process  does  not  extend; 
and  in  a  very  brief  time,  after  a  day  or  two,  the  fever  ceases  (rudimentary 
pneumonia;  abortive  pneumonia). 

In  this  connection  we  may  remark  that  the  diplococcus  infection  may  be 
localized  in  still  other  places.  Thus,  for  example,  we  regard  it  as  very  prob- 
able that  many  cases  of  sore  throat  or  acute  enteritis,  associated  with  the 
sudden  onset  of  high  fever  and  with  herpes,  and  especially  when  seen  at  the 
time  of  an  epidemic  of  pneumonia,  are  due  to  diplococcus  infection.  Asso- 
ciated with  these  attacks  there  may  also  be  a  late  development  of  pulmonary 
symptoms. 

7.  Typhoid  Pneumonia — Asthenic  Pneumonia. — By  typhoid  pneumonia 
we  mean  those  cases  in  which,  besides  the  local  pulmonary  symptoms,  which 
may  be  either  slight  or  well  marked,  there  are  remarkably  severe  general 


CROUPOUS   PNEUMONIA  207 

symptoms.  The  cases  do  nol  often  begin  as  suddenly  as  ordinary  pneumonia, 
but  more  gradually,  like  typhoid.  Even  al  firs!  the  general  symptoms,  such 
as  greal  dullness,  Loss  of  appetite,  or  headache,  predominate  over  the  thoracic 
symptoms.  At  the  height  of  the  disease  there  is  a  decided  typhoidal  state, 
stupor,  delirium,  a  very  dry  tongue,  great  general  weakness,  and  also  enlarge- 
ment of  the  spleen,  and  frequently  mild  jaundice,  albuminuria,  etc.  Such 
cases  are  to  be  regarded  as  pneumonia  with  an  unusually  severe  gi  neral  infec- 
tion (or  intoxication).  They  sometimes  occur  in  epidemics.  It  is  said  that 
pneumonia  of  the  upper  lobes  shows  a  somewhat  more  frequent  tendency  to 
severe  nervous  symptoms  than  pneumonia  of  the  lower  lobes.  Recovery  from 
this  typhoid  or  asthenic  pneumonia,  which  may  last  two  weeks  or  more,  often 
follows  by  lysis.  Typhoid  pneumonia  is  by  no  means  a  sharply  defined  dis- 
ease. The  term  serves  merely  as  a  short  name  for  the  grave  constitutional 
disturbance.  Clinically  it  is  impossible  to  distinguish  it  sharply  from  pneu- 
monia migrans,  bilious  pneumonia,  and  other  forms.  "We  must  await  fur- 
ther bacteriological  investigations  to  determine  whether  there  may  not  be 
some  other  special  pathogenic  organism  in  man)'  cases  of  severe  character. 

Some  especially  severe  forms  of  pneumonia,  of  apparently  epidemic  or 
contagious  nature,  have  been  recognized  as  streptococcus  pneumonias.  In 
this  connection  may  be  briefly  mentioned,  also,  the  peculiar  and  severe  pneu- 
monia which  is  contracted  from  diseased  parrots  (so-called  psittacosis).  On 
the  other  hand,  it  is  not  improbable  that  another  important  factor  may  be  a 
variation  in  the  virulence  of  the  ordinary  pneumococcus  as  well  as  the 
greater  or  lesser  invasion  of  the  blood  by  the  pneumococcus. 

Pneumo-typUoid  is  to  be  carefully  distinguished  from  typhoid  pneumonia, 
although  from  a  clinical  point  of  view  the  diagnosis  between  them  is  often 
no  easy  matter.  By  pneumo-typhoid  is  meant  typhoid  fever  with  a  localiza- 
tion of  the  typhoid  bacilli  in  the  lungs  (see  page  16),  but  it  is  also  true  that 
ordinary  croupous  jmeunionia  may  occasionally  appear  as  a  complication  of 
typhoid  fever. 

8.  Pneumonia  with  Delayed  Resolution. — While  the  resolution  of  pneu- 
monia is  complete,  as  a  rule,  in  three  days  to  a  week  after  the  occurrence  of 
the  crisis,  there  are  cases  in  which  this  process  demands  a  much  longer  time. 
Not  infrequently,  and  particularly  in  severe  cases  of  pneumonia,  one  sees 
after  the  crisis  a  surprisingly  rapid  disappearance  of  all  the  physical  signs, 
while,  on  the  other  hand,  recovery  is  sometimes  remarkably  slow  in  appar- 
ently mild  cases;  but  this  rule  is,  of  course,  not  without  exceptions.  The 
course  of  the  disease  is  often  enough  precisely  the  opposite.  Just  what  are 
the  conditions  upon  which  the  rapidity  or  the  slowness  of  resolution  depends 
we  do  not  know.  Sometimes  unfavorable  constitutional  conditions,  such  as 
anasmia,  debility,  phthisical  tendencies,  and  kyphoscoliosis,  appear  to  delay 
resolution.  Sometimes,  on  the  other  hand,  no  such  explanation  can  be  found. 
It  seems  to  us  that  at  certain  times  all  the  cases  of  pneumonia  exhibit  more 
of  a  tendency  to  delayed  resolution  than  at  others,  so  that  it  is  not  impossible 
that  there  are  variations  in  the  pathological  process  itself.  In  many  cases 
of  delayed  resolution  it  is  our  opinion  that  we  have  to  do  with  genuine 
secondary  diseases,  or  a  mixed  infection  of  the  lungs  for  the  develop- 
ment of  which  the  precedent  croupous  pneumonia  had  prepared  a  favor- 
able soil. 


268  DISEASES   OF  THE   RESPIRATORY   ORGANS 

With  regard  to  the  symptoms  of  delayed  resolution,  there  are  various 
forms.  In  the  first  place,  we  see  eases  where  the  crisis  takes  place  in  the 
usual  way,  and  the  temperature  thereafter  remains  permanently  normal.  The 
patients  perhaps  feel  quite  well,  and  are  troubled  little  by  thoracic  symptoms ; 
nevertheless,  the  dullness  upon  percussion  remains  unchanged,  or  diminishes 
at  best  very  gradually,  and  the  bronchial  breathing  and  moist  rales  can  still 
be  heard.  All  the  signs  diminish  very  slowly,  sometimes  occupying  several 
weeks  in  their  disappearance,  and  then  complete  recovery  ensues.  In  a  few 
cases  it  is  striking  that,  after  the  crisis,  bronchial  respiration  and  dullness 
persist,  while  there  are  scarcely  any  rales  and  no  expectoration.  In  these 
cases  it  seems  as  if  the  pneumonic  exudation  does  not  really  liquefy  at  all, 
and  is  very  slowly  absorbed.  In  other  cases  there  is  no  distinct  crisis,  but 
the  fever  continues,  although  lower  than  at  first,  and  the  physical  signs  per- 
sist to  a  greater  or  less  extent.  At  the  end  of  two  or  three  weeks,  or  even 
still  later,  the  fever  slowly  ceases,  and  thereupon  normal  resonance  and 
vesicular  breathing  gradually  return. 

In  still  other  cases  the  patients  remain  free  from  fever  for  the  first  few 
days  after  the  crisis  has  taken  place,  although  the  pneumonia  is  not  com- 
pletely resolved.  Then  there  appears  again  a  rise  of  temperature  which  is 
mostly  moderate,  100.5°  to  103.5°  F.  (38°  to  39.5°  C),  while  the  dullness 
continues  and  there  are  an  abundance  of  moist  rales  and  catarrhal  expecto- 
ration. After  two  or  three  weeks  the  fever  gradually  ceases  and  the  abnor- 
mal pulmonary  signs  also  slowly  disappear.  In  such  cases  we  may  indeed 
suppose  that  some  secondary  infection,  a  sort  of  secondary  catarrhal  pneu- 
monia, has  developed  upon  the  seat  of  the  croupous  pneumonia.  The  disease 
may  take  still  another  course  somewhat  different  from  those  thus  far  described, 
and  of  this  we  have  seen  repeated  instances  much  resembling  one  another. 
After  the  occurrence  of  the  crisis  the  patient  remains  for  about  a  week  with- 
out fever.  During  this  time  the  dullness  and  the  not  very  loud  bronchial 
breathing  remain  unchanged.  Then  appears  a  moderate  intermitting  fever, 
with  elevations  to  about  102°  or  103°  F.  (39.5°  C).  This  fever  may  last 
two  to  four  weeks,  or  even  longer.  Over  the  affected  portion  of  the  lungs 
are  heard  either  no  moist  rales  or  only  a  very  few.  Gradually  there  appears 
a  moderate  but  distinct  contraction  of  the  side  involved,  then  the  resonance 
gradually  grows  clear,  the  respiratory  sounds  louder  and  vesicular,  the  fever 
ceases,  and  finally  health  is  completely  restored.  In  many  other  cases  of 
delayed  resolution,  as  we  have  already  said,  we  see  this  same  striking  absence 
of  moist  rales  and  the  development  of  a  moderate  degree  of  contraction. 
Under  such  circumstances  it  is  often  very  difficult  to  exclude  a  secondary 
pleurisy,  and  we  cannot  make  sure  except  by  repeated  exploratory  puncture. 
Moreover,  it  is  not  exceptional  to  find  delayed  resolution  and  secondary 
pleurisy  both  present  in  the  same  patient. 

9.  Termination  of  Pneumonia  in  Phthisis,  Contraction  of  the  Lungs, 
Pulmonary  Gangrene,  or  Pulmonary  Abscess. — Four  terminations  of  pneu- 
monia are  ordinarily  mentioned  as  unusual  and  anomalous — the  termination 
in  "  chronic  pneumonia,"  in  tuberculosis,  in  gangrene,  and  in  abscess. 

Concerning  the  termination  in  chronic  pneumonia,  we  have  already  men- 
tioned a  process  belonging  here,  the  termination  in  contraction  with  ultimate 
recovery.      In   rare   cases   the   contraction   is   permanent.      The    anatomical 


CROUPOUS   PNE1  MONIA 


269 


process  consists  in  the  development  of  pulmonary  cirrhosis,  with  Hie  forma- 
tion of  a  large  amounl  of  connective  tissue.    This  proliferation,  it  should  be 

said,  lakes  place  nol  only  in  the  interstitial  tissue,  bul  also  in  the  interior  of 
the  alveoli  by  extension  from  the  alveolar  walls.  Few  clinical  observations 
of  the  further  course  of  these  cases,  provided  death  Hoes  uol  shortly  ensue, 
have  as  yet  been  published. 

When  croupous  pneumonia  is  said  to  terminate  in  pulmonary  tubercul 
of  course  the  statement  can  be  understood  to  mean  only  that  the  symptoms 
of  tuberculosis  follow  immediately  upon  an  attack  of  pneumonia.  When  this 
is  the  case — it  does  not  occur  often — it  is  probable  thai  the  pneumonia 
attacked  a  person  already  suffering  from  tuberculosis,  in  whom,  however,  the 
symptoms  did  not  become  evident  until  after  the  pneumonia  had  run  its 
course.  It  may  also  be  that  exceptionally  the  pneumonia  furnishes  a  soil  for 
a  secondary  infection  with  tubercle  bacilli. 

Pneumonia  results  in  pulmonary  gangrene  in  rare  instances,  when  the 
patient  is  elderly,  delicate,  or  diabetic.  Here,  too,  in  our  opinion,  a  new 
infection,  with  a  foul  and  putrid  substance,  must  always  take  place,  and  this 
excites  the  gangrene.  The  previous  pneumonia  furnishes  only  the  occasion 
for  the  development  of  gangrene,  and  perhaps  prepares  the  soil  for  the  agents 
of  decomposition.  The  development  of  gangrene  is  appreciated  clinically 
(see  the  appropriate  chapter)  by  the  change  in  the  sputum  and  the  persistent 
fever. 

The  transition  from  pneumonia  to  pulmonary  abscess  is  very  rare.  We 
cannot  decide  whether  a  further  specific  cause  is  also  needed  for  this,  or 
whether  the  pneumonic  process  may  excep- 
tionally go  on  into  the  formation  of  abscess. 
We  know  that  the  pneumococci  sometimes  ex- 
cite purulent  inflammation  in  the  pleura  and 
in  the  meninges,  and  so  it  would  not  seem 
impossible  that,  under  peculiar  circum- 
stances, they  should  also  cause  the  develop- 
ment of  an  abscess  in  the  lungs.  The  transi- 
tion to  an  abscess  may  be  recognized  by  the 
character  of  the  sputum,  which  contains  frag- 
ments of  pulmonary  tissue,  such  as  elastic 
fibers,  besides  abundant  pus.  Moreover,  we 
sometimes  find,  on  microscopic  examination 
of  the  sputum  in  abscess,  scales  of  cholesterin 
(Fig.  49)  and  hematoidin  crystals;  the  latter  may  be  so  abundant  as  to  give 
the  expectoration  a  brownish  color.  Sometimes  we  have  seen  a  peculiar  green- 
ish color  of  the  sputum.  The  signs  of  a  pulmonary  cavity  are  found  if  the 
abscess  bursts. 

Diagnosis. — No  special  remarks  on  diagnosis  need  to  be  added  to  the  de- 
scription we  have  given  of  all  the  important  symptoms  which  may  occur  in 
croupous  pneumonia.  In  the  first  place,  we  must  consider  the  sudden  onset 
with  a  chill  and  high  fever,  shortly  followed  by  subjective  thoracic  symptoms, 
such  as  cough  and  pain  in  the  side;  also  the  characteristic  sputum  and  the 
objective  physical  signs,  the  appearance  in  many  cases  of  herpes  on  the  face, 
and  finally  the  general  course  of  the  disease,  particularly  the  temperature 


Fig.  49. — Cholesterin  crystals. 


270  DISEASES   OF  THE   RESPIRATORY   ORGANS 

curve  with  its  final  sudden  drop.  We  will  discuss  the  differential  diagnosis 
between  pneumonia  and  pleurisy  with  effusion  more  fully  in  the  description 
of  the  latter  affection. 

Prognosis. — Croupous  pneumonia  belongs  in  general  to  the  benign  infec- 
tious diseases.  The  great  majority  of  cases,  in  previously  strong  and  healthy 
individuals,  run  a  favorable  course,  and  end  in  complete  recovery.  On  the 
other  hand,  pneumonia  brings  a  number  of  perils  with  it,  the  knowledge  of 
which  should  always  make  us  cautious  in  giving  a  prognosis. 

One  grave  danger  lies  in  the  extension  of  the  process.  If  the  advance  of 
the  pneumonia  cannot  be  stopped,  if  the  whole  of  one  lung  is  involved,  and, 
besides  that,  a  great  portion  of  the  other  lung,  the  diminution  of  the  respira- 
tory surfaces  may  of  itself  occasion  a  fatal  termination. 

A  further  danger  lies  in  the  onset  of  certain  complications.  An  intense 
pleurisy,  with  effusion,  especially  if  purulent,  causes  greater  difficulty  in 
respiration,  and  thus  increases  the  danger.  Still  worse  is  a  serofibrinous  or 
purulent  pericarditis,  which,  in  not  very  rare  cases,  is  revealed  at  the  autopsy 
as  the  special  cause  of  death.  We  must  note,  however,  that  recovery  some- 
times finally  takes  place  in  spite  of  an  empyema  or  of  a  purulent  pericarditis. 
The  complication  with  a  purulent  meningitis,  which  is  fortunately  very  rare, 
is  probably  invariably  fatal. 

The  dangers  of  constitutional  infection  and  constitutional  intoxication  are, 
on  the  whole,  much  smaller  in  pneumonia  than  in  other  infectious  diseases; 
e.  g.,  typhoid  fever ;  but  yet,  this  possibility  deserves  some  consideration,  par- 
ticularly in  certain  forms  of  pneumonia  already  referred  to  and  termed 
"  typhoid  "  or  "  asthenic."  Such  particularly  severe  and  malignant  forms  of 
pneumonia,  with  a  high  rate  of  mortality,  sometimes  appear  as  endemics  and 
epidemics;  but  it  should  be  added  that  these  cases  are  also  often  marked  by 
the  extent  of  the  local  process  and  the  development  of  the  dangerous  compli- 
cations above  enumerated. 

The  individuality  of  the  patient  plays  the  most  important  part  in  the  prog- 
nosis of  pneumonia.  While  a  constitution  that  was  previously  healthy  and 
uninjured  usually  survives  the  disease,  one  that  was  previously  weak  and  dis- 
eased readily  succumbs.  In  this  fact  lies  the  danger  of  pneumonia  in  old, 
weak,  badly  nourished  persons,  and  in  persons  with  a  preexisting  emphysema, 
kyphoscoliosis,  heart  disease,  etc.  In  this,  too,  lies  the  great  danger  of  every 
pneumonia  in  drunkards.  Since  the  nervous  system  is  much  affected  by 
chronic  alcoholism,  we  very  often  see  outbreaks  of  delirium  tremens  in  pneu- 
monia. In  like  manner  the  other  nerve  centers  are  weakened  and  incapable 
of  resistance,  especially  the  regulatory  centers  for  the  heart  and  respiration. 
Hence  we  can  understand  why  even  moderate  drinkers,  though  previously 
strong  and  well  to  all  appearances,  succumb  to  pneumonia  from  failure  of  the 
heart  and  impairment  of  respiration. 

If  we  ask  upon  what  symptoms  our  prognosis  in  any  given  case  should  de- 
pend, we  must  reply  that  no  single  factor  can  be  given  especial  prominence. 
Chief  stress  must  always  be  laid  upon  the  state  of  the  lungs  and  the  respira- 
tion, but  attention  must  also  be  given  to  the  general  condition,  the  heart's 
action,  the  height  of  the  fever,  etc.  The  worst  dangers  of  pneumonia  have  just 
been  mentioned. 

Of  the  abnormal  terminations  of  pneumonia,  contraction  gives  the  best 


CROUPOUS  PNEUMONIA  271 

prognosis;  bul  recovery,  or  at  least  a  marked  subsidence  of  all  the  symptoms, 
may  sometimes  lake  place  after  gangrene  and  abscess. 

Treatment. — Many  of  the  milder  cases  of  typical  pneumonia  aeed  no  spe- 
cial active  treatment  when  the  disease  takes  a  favorable  course.  Most  cases 
get  well  under,  or,  we  can  almost  say,  in  spite  of  any  treatment.  From  the 
now  obsolete  method  of  treatment  by  large  bleedings,  and  from  the  u*'  of 
certain  drugs  (veratrin,  tartar  emetic),  which  are  even  now  sometimes  em- 
ployed, we  should  expect  harm  rather  than  any  benefit,  yet  under  such  treat- 
ment many  patients  have  recovered. 

We  do  not  know  of  any  certain  means  favorably  to  influence  the  pneumonic 
process.  Whether  we  are  destined  to  learn  of  some  specific  mode  of  treatment, 
perhaps  by  means  of  some  serum,  after  the  analogy  of  other  infectious  diseases, 
as  diphtheria,  we  cannot  say.  A  few  beginnings  have  already  been  made  in 
this  direction,  but  without  any  practical  results  as  yet.  We  are  at  present 
obliged,  therefore,  to  fall  back  upon  a  purely  symptomatic  and  constitutional 
treatment  of  pneumonia.  [Of  late,  interest  has  turned  to  vaccination  treat- 
ment, by  injecting  sterilized  cultures  of  pneumonia  bacilli,  sometimes  employ- 
ing bacilli  which  have  been  grown  from  the  patient's  sputum  (autogenous)  ; 
but  thus  far  the  success  has  been  partial  or  doubtful.] 

The  symptoms  which  are  usually  prominent  in  pneumonia,  even  in  the 
milder  cases,  and  of  which  the  patient  is  especially  desirous  to  be  relieved, 
are  the  pain  in  the  side,  the  troublesome  cough,  and  the  difficulty  and  distress 
in  breathing.  Since  the  respiratory  symptoms,  as  we  have  seen,  are  partly 
due  to  the  pain,  as  this  improves  the  patient's  breathing  often  undergoes  a 
decided,  improvement.  For  the  pain,  we  may  first  mention  a  number  of  ex- 
ternal applications  to  the  skin  on  the  affected,  side.  An  ice  bag  sometimes 
gives  marked  relief.  Many  patients  cannot  bear  this,  but  prefer  warm  poul- 
tices or  cold  wet  compresses.  The  application  of  mustard  plasters  or  dry  cups 
to  the  skin  may  be  of  advantage.  Subcutaneous  injections  of  morphin,  how- 
ever, are  the  most  effective  remedy,  and  are  often  indispensable.  There  is  no 
reason  why  we  should  not  use  this  remedy,  with  care  and  in  moderate  doses, 
for  the  relief  of  pain;  and,  as  the  disease  is  of  short  duration,  we  need  not 
particularly  fear  the  morphin  habit.  Small  doses  of  morphin,  subcutaneously 
or  by  the  mouth,  may  also  be  required  to  alleviate  the  cough. 

Local  bloodletting  is  a  remedy  the  action  of  which  cannot  be  explained 
physiologically,  and  yet  experience  has  shown  that  it  is  of  undoubted  advan- 
tage. The  relief  which  many  patients  feel  after  the  application  of  eight  or 
twelve  leeches  to  the  affected  side  is  very  striking;  but  we  should  prescribe 
them  only  when  there  are  severe  symptoms  at  the  beginning  of  the  disease,  and 
in  persons  who  were  strong  and  healthy  before  the  attack.  Wet  cups  accom- 
plish the  same  thing,  but  their  effect  is  somewhat  more  powerful,  and  hence 
they  should  be  reserved  for  strong  and  robust  persons,  such  as  laborers. 

The  tepid  or  cold  bath  serves  as  the  most  effective  means  of  improving  the 
respiration,  of  aiding  expectoration,  and  of  stimulating  and  refreshing  the 
whole  system.  We  hold  it  useless,  if  not  injurious,  to  give  a  patient  baths  if 
the.  disease  is  progressing  favorably,  for  almost  every  bath  has  some  disagree- 
able feature.  These  disadvantages,  however,  are  always  less,  in  severe  cases, 
than  the  benefit  and  improvement  which  baths  give  the  patient,  and  which 
most  patients  recognize  with  gratitude.     The  main  point  is  that  the  patient 


272  DISEASES   OF   THE   RESPIRATORY   ORGANS 

should  make  no  physical  exertion  while  in  the  hath,  that  he  should  he  lifted 
into  it,  held  and  supported  while  in  it,  and  lifted  into  bed  again  after  it. 
Since  the  baths  are  given  primarily  not  on  account  of  the  fever,  but  to  im- 
prove the  respiration,  and  because  of  their  favorable  influence  on  the  nervous 
system,  their  temperature  need  not  be  especially  low.  We  give  them  from  77° 
to  86°  F.  (25°  to  30°  C.)  ;  somewhat  warmer  with  sensitive  and  weak  people, 
and  cooler,  down  to  73°  F.  (20°  C),  with  strong  persons,  or  with  very  high 
fever  or  severe  nervous  symptoms.  We  need  not  employ  more  than  two  or 
three  baths  a  day,  and  at  night  we  employ  them  only  when  there  are  threaten- 
ing symptoms.  The  favorable  action  of  the  baths  is  seen  especially  in  the 
great  relief  and  refreshment  that  the  patient  feels.  The  respiration  is  quieter 
and  slower,  but  deeper.  The  patient  often  falls  into  a  quiet  sleep  after  the 
bath.  Of  late  years  we  have  often  replaced  the  baths  by  a  wet  pack,  even  in 
adults.  This  has  been  almost  always  very  well  received,  and  indeed  seemed  to 
make  the  patients  quieter,  with  easier  respiration  and  less  discomfort.  We 
would  particularly  and  strongly  recommend  the  pack  for  private  patients,  in 
whose  case  the  employment  of  baths  is  associated  with  many  difficulties. 

Among  internal  remedies  for  pneumonia,  antipyretics  are  frequently  em- 
ployed. We  do  not  believe  they  are  capable  of  exerting  any  decided  influence 
upon  the  general  course  of  the  disease,  although  we  admit  that  antipyrin  and, 
under  some  circumstances,  also  phenacetin  and  antifebrin  have  a  good  effect, 
since  they  not  only  modify  the  fever,  but  improve  the  nervous  symptoms  and 
the  general  condition.  Antipyrin  is  prescribed  in  doses  of  15  to  30  gr.  (gm. 
1  to  2),  particularly  toward  night.  [It  is  seldom  that  antipyretics  are  justified 
in  pneumonia.] 

To  make  the  cough  somewhat  more  effective,  expectorants  are  prescribed. 
We  ourselves  most  frequently  employ  infusion  of  ipecac,  apomorphin,  infusion 
of  senega,  liquor  ammonii  anisatus,  and  benzoin.  The  last  two  remedies  are 
especially  favorable  if  the  heart  is  feeble.  It  also  seems  to  us  of  some  impor- 
tance, with  regard  to  expectoration,  to  prescribe  an  abundance  of  liquid  in  the 
form  of  water,  tea,  lemonade,  and  similar  drinks. 

The  behavior  of  the  heart  should  always  be  watched  with  vigilance,  espe- 
cially in  elderly  and  delicate  persons,  and  in  the  obese  and  alcoholic.  If  the 
pulse  becomes  very  frequent,  an  ice  bag  is  placed  upon  the  heart.  If  the  pulse 
rate  is  remarkably  rapid  from  the  start,  we  may  order  digitalis  at  once,  either 
in  infusion,  or,  still  better,  in  powders  containing  1.5  to  3  gr.  (gm.  0.1  to  0.2), 
repeated  several  times  a  day;  and  as  digitalis  acts  slowly,  requiring  twelve  to 
twenty-four  hours  to  make  its  influence  felt,  if  the  weakness  of  the  heart  is 
dangerous,  stimulants  which  act  more  promptly  must  be  employed.  As  such, 
caffein  and  tincture  of  strophanthus  are  to  be  recommended,  and,  above  all, 
subcutaneous  injections  of  oleum  camphoratum  (1  to  4),  of  which  three  or 
four  syringefuls  (Tllxv),  and  more,  may  be  employed  (5ss.  to  5j).  Again, 
ether  injected  subcutaneously  is  a  powerful  cardiac  stimulant,  but  it  should 
be  employed  cautiously  because  of  its  marked  local  effect  (tissue  necrosis  and 
paralysis  of  the  muscles),  and  the  place  of  injection  should  be  the  skin  of  the 
abdomen  or  the  thigh. 

We  have  yet  to  make  some  remarks  upon  the  very  extensive  use  of  large 
amounts  of  alcohol  in  pneumonia.  A  free  use  of  alcohol  is  generally  consid- 
ered necessary  in  drunkards,  especially  when  delirium  tremens  is  beginning 


CROUPOUS   PNEUMONIA  273 

or  is  already  pronounced.     Since  the  withdrawal  of  any  poison  that   is  taken 
habitually,  like  uicotin  or  morphin,  may  excite  the  severesi   symptoms,  the 

sudden  withdrawal  of  alcohol  from  drunkards  may  have  the  \\<>i>t  results, 
while,  if  we  give  an  abundant  supply  of  the  stimulant  to  which  the  nervous 
system  is  accustomed,  we  sometimes  succeed  in  avoiding  the  onsel  of  severe 
nervous  symptoms,  such  as  collapse  and  failure  of  the  hearl  and  respiration. 
It  is  questionable  if  this  view  is  correct.  All  in  all,  I  have  not  gotten  the 
impression,  from  my  personal  experience,  that  the  withdrawal  of  alcohol  leads 
to  any  serious  manifestations.  I  shall  not,  however,  question  the  propriety 
of  the  exhibition  of  alcohol  in  the  pneumonia  of  alcoholics,  but  I,  myself,  never 
insist  upon  the  same.  Likewise  wine  should  be  given  to  persons  who  are 
accustomed  to  it  and  themselves  desire  it.  It  is  quite  a  different  matter  with 
patients  who  before  their  illness  have  not  been  accustomed  to  take  alcohol  at 
all,  or  who  took  it  only  in  small  amounts.  It  may  be  true  that  in  these  cases 
moderate  amounts  of  wine  may  have  a  stimulating  and  exciting  action,  al- 
though we  never  could  satisfy  ourselves  of  the  often  praised  influence  of 
alcohol  upon  the  action  of  the  heart.  We  hold  it,  however,  unjustifiable  to 
force  large  amounts  of  alcohol  indiscriminately  upon  every  patient  with  pneu- 
.  monia,  perhaps  in  spite  of  great  resistance  on  his  part.  Why  should  we  expect 
sick  persons  to  be  benefited  b}^  doses  of  alcohol  which  have  only  bad  results  on 
healthy  men  unaccustomed  to  them  ?  The  assertion  that  fever  patients  "  bear  " 
alcohol  better  than  healthy  persons  lacks  proof.  It  should  be  admitted  that 
perhaps  alcohol  is  more  rapidly  consumed  in  fever  than  in  health,  but  it  should 
also  be  considered  that  the  toxic  effects  of  alcohol  are  less  easily  noticeable  in 
comatose  patients  than  in  persons  possessing  normal  consciousness. 

[Probably  a  moderate  amount  of  alcohol  may  contribute  to  the  support  of 
a  patient  who  is  beginning  to  fail  in  pneumonia,  but  it  is  not  wise  to  give  very 
large  doses,  even  if  the  patient  is  very  feeble.  Better  are  strychnin  given  sub- 
cutaneously  in  full  doses,  but  stopping  short  of  physiological  effect,  and  caffein 
also  subcutaneously.  If  the  pulse  tension  is  low  and  the  abdomen  distended, 
a  flannel-covered  ice  bag  placed  on  the  abdomen  may  act  favorably  by  stimu- 
lating the  splanchnic  nerve.  Oxygen  inhalations  do  not  seem  to  be  of  very 
great  value,  much  less  so  than  in  broncho-pneumonia.  Emphasis  must  be 
placed  on  fresh-air  treatment.  Apparently  a  low  temperature  makes  the 
air  better.  The  patient  should  be  warmly  but  lightly  covered.  He  may  be  in 
a  room  with  the  windows  all  open,  or,  still  better,  actually  in  the  open  air. 
The  benefit  is  fully  as  great  with  children  as  adults.  Speaking  of  the 
Baby's  Hospital,  in  New  York,  LaFetra  says :  "  1.  In  the  acute  congestive 
stages  of  inflammations  of  the  upper  respiratory  tract  (rhinitis,  laryngitis, 
bronchitis,  especially  of  the  small  tubes,  with  or  without  bronchial  pneu- 
monia) warm,  moist  air  is  of  greater  help  than  cold,  dry  air.  2.  In  lobar 
pneumonia,  with  high  temperature  and  little  or  no  bronchitis,  cold,  dry  air  is 
of  great  advantage.  The  same  is  true  of  pulmonary  tuberculosis  and  of  em- 
physema. 3.  After  the  acute  stage  has  passed,  and  when  there  is  no  inflam- 
matory spasm  of  the  larynx  or  bronchi,  the  cold-air  treatment  is  of  advantage 
in  cases  of  rhinitis,  laryngitis,  bronchitis,  and  bronchial  pneumonia."] 

We  scarcely  need  to  lay  special  emphasis  on  the  fact  that  the  physician 
should  endeavor,  so  far  as  possible,  to  maintain  the  bodily  strength  by  means 
of  appropriate  and  sufficient  nourishment.     Soups,  bouillon  with  toast  or  rusk, 


274  DISEASES   OF  THE   RESPIRATORY   ORGANS 

milk,  and  eggs  are  the  most  suitable  articles  of  diet,  and  it  is  sometimes  proper 
to  give  small  amounts  of  finely  minced  meat.  Care  should  be  taken  that  the 
patient  has  an  abundance  of  refreshing  beverages.  Wine  and  also  moderate 
amounts  of  good  beer  may  be  allowed  without  hesitation. 

The  treatment  of  complications  follows  the  ordinary  rules  which  have  been 
given  under  the  individual  affections.  We  must  also  mention  that,  in  delirium 
tremens,  tepid  baths  with  cold  douches  sometimes  have  a  very  good  effect.  Be- 
sides this,  we  may  try  subcutaneous  injections  of  strychnin,  7  to  15  minims  of 
a  one-per-cent  solution  once  or  twice  a  day.  We  cannot  wholly  dispense  with 
narcotics,  such  as  morphin  and  chloral,  but  we  must  warn  against  the  impru- 
dent use  of  large  doses  of  chloral,  above  35  gr.  (gm.  2.5).  Paraldehyd,  in 
doses  of  45  to  75  minims  (gm.  3.0  to  5.0),  is  to  be  recommended. 


CHAPTER    VI 

TUBERCULOSIS    OF    THE   LUNGS 

{Pulmonary  Phthisis.     Pulmonary  Consumption) 

GENERAL  PATHOLOGY  AND  AETIOLOGY  OF  TUBERCULOSIS 

Ever  since  Bayle,  in  1810,  demonstrated  the  extensive  distribution  of  pe- 
culiar nodules  in  the  various  organs,  and  their  relation  to  pulmonary  consump- 
tion, few  questions  have  so  taxed  clinical  observers  and  pathologists  as  those 
relating  to  the  cause  and  nature  of  tuberculosis.  Harmony  could  not  be 
reached,  however,  so  long  as  the  criterion  for  the  decision  of  the  questions 
was  sought  in  the  presence  of  definite  anatomical  changes,  which  were  regarded 
as  specific  of  tuberculosis.  Laennec  considered  the  peculiar  change  in  the 
tuberculous  products,  which  later  was  named  caseation  by  Virchow,  to  be  char- 
acteristic, and  called  everything  tuberculous  in  which  it  was  found.  He  dis- 
tinguished the  isolated  tubercle  from  diffuse,  tuberculous,  cheesy  infiltration. 
Thus,  Laennec  recognized  that  many  processes  were  allied  whose  affinity  was 
often  disputed  afterwards,  and  which  has  only  recently  been  established,  such 
as  the  affinity  between  "  scrofulous  "  enlargement  of  the  glands  and  tubercu- 
losis. Another  opinion  became  quite  prevalent,  after  Virchow  discovered  that 
precisely  the  same  anatomical  process  as  tuberculous  caseation  was  also  found 
in  inflammatory  products,  which  were  certainly  not  tuberculous,  and  in  can- 
cerous ulcerations.  Hence,  Virchow  made  a  sharp  distinction  between  tubercle 
and  those  new  growths  and  inflammatory  processes  which  had  become  cheesy. 
The  anatomical  criterion  of  tuberculosis  was,  in  his  view,  the  presence  of  the 
miliary  tubercle,  a  gray  nodule,  the  size  of  a  millet  seed  at  the  largest,  made 
up  of  cells  like  lymph  corpuscles.  The  study  of  the  finer  structure  of  the  mil- 
iary tubercle  was  now  pushed  most  eagerly  by  Wagner,  Schiippel,  Langhans, 
and  others,  but  they  were  unable  to  reach  perfect  harmony  regarding  its  origin 
and  significance. 

As  long  ago  as  1865,  however,  a  discovery  was  made  which  pointed  une- 
quivocally to  the  only  way  which  could  lead  to  a  correct  knowledge  of  tuber- 
culosis.   It  was  the  fact,  discovered  by  Villemin,  that  tuberculosis  can  be  pro- 


TUBERCULOSIS  OF  THE  LUNGS  275 

duced  artificially  by  inoculating  healthy  animals  with  small  amounts  of  tuber- 
culous and  cheesy  substances.     Although  doubted  and  misinterpreted  al   firsl 
in  various  quarters,  the  fact  that  tuberculosis  can  be  transmitted,  and  cod 
quently  the  fact  of  Us  infectious  character,  musl  now  be  regarded  as  proved 

beyond  a  doubt.  In  the  general  change  which  our  opinions  upon  the  nature  of 
infectious  diseases  has  undergone,  especially  in  the  last  few  years,  the  exist- 
ence of  a  specific,  organized  cause  of  tuberculosis,  too,  had  to  be  assumed. 
Klebs,  and  later  Cohnheim,  had  already  without  reserve  defined  tuberculosis 

as  a  specific,  infectious  disease,  and,  sooner  than  we  dared  to  hope,  R.  Koch 
discovered  the  special  carriers  of  the  disease  in  the  shape  of  the  tubercle  bacilli, 
in  the  year  1881.  The  definition  of  tuberculosis  no  longer  rests  upon  any  ex- 
ternal anatomical  character.  Every  disease  is  tuberculous  which  is  excited  by 
the  pathogenic  action  of  a  specific  kind  of  bacteria,  the  tubercle  bacilli  dis- 
covered by  Koch. 

The  pathogenic  bacteria  of  tuberculosis  belong  to  the  group  of  bacilli.  The 
tubercle  bacilli  are  rod-like,  of  small  diameter,  slightly  rounded  at  their  ex- 
tremities, and  either  straight  or  somewhat  bent.  Their  length  is  perhaps  a 
fourth  or  a  half  that  of  the  diameter  of  a  red  blood  corpuscle.  In  the  interior 
of  these  rods  it  is  not  infrequently  possible  to  distinguish  very  minute  colorless 
spots  which  are  probably  to  be  regarded  as  endogenous  spores.  The  tubercle 
bacilli  have  no  independent  motion  whatever.  Their  reaction  to  certain  color- 
ing matters  is  very  characteristic,  and  of  the  highest  importance  with  regard 
to  their  recognition  (vide  infra). 

We  know  with  absolute  certainty  that  the  tubercle  bacilli  are  always  pres- 
ent in  all  the  different  forms  of  pulmonary  tuberculosis,  both  in  the  lung  itself 
and  in  the  expectoration  (vide  infra),  and  also  in  tuberculous  diseases  of  other 
organs,  the  brain,  the  intestines,  the  spleen,  the  liver,  and  the  kidneys,  and 
also  in  "  scrofulous  lymph-glands,"  in  "  fungous  "  diseases  of  the  bones  and 
joints,  and  in  the  so-called  lupus,  which  is  nothing  but  a  local  tuberculosis  of 
the  skin.  Precisely  the  same  bacilli  are  also  found  in  the  K  spontaneous " 
tuberculosis  of  animals,  such  as  monkeys,  puppies,  and  guinea  pigs,  and  in 
every  tuberculosis  that  is  artificially  produced  in  animals  by  inoculation. 
Finally,  by  the  discovery  of  tubercle  bacilli  in  the  "  pearly  distemper  "  of  cat- 
tle, the  close  relationship  of  this  disease  with  tuberculosis  has  been  established. 

Koch,  by  his  successful  "  pure  cultures  "  and  inoculations  with  the  culti- 
vated bacilli,  has  established  the  fact  that  these  tubercle  bacilli  are  to  be 
regarded  as  the  cause  of  tuberculosis.  Bacilli  coming  from  any  fresh  product 
of  tuberculous  disease  may  be  grown  in  pure  culture  at  a  constant  temperature 
of  98°  to  100°  F.  (37°  to  38°  C.)  upon  blood  serum  which  has  been  stiffened 
by  heating,  and  upon  several  other  artificially  prepared  soils.  In  this  cultiva- 
tion they  show  certain  characteristic  properties  in  their  growth,  which  cannot 
be  fully  described  here,  and  they  multiply  to  an  unlimited  extent.  By  the 
subcutaneous  injection  of  the  smallest  amounts  of  sputum  containing  tubercle 
bacilli  into  guinea  pigs,  the  local  lymph-nodes  first  become  swollen,  and  after 
about  thirty  days  tuberculosis  of  the  spleen  is  to  be  found,  and  after  some 
forty  days  tuberculosis  of  the  liver.  Death  occurs  seven  to  eight  weeks  after 
the  injection,  durjng  which  period  the  animal  becomes  markedly  emaciated. 
If  the  animals  inhale  the  infectious  material,  numerous  tuberculous  foci  are  to 
be  found  in  their  lungs  about  three  weeks  later.     Tuberculosis  may  likewise 


276  DISEASES   OF  THE   RESPIRATORY   ORGANS 

be  developed  in  animals  fed  with  tubercle  bacilli,  but  for  this  purpose,  however, 
exceedingly  large  quantities  of  the  infectious  material  are  required.  Accord- 
ing to  Fliigge,  400,000,000  bacilli,  in  a  single  feeding,  are  an  effectual  dose 
for  a  guinea  pig.  The  most  instructive  inoculations  are  those  into  the  ante- 
rior chamber  of  the  eye  in  puppies  or  guinea  pigs,  which  were  first  tried  by 
Cohnheim  and  Salomonsen.  After  an  incubation  of  two  or  three  weeks  we 
see  here  very  plainly  an  eruption  of  the  first  nodules  of  tubercle  in  the  iris, 
and  the  tuberculosis  spreads  to  the  other  organs  of  the  body  later.  By  all  of 
these  experiments  it  was  demonstrated  that  tuberculosis  is  always,  at  the  start, 
a  purely  local  disease,  and  that  its  further  extension  depends  upon  the  spread 
of  its  germs. 

^Etiology  of  Tuberculosis  in  Man 

The  distribution  of  tubercle  bacilli  must  be  remarkably  extensive,  for  tu- 
berculous diseases  occur  in  almost  every  country  on  earth.  The  predisposition 
of  mankind  to  the  disease  is  also  very  great,  and  thus  we  understand  the  fright- 
ful fact,  which  statistics  show,  that  about  one  eighth  of  all  deaths  are  from 
tuberculosis !  The  number  of  individuals  who  are  at  all  infected  is  very  much 
larger  still.  According  to  some  statistics,  tuberculosis  is  present  in  from 
eighty  to  ninety  per  cent  of  all  post-mortem  cases.  The  greatest  number  of 
these  cases,  to  be  sure,  show  healed  lesions.  It  has  neither  been  proved,  nor 
is  it  probable,  that  tubercle  bacilli  multiply  outside  of  the  human  body,  like 
the  bacilli  of  splenic  fever,  since  they  can  develop  only  in  a  constant  and  uni- 
formly warm  temperature  between  85°  and  104°  F.  (30°  to  40°  C).  We  must 
therefore  regard  them  as  true  parasites,  which  can  live — that  is,  which  can 
propagate  and  multiply — only  in  the  bodies  of  animals,  but  they  (or  their 
spores)  seem  to  preserve  their  virulence  and  their  ability  to  multiply  outside 
of  the  body  for  a  long  time.  Phthisical  sputum  may  be  used  for  inoculation 
with  success,  even  if  it  has  been  dried  for  several  weeks.  The  tubercle  bacilli 
also  resist  most  chemical  reagents,  such  as  nitric  acid,  very  decidedly. 

If  the  body  becomes  infected,  then,  with  tubercle  bacilli,  it  is  always  prob- 
able that  they  have  come  from  some  other  individual — man  or  beast — with  tu- 
berculous disease.  We  need  not  mention  how  numerous  the  opportunities  for 
infection  may  be,  considering  the  present  general  distribution  of  tuberculosis. 
The  chief  stress  in  this  respect  is  very  evidently  to  be  laid  upon  the  expectora- 
tion of  phthisical  patients,  which  contains  the  bacilli.  The  extensive  investi- 
gations of  Cornet  have  well  shown  how  frequently  it  is  possible  to  obtain  tuber- 
culous material,  which  is  capable  of  causing  infection,  from  the  dust  in  the 
neighborhood  of  phthisical  patients  who  carelessly  deposit  their  expectoration 
upon  the  floor  and  in  handkerchiefs  and  elsewhere.  On  the  other  hand, 
Fliigge's  studies  have  shown  that  dried  sputum  does  not  readily  become  pul- 
verized and  whirled  about  in  dust.  Tubercle  bacilli  were  only  exceptionally 
found  in  the  dust  gathered  at  a  height  of  about  that  of  an  adult's  head  from 
the  floor  in  waiting  rooms,  factories,  street  cars,  etc.  For  these  reasons, 
Fliigge  considers  another  mode  of  infection  to  be  of  greater  significance. 
He  has  demonstrated  that  the  consumptive  with  a  cough  can  defile  the  sur- 
rounding air  with  numerous  minute  drops  of  sputum  containing  tubercle  bacilli. 
These  hover  for  a  time  in  the  air,  and  may  be  inhaled  by  other  persons.    This 


TUBERCULOSIS  OF  THE   LUNGS  277 

mode  of  infection  is  frequently  importanl  in  the  direcl  transmission  of  tuber- 
culosis, and  such  direcl  transmission  is  shown,  above  all,  by  the  cases  of  tuber- 
culosis in  married  couples,  in  nurses,  and  in  patients  who  for  a  long  time 
occupy  a  ward  in  which  there  arc  many  consumptives.  Still,  the  experience  of 
physicians  proves  thai  such  direct  infection  with  tuberculosis  ie  of  very  infre- 
quent occurrence  (vide  infra ).  There  arc  very  many  who  fall  sick  with  tuber- 
culosis who  have  never  been  in  close  contad  with  other  consumptives.  In  such 
cases  it  must  he  that  the  tubercle  bacilli  enter  the  body  indirectly.  This  may 
naturally  occur  in  the  most  diverse  ways.  The  tubercle  bacilli  may  be  .-'al- 
tered by  the  diseased  individual  by  means  of  the  sputum  itself,  as  well  as  by 
the  expulsion  of  drops  of  mucus  containing  bacilli  during  coughing. 

The  material  which  contains  the  bacilli  or  spores  is  taken  into  the  body,  in 
the  majority  of  cases,  along  with  the  inspired  air.  This  is  probable,  because, 
in  most  cases,  tuberculosis  has  its  starting-point  in  the  air-passages,  the  lungs, 
or  the  larynx.  Inoculation  experiments  show,  as  we  have  indicated,  that  the 
first  extension  of  the  process  depends  upon  the  point  of  inoculation.  Hence 
it  seems  very  probable  that,  in  tuberculosis  in  man,  the  infect  ion-  matter  is 
taken  directly  into  the  air-passages  by  the  breath.  In  this  way  it  sometimes, 
though  rarely,  attacks  the  upper  air-passages,  as  in  primary  tuberculosis  of  the 
nose,  the  pharynx,  and  the  larynx,  but  more  frequently  it  affects  the  deeper  por- 
tions of  the  respiratory  apparatus,  as  in  primary  tuberculosis  of  the  lungs  and 
bronchi. 

It  cannot  be  denied,  however,  that  even  in  the  presence  of  an  apparently 
primary  pulmonary  tuberculosis,  the  possibility  of  an  indirect  infection  of  the 
lungs  cannot  be  absolutely  excluded.  Certain  experiments  seem  to  show  that 
tubercle  bacilli  that  have  perhaps  first  passed  by  way  of  the  tonsils  or  through 
small  wounds  of  the  skin  into  the  neighboring  lymph-glands,  finally  reach  the 
lungs  via  the  blood  or  lymph-channels,  where  they  at  last  find  conditions  favor-  • 
able  to  their  settlement  and  to  the  development  of  their  harmful  effects.  At 
the  present  time  it  can  by  no  means  be  definitely  stated  to  what  extent  the 
direct,  and  to  what  extent  the  indirect,  mode  of  infection  plays  a  part  in 
primary  pulmonary  tuberculosis.  The  fact  that  pulmonary  tuberculosis  is  so 
often  apparently  first  situated  at  the  apex,  and  that,  on  the  other  hand,  the 
lower  lobes  are  most  often  involved  in  all  the  other  inhalation  diseases  of  the 
lungs,  may  be  advanced  as  an  argument  in  favor  of  the  indirect  infection  of  the 
lungs.  The  important  X-ray  examinations  (vide  infra)  that  have  been  made 
in  incipient  tuberculosis  (H.  Rieder)  have,  however,  led  to  the  interesting 
result  that  in  many  cases,  at  least,  the  apices  are  by  no  means  the  first  seat 
of  the  disease,  but  are  only  involved  during  the  second  stages  of  tuberculosis. 
The  bronchial  lymph-glands  are  primarily  affected,  an  observation  clinically 
not  demonstrable  without  X-ray  examination.  In  the  X-ray  picture  strands 
(probably,  for  the  most  part,  tuberculous  lymphangitis)  may  be  seen  extend- 
ing from  the  lymph-nodes  to  one  or  both  of  the  upper  pulmonary  lobes, 
whence  the  disease  establishes  itself  and  spreads  further.  In  most  cases  the 
bronchial  glands  certainly  become  diseased  through  inhalation  of  the  tuber- 
culous virus.  Here  the  latter  first  passes  through  the  lungs,  leaving  them  un- 
affected, and  only  being  taken  up  by  the  bronchial  glands,  where  it  remains. 
(Compare  with  the  chapter  on  Pneumonoconiosis.) 

In  addition  to  infection  through  the  atmosphere,  the  possibility  of  infection 
18 


278  DISEASES  OP  THE  RESPIRATORY  ORGANS 

of  the  intestinal  canal  from  the  swallowing  of  infectious  material  must  be 
considered.  The  transmission  of  tuberculosis  from  domestic  animals  to  man 
plays  a  part  in  this  connection  which  perhaps  is  not  unimportant.  Since  the 
pearly  distemper  of  cattle  is  identical,  or  at  least  closely  related  to  tuberculosis 
in  man,  the  use  of  the  flesh  of  such  animals  as  food  furnishes  a  possible  means 
of  infection.  It  is  a  still  more  important  circumstance  that,  when  pearly 
nodules  are  present  on  the  udder,  the  milk  of  the  diseased  animal  may  be  pol- 
luted by  tubercle  bacilli,  and  that  the  use  of  such  uncooked  milk  or  butter 
made  from  it  as  food  certainly  involves  the  danger  of  the  transmission  of  tuber- 
culosis. Indeed,  Behring  has  expressed  the  opinion  that  the  greater  proportion 
of  cases  of  pulmonary  tuberculosis  are  referable  to  an  infection  of  the  intestinal 
canal  dating  from  earliest  childhood.  This  assertion  is  not  in  accordance  with 
general  experience,  and  has  met  with  but  little  approbation  in  medical  circles. 
It  is  all  the  more  improbable  because  Koch,  Kossel,  and  others  have  demon- 
strated that  the  bacilli  of  human  and  of  bovine  tuberculosis  are  not  identical. 
Two  different  types  of  the  tubercle  bacillus,  the  typus  bovinus  and  typus  hu- 
manus,  can  be  readily  distinguished.  Human  tubercle  bacilli  usually  produce 
only  a  local  tuberculosis  in  cattle,  whereas  a  general  tuberculosis  may  readily 
be  given  to  them  by  inoculation  with  the  bacillus  of  bovine  tuberculosis.  On 
the  other  hand,  the  bovine  bacilli  do  not  seem  to  have  any  great  virulence 
for  human  beings.  That  some  virulence  exists,  however,  is  shown  by  some 
cases  of  intestinal  and  peritoneal  tuberculosis  in  children,  in  which  just  the 
bovine  type  of  bacilli  can  be  demonstrated.  The  danger  of  milk  infection, 
especially  in  children,  cannot  therefore  be  overlooked,  but  its  importance 
should  not  be  overestimated.  In  most  cases,  tuberculosis  in  children  certainly 
does  not  begin  in  the  intestine,  but  in  the  lymph-nodes,  and,  above  all,  in  the 
bronchial  nodes  surrounding  the  roots  of  the  lungs. 

In  some  cases  the  tuberculous  infection  may  probably  arise  from  little  fis- 
sures and  excoriations  of  the  skin.  In  this  way  either  we  get  a  local  tuber- 
culosis of  the  skin,  such  as  lupus,  or  the  bacilli  are  carried  by  the  lymphatics 
to  the  neighboring  glands  of  the  neck  or  axilla,  establish  themselves  there,  and 
set  up  a  tuberculous  disease  in  them.  It  has  been  pointed  out  above  that 
tubercle  bacilli  may  also  pass  from  the  lymph-nodes  into  the  blood  and  thus 
reach  distant  organs.  Because  of  its  importance,  it  should  again  be  stated 
that  even  when  the  tubercle  bacilli  are  taken  into  the  body  through  the  lungs 
or  the  intestine,  the  infectious  material  often  passes  the  primary  seat  of  in- 
fection without  fastening  itself  there,  and  does  not  take  root  until  it  reaches 
the  nearest  lymph-glands;  or  perhaps,  often,  still  more  distant  regions,  such 
as  the  kidneys  or  the  bones  (?).  Thus  arises  the  so-called  primary  tubercu- 
losis of  the  bronchial  or  mesenteric  glands,  leading  sometimes,  as  we  shall  see 
later,  to  various  severe  tuberculous  diseases  in  other  parts,  such  as  the  pleura 
or  peritoneum. 

It  remains  to  mention  the  possibility  of  a  primary  genito-urinary  tubercu- 
losis. Primary  infection  of  the  uterus  and  ovaries  might  be  referable  to  direct 
infection  from  without;  but  it  is  questionable  whether  genito-urinary  tubercu- 
losis of  the  male,  affecting  the  kidneys,  testicles,  and  prostate,  arises  in  this 
manner.  In  such  cases  we  are  probably  generally  dealing  with  infection  due  to 
the  excretion  by  the  kidneys  of  tubercle  bacilli  which  have  got  into  the  body  in 
some  way,  and  have  reached  the  general  circulation. 


TUBERCULOSIS  OF  THE   LUNGS  279 

Considering  the  wide  distribution  of  the  tubercle  bacilli,  and  the  many 
chances  for  infection,  it  seems  wonderful  thai   in  spite  of  L1  so  many  human 

beings  escape  tbe  disease.  One  factor,  wbicli  lias  been  already  mentioned  by 
Koch,  must  be  borne  in  mind,  however,  and  that  is  the  extremely  slow  growth 
of  the  tubercle  bacilli.  This  is  the  reason  why  the  bacilli  do  no!  always  remain 
in  the  body,  but  in  many  cases  are  eliminated  again  before  they  have  gained  a 
definite  foothold. 

Individual  predisposition,  however,  is  another  factor  wbicli  i-  probably  still 
more  important — a  factor  wbicli  we  cannot  well  explain,  but  wbicli  we  cannot 
get  on  without,  at  tbe  present  time,  in  tbe  pathology  of  many  infectious  dis- 
eases. In  our  conception  of  most  of  the  other  infectious  diseases  as  well  as 
of  tuberculosis,  we  must  assume  provisionally  an  unequal  predisposition  to  dis- 
ease in  different  individuals.  Of  all  individuals  who  are  exposed  to  the  inva- 
sion of  tubercle  bacilli,  only  those  become  diseased  in  whom  the  poison  can 
establish  itself  in  the  tissue  cells  where  it  exerts  its  deleterious  influences,  and 
whence  it  further  increases  and  spreads. 

The  basis  for  this  "  predisposition  to  tuberculosis  "  is  not  well  understood. 
According  to  our  present  views  on  the  general  principles  of  immunity,  how- 
ever, it  is  by  no  means  impossible  that  the  variation  in  the  predisposition  to 
tuberculosis  is  at  least  in  part  dependent  on  the  varying  individual,  chemical 
state  of  tbe  blood  serum  and  the  tissue  juices.  In  this  connection,  the  recent 
investigations  of  E.  Koch,  Behring,  and  others  have  taught  that  there  are 
decided  differences  in  the  agglutinating  effect  of  the  serum  of  tuberculous  and 
of  nontuberculous  individuals  on  cultures  of  tubercle  bacilli.  Yet  it  is  very 
striking  that  the  existence  of  the  tendency  to  tuberculosis  is  often  expressed  in 
tbe  general  constitutional  debility  of  the  individual,  and — still  more  remark- 
able— in  certain  peculiarities  of  his  bodily  frame,  e.  g.,  the  shape  of  his  thorax. 
This  phthisical  habitus  (vide  infra)  is  especially  common  in  persons  who  come 
from  families  with  a  tendency  to  tuberculosis,  and  it  is  a  peculiar  yet  quite 
inexplicable  expression  of  the  predisposition  to  tuberculosis,  due  to  family  and 
hereditary  influence  (vide  infra).  It  should  be  said  that  the  hereditary  tend- 
ency to  tuberculosis  is  not  invariably  associated  with  any  striking  and  self- 
evident  weakness  of  the  constitution.  Persons  who  spring  from  tuberculous 
families  may  have  a  vigorous  frame  and  yet  fall  victims  to  the  disease;  and 
likewise,  also,  when  there  is  no  hereditary  tendency,  the  most  powerful  build 
does  not  by  any  means  render  one  invulnerable  to  the  disease. 

We  now  believe  that  many  evil  influences  which  were  once  thought  to  be 
causes  of  tuberculosis  act  only  in  increasing  the  predisposition  to  the  disease. 
Insufficient  food,  bad  air,  severe  illness,  childbirth,  want,  and  care — these 
alone,  of  course,  can  never  produce  tuberculosis;  but  innumerable  observa- 
tions show  that  the  body  which  has  become  weakened  affords  less  resistance 
to  the  injurious  influence  of  the  tuberculous  poison  than  does  the  strong  and 
healthy  body.  Thus  it  seems  to  us,  from  our  own  observations,  to  be  in  the 
highest  degree  probable  that  chronic  alcoholism  increases  the  liability  of  the 
individual  to  tuberculosis.  It  is  surprising  how  often  drunkards,  possessed 
of  a  naturally  most  vigorous  constitution,  fall  victims  to  tuberculosis. 

People  used  often  to  speak  of  the  transition  of  other  affections  of  the  lungs 
into  pulmonary  consumption — that  is,  into  tuberculosis.  It  was  imagined 
that  an  old  bronchial  catarrh,  croupous  inflammation  of  the  lungs,  or  the 


280  DISEASES   OF  THE   RESPIRATORY   ORGANS 

catarrhal  pneumonia  accompanying  measles,  or  whooping  cough,  could  readily 
become  "  tuberculous."  Of  course  the  proper  interpretation  of  such  a  connec- 
tion is  that  the  precedent  disease  prepares  a  favorable  soil  for  infection  with 
the  tuberculous  virus,  and  that  consequently  the  tubercle  bacilli  fasten  more 
readily  upon  the  mucous  membrane,  which  has  been  previously  affected,  than 
under  normal  conditions.  Moreover,  many  of  the  infections  which  we  for- 
merly supposed  to  be  apt  to  change  into  tuberculosis  are  themselves  tubercu- 
lous. This  is  true  in  most  of  the  so-called  scrofulous  diseases  of  the  lymph- 
glands,  bones,  etc.,  and  also,  as  we  shall  see  later,  in  the  overwhelming 
majority  of  cases  of  apparently  primary  pleurisy. 

No  single  factor,  however,  of  those  which  favor  the  predisposition  to 
tuberculosis,  plays  so  manifest  and  so  visible  a  part  ■  as  does  the  hereditary 
tendency  above  mentioned — that  is,  the  inborn  predisposition  of  the  indi- 
vidual. The  fact  of  the  heredity  of  phthisis  meets  us  with  such  uncommon 
frequency  that  it  must  have  forced  itself  upon  the  notice  of  the  older  physi- 
cians. In  the  great  majority  of  all  cases  of  phthisis  we  can  make  out,  by 
close  questioning,  that  in  the  family,  either  among  the  older  members  or 
among  the  brothers  and  sisters,  one  or  more  cases  of  tuberculous  disease  have 
already  occurred.  The  closer  we  investigate,  and  the  more  we  search  for 
some  one  of  the  different  forms  in  which  tuberculosis  can  show  itself,  like 
pleurisy,  or  affections  of  the  bones  and  joints,  the  more  frequently  we  can 
make  out  this  hereditary  predisposition.  Some  persons  are  indeed  of  the 
opinion  that  the  hereditary  transmission  of  the  disease  is  often  merely  appar- 
ent, and  not  real,  from  the  fact  that  the  close  relations  between  the  children 
and  their  diseased  parents,  or  brothers  and  sisters,  greatly  increases  the 
danger  of  infection  of  the  ordinary  kind.  Certainly  this  consideration  should 
not  be  forgotten  with  regard  to  the  occasional  appearance  of  tuberculosis  in 
families,  but  yet  it  would  be  impossible  to  explain  in  this  way  alone  the 
extremely  frequent  development  of  tuberculosis  in  special  families. 

There  can  be,  therefore,  scarcely  any  doubt  as  to  the  inheritance  of  tuber- 
culosis, but  the  explanation  of  this  fact  is  far  from  clear.  The  hereditary 
character  of  tuberculosis  may  very  well  harmonize  with  its  infectious  character. 
We  might  assume  in  this  case  a  perfect  analogy  with  syphilis — namely,  a 
transition  of  the  infectious  material  itself  from  the  parent  to  the  child  before 
birth.  There  is  only  one  striking  difference  between  syphilis  and  tuberculosis 
— that  the  children  of  syphilitic  parents  very  often  come  into  the  world  with 
definite  signs  of  infection,  while  congenital  tuberculosis  in  this  sense  is  an 
extremely  rare  occurrence.  We  must  accordingly  compare  tuberculosis  to 
that  form  of  hereditary  syphilis  (lues  hereditaria  tarda)  in  which  the  first 
symptoms  of  the  affection  come  on  at  a  late  period.  Since  certain  considera- 
tions, however,  oppose  such  a  theory,  we  are  of  late  far  more  disposed  to 
assume  that,  as  a  rule,  tuberculosis  in  itself  is  not  inherited,  but  only  the  pre- 
disposition to  tuberculous  disease.  This  opinion  agrees  with  the  facts  that 
members  of  a  family  in  which  tuberculosis  prevails  very  often  show  the 
so-called  tuberculous  babit  even  without  any  real  tuberculous  disease ;  and  that 
they  often  have  "  weak  lungs  " — that  is,  that  they  easily  get  out  of  breath, 
and  manifest  a  distinct  tendency  to  catarrh  of  the  respiratory  organs.  An- 
other fact,  which  to  a  certain  extent  may  be  regarded  as  an  argument  against 
the  assumption  of  a  direct  hereditary  transmission  of  the  disease,  is  that,  in 


TIIHERCULOSIS   OF  THE   LUNGS  281 

cases  of  apparently  hereditary  tuberculosis,  as  a  rule  those  organs  first  show 
evidence  of  disease  which  are  most  exposed  to  an  infection  from  the  outer 
world — namely,  the  lungs  and  larynx.  This  is  also  an  argument  againsl  the 
acceptance  of  an  exclusively  hereditary  predisposition  to  tuberculosis. 

The  age  of  the  patient  has  an  important  influence  upon  the  predisposition 
to  tuberculous  disease.  Pulmonary  tuberculosis  occurs  with  special  frequi 
in  youth,  between  fifteen  and  thirty.  It  is  not  rare  in  children.  After  forty 
it  is  much  rarer  in  its  pronounced  and  rapid  forms,  but  it  is  seen  even  in  the 
most  advanced  age.  Slight  tuberculous  changes  are  very  frequently  found  at 
autopsy  in  the  lungs  of  old  persons.  These  changes  have,  as  a  rule,  no  clin- 
ical significance.  They  are  in  all  probability  due  to  the  inhalation  of  tuber- 
culous germs  with  scarcely  any  tendency  to  further  extension  because  of  the 
lack  of  individual  predisposition  to  the  disease.  It  has  not  yet  been  shown 
that  sex  has  a  special  influence  upon  liability  to  the  disease. 

PATHOLOGICAL  ANATOMY  OF  TUBERCULOSIS,  ESPECIALLY 
OF  PULMONARY  TUBERCULOSIS 

If  now  we  inquire  wherein  consists  the  injury  which  the  tubercle  bacilli 
inflict  upon  the  body,  the  first  point  to  emphasize  is  that  the  action  of  the 
tubercle  bacilli  is  at  first  invariably  purely  local.  Tuberculosis  does  not 
belong  to  the  "general  infectious  diseases,"  in  which  the  infection  of  the 
whole  organism,  the  general  infection  of  the  body,  predominates  over  the 
local  disturbances.  The  essence  of  tuberculosis,  at  least  in  the  great  majority 
of  cases,  is  the  local  disease.  The  tubercle  bacilli  give  rise  to  definite  ana- 
tomical changes  in  the  organs  where  they  settle,  and  the  consequent  disturb- 
ance of  function  in  the  organ  has  an  effect  on  the  rest  of  the  body. 

The  danger  of  tuberculous  diseases,  however,  consists  in  the  fact  that  the 
local  affection  often  attacks  the  most  important  organs,  as  the  lungs  and  the 
brain,  and  sets  up  such  extensive  anatomical  changes  in  them  that  because 
of  these  changes  alone  it  becomes  impossible  for  life  to  continue  longer.  Be- 
sides this,  the  infection  in  many  cases  does  not  always  confine  itself  to  one 
organ,  but  the  infectious  material  extends  over  the  body  by  ways  and  means 
which  we  shall  learn  in  part  later  on,  and  attacks  one  organ  after  another, 
or  even  many  at  once.  Finally,  it  is  to  be  said  that  the  peculiar  character  of 
the  changes  caused  by  tuberculosis  explains  why  these  are  often  the  cause 
of  manifold  secondary  processes,  particularly  secondary  infections.  Thus 
arise  fever,  suppuration,  secondary  inflammation,  and  other  important  phe- 
nomena, which  will  be  minutely  considered  later. 

The  entire  local  action  of  the  tubercle  bacilli — that  is,  the  pathological 
anatomy  of  tuberculosis — is  almost  wholly  independent  of  the  organ  attacked. 
Tuberculosis  belongs  to  the  group  of  so-called  "  infectious  tumors  " — that  is, 
the  local  action  of  the  tubercle  bacilli  consists  chiefly  in  the  production  of  a 
proliferation  and  accumulation  of  cells  at  their  place  of  settlement,  which, 
as  a  whole,  is  termed  a  tubercular  new  growth.  Without  going  into  histolog- 
ical details  we  may  say,  briefly,  that  the  whole  process  consists  in  a  primary 
injury  of  the  tissue,  due  to  the  invasion  of  the  tubercle  bacilli,  followed  by  a 
hyperplasia  of  the  cells  peculiar  to  the  tissue  itself,  and  involving  not  only 
the  connective-tissue  cells  and  the  endothelial  cells  of  the  lymph  and  blood 


282  DISEASES  OF  THE   RESPIRATORY   ORGANS 

vessels,  but  also,  possibly,  the  epithelial  cells.  The  so-called  epithelioid  cells, 
which  are  large  cells,  rich  in  protoplasm,  and  the  multinucleated  giant  cells, 
most  often  found  in  the  center  of  tuberculous  nodules,  are  derived  from  the 
hyperplasia  of  the  connective-tissue  cells.  The  giant  and  epithelioid  cells  are 
surrounded  by  numerous  round  cells.  These,  at  first,  are  ordinary  leucocytes, 
for  the  most  part  of  the  mononuclear  lymphocyte  type,  and  then  usually 
later  on  migrating  polymorphonuclear  leucocytes  appear.  The  round  cells 
referred  to  may,  in  some  cases,  finally  include  nearly  the  entire  tubercle.  A 
network,  or  reticulum,  is  found  between  the  individual  new-formed  cells  and 
the  wandering  cells.  This  probably  represents  the  remains  of  the  original 
interstitial  tissue,  crowded  apart  by  the  increased  number  of  cells.  There 
is  no  new  formation  of  vessels.  The  tubercle  contains  no  blood  vessels.  The 
tubercle  bacilli  lie  especially  inside  the  giant  cells,  but  also  in  their  vicinity. 

If  these  changes  have  progressed  far  enough,  they  become  visible  to  the 
naked  eye  as  a  small,  circumscribed  grayish  point,  the  so-called  miliary  tuber- 
cle. From  these  minute  nodules  the  disease  itself  obtained  its  name  of 
tuberculosis.  By  approximation  and  coalescence  of  neighboring  tubercles — 
for  these  keep  developing  because  of  the  spread  of  the  local  infection — the 
tubercular  formation  continually  extends  itself,  and  thus  are  gradually  formed 
the  large  tubercular  nodules,  and  finally  the  diffuse  tubercular  new  growth 
or  the  diffuse  tubercular  infiltration. 

The  tubercular  new  growth,  as  such,  differs  but  little  histologically  from 
other  infectious  tumors,  such  as  those  seen  in  syphilis  and  leprosy.  Tuber- 
culosis, however,  has  a  characteristic  difference  in  its  final  stages  of  cheesy 
degeneration  and  eventual  disintegration  of  the  new-formed  tissue,  processes 
which  are  connected  in  part  with  the  absence  of  blood  vessels  and  the  conse- 
quent deficiency  of  nutrition  of  the  new  formation,  in  part  with  the  toxins 
that  are  elaborated  by  the  tubercle  bacilli.  Both  the  tubercular  infiltration 
and  also  the  portions  of  the  original  tissues  inclosed  by  it  perish,  lose  their 
nuclei,  and  finally  become  disintegrated.  The  manner  in  which  they  are 
destro}red — namely,  "  fatty  degeneration  " — belongs  in  the  group  of  the  so- 
called  coagulation  necroses  (Weigert).  This  process  is  recognizable  to  the 
naked  eye,  because  the  tubercular  infiltration  when  it  becomes  thus  degen- 
erated takes  on  a  pronounced  yellowish  color.  Wherever  the  necrotic  portions 
of  tissue  are  superficially  situated  they  are  cast  off,  giving  rise  to  tubercular 
ulcers. 

Alongside  the  tubercular  new  formation  there  are  found  in  the  organs 
affected  with  tuberculosis  various  inflammatory  processes,  either  simple  or 
suppurative  or  hemorrhagic.  We  may  therefore  surmise  that  the  tubercle 
bacilli  (or  the  chemical  toxins  formed  by  them),  besides  their  characteristic 
effects,  act  simultaneously  in  another  role  as  excitants  of  inflammation;  but 
it  is  very  probable,  and  especially  so  in  pulmonary  tuberculosis,  that  many  of 
the  inflammatory  changes  which  arise  are  not  peculiar  to  the  tuberculosis  as 
such,  but  are  to  be  regarded  as  secondary  processes  {vide  infra)  for  the  devel- 
opment of  which  the  preceding  tubercular  new  growth,  as  it  disintegrates, 
furnishes  a  suitable  soil. 

As  regards  the  special  anatomical  processes  and  appearances  in  pulmonary 
tuberculosis,  the  tuberculous  change  usually  begins  in  the  walls  of  the  smallest 
bronchi,  or  not  rarely  in  the  alveoli  themselves.    At  any  rate,  the  disease  does 


TUBERCULOSIS  OF  THE   LUNGS  283 

not  begin  in  many  different  parts  of  the  lung  al  once,  but  probably  in  one  <>r 
two  circumscribed  spots  only,  and  in  a  greal  majority  of  cases  in  one  apex. 
The  tubercular  infiltration  begins  in  the  walls  of  the  bronchi,  and  thence 
gradually  extends  toward  tbe  periphery.  The  original  tuberculous  bronchitis 
becomes  a  tuberculous  peribronchitis.  Tbe  infectious  material  extends  from 
its  original  focus  by  means  of  the  lymph  and  blood  channels  out  into  the  sur- 
rounding tissue;  and  also  as  soon  as  superficial  ulceration  takes  place,  the  in- 
fectious matter  is  liable  to  be  carried  by  tbe  inspired  air  into  other  bronchi. 
Thus  tbe  diseased  spot,  small  at  first,  keeps  gradually  extending.  Tubercu- 
lous peribronchitis  is  usually  easily  recognized  with  the  naked  eye.  We  not  ire 
the  little  lumen  of  the  bronchus  in  the  middle  of  the  "  cheesy  "  nodule,  which 
at  first  is  gray  and  later  yellowish.  Many  of  tbe  adjacent  nodules  run 
together  in  part,  and  even  entirely.  The  lumen  of  the  bronchus  is  either 
wholly  plugged  by  the  infiltration,  or  the  destruction  of  tbe  necrotic  cells 
begins  in  the  midst  of  the  peribronchitis.  In  the  latter  case  the  lumen  is 
enlarged  to  a  little  irregular  hole — the  first  beginning  of  the  formation  of  a 
cavity. 

The  alveolar  tissue  of  the  lung  cannot  long  remain  unaffected,  with  such 
a  disease  of  the  smaller  bronchi.  Lobular  atelectasis,  the  necessary  result  of 
every  permanent  bronchial  obstruction,  must  arise,  but  this  soon  passes  (by 
penetration  or  aspiration  of  the  germs)  into  a  lobular  pneumonia,  which  from 
its  specific  nature  later  becomes  caseous.  We  cannot  go  into  the  histological 
details  here.  The  alveoli  are  filled  with  pus  corpuscles  and  large  epithelioid 
cells,  which  are  considered  by  many  authors  to  be  the  offspring  of  the  alveolar 
epithelium.  The  alveolar  walls  are  also  infiltrated.  This  finally  results  in 
the  destruction  of  the  cheesy  and  necrotic  tissue,  and  consequently  in  the 
formation  of  cavities.  At  other  times  the  neighboring  nodules  run  together, 
and  the  tubercular  infiltration  thus  extends,  giving  rise  to  a  diffuse  caseous 
pneumonia.  These  processes  may  all  be  readily  recognized  by  the  naked  eye. 
The  earlier  stages  of  atelectasis  and  infiltration  correspond  to  the  jelly-like, 
gray  coloring  seen  in  the  so-called  gelatinous  infiltration  of  Laennec,  and  the 
transition  to  caseation  is  recognized  by  the  eye  from  the  yellowish  color. 

Although  all  the  processes  thus  far  described  are  destructive  in  their 
nature,  changes  are  also  found  in  the  lungs  in  tuberculosis  which  seem  to  have 
a  tendency  toward  circumscribing  the  disease  and  toward  healing.  Promi- 
nent among  these  are  the  chronic  interstitial  processes.  We  meet  with  the 
formation  of  new  connective  tissue,  partly  about  the  tubercular  infiltration, 
but  especially  where  there  is  already  destruction  of  tissue,  and  this  may  lead 
to  contraction  and  the  formation  of  a  firm  cicatrix.  The  encapsulated  cheesy 
masses  may  then  be  in  part  reabsorbed;  in  part  they  undergo  calcification. 
The  possibility  of  such  a  halt  in  the  tubercular  process  depends,  however, 
upon  certain  conditions.  The  tubercular  new  growth  and  its  destruction 
must  not  advance  too  rapidly,  and  the  new-formed  tissue  must  not  itself  be 
destroyed  before  it  becomes  cicatrized.  We  see  the  cicatricial  formation, 
therefore,  more  especially  in  chronic  cases;  we  find  it  in  places  which  have  been 
affected  the  longest,  and  where  the  tubercular  process,  perhaps,  has  finally 
cot ne  to  a  standstill  of  its  own  accord.  Macroscopically,  this  cicatricial  con- 
nective tissue  is  composed  of  a  thick,  firm  substance,  usually  pigmented — the 
so-called  pigment  induration.     If  the  cicatricial  formation  follows  a  previous 


284  DISEASES  OF  THE   RESPIRATORY   ORGANS 

extensive  destruction  of  the  pulmonary  tissue,  the  affected  portion  of  the 
lung  may  thus  be  diminished  to  less  than  half  its  original  bulk.  Cavities 
and  firm  cicatricial  tissue  form  the  anatomical  basis  of  such  an  extensive 
"pulmonary  contraction."  Either  the  cavities  are  formed  in  the  usual  way 
from  the  destruction  of  lung  tissue,  or  they  may  be  simple  bronchial  dilata- 
tions due  to  the  traction  of  the  contracted  tissue — bronchiectatic  cavities. 

The  contractile  changes  in  pulmonary  tuberculosis  teach  us  that  the  tuber- 
cular process  is  in  itself  capable  of  healing.  The  incurability  of  most  cases 
of  phthisis  is  due  to  the  fact  that  the  infectious  material  from  every  exist- 
ing tubercular  noclule  is  carried  into  other  bronchi,  and  there  sets  up  a  new 
tuberculosis.  Thus  the  disease  is  constantly  extended.  The  original  tuber- 
culosis, which  was  localized  in  one  apex  only,  gradually  spreads  to  the  lower 
portion  of  the  lung.  The  infectious  material  is  carried  by  coughing  into  the 
trachea,  and  from  this  point  may  be  carried  by  inspiration  into  the  other  lung. 
This  becomes  diseased,  and  finally  there  is  such  an  extensive  destruction  of  the 
lungs  as  to  make  the  further  continuance  of  life  impossible. 

Besides  the  specific  tuberculous  lesions  in  phthisical  lungs,  there  are  very 
often  found  simple  inflammatory  processes,  such  as  bronchitis  and  lobular 
catarrhal  pneumonia ;  sometimes,  also,  although  seldom  of  great  extent,  croup- 
ous pneumonia ;  and  finally,  in  exceptional  instances,  limited  foci  of  gangrene. 
These  secondary  diseases  not  specifically  tuberculous,  and  yet  almost  always 
associated  with  tuberculosis,  are  of  the  greatest  clinical  importance.  They 
probably  are  due  in  most  instances  to  the  influence  of  secondary  pathogenic 
germs  (particularly  streptococci,  less  often  diplococci,  etc.),  for  which  the 
tuberculosis  has  merely  prepared  a  favorable  soil.  Many  clinical  phenomena 
(particularly  most  of  the  febrile  exacerbations  of  the  disease)  depend  upon 
these  secondary  inflammatory  processes  which,  in  their  turn,  promote  the  fur- 
ther extension  of  the  tuberculosis.  Thus,  frequently,  inflammatory  lesions 
which  are  due  to  secondary  infection  finally  are  transformed  by  the  invasion 
of  tubercle  bacilli  into  foci  of  tuberculosis. 

If  we  consider  the  list  of  anatomical  processes  which  are  found  in  tuber- 
culosis of  the  lungs,  and  which  may  be  combined  in  the  most  manifold  ways, 
we  can  understand  the  great  diversity  in  the  anatomical  picture  in  different 
cases.  Primary  tuberculosis  of  the  bronchial  wall  and  tuberculous  peribron- 
chitis, diffuse  cheesy  pneumonia,  and  destruction  of  the  tubercular  new 
growths,  with  the  formation  of  cavities,  on  the  one  hand;  contracting  inter- 
stitial pneumonia,  cicatricial  formation,  and  pigment  induration  on  the  other 
- — these  are  the  comparatively  simple  anatomical  lesions  from  which  the  whole 
process  of  pulmonary  tuberculosis  in  its  most  varied  forms  is  composed.  Be- 
sides this,  we  often  find  here  and  there  one  or  more  miliary  tubercles  scattered 
through  the  lungs,  which  are  probably  due  very  largely  to  an  extension  of  the 
infectious  material  by  means  of  the  blood  or  lymph  current;  and  finally  the 
already  mentioned  processes  of  secondary  inflammation,  such  as  bronchitis 
and  pneumonia. 

The  secondary  tuberculous  diseases  of  the  pleura,  the  bronchial  glands, 
and  other  organs,  will  receive  a  special  description. 


TUBERCULOSIS  OF  THE  LUNGS  285 

CLINICAL   HISTORY   OF   TUBERCULOSIS  IN   GENERAL  AND    OF 
PULMONARY   TUBERCULOSIS   IN   PARTICULAR 

In  judging  of  the  various  appearances  in  the  clinical  picture  of  tubercu- 
losis we  must  especially  consider  the  following  points:  The  place  of  the  firsl 
infection  is  of  chief  importance — that  is,  the  place  where  a  local  affection, 
set  up  by  the  tuberculous  poison,  first  arises.  One  can  readily  understand 
why  all  those  organs  which  are  directly  exposed  to  infection  from  without 
are  most  frequently  affected  with  primary  tuberculosis.  Very  often,  as  we 
have  said,  the  lungs  are  the  organs  first  attacked.  Less  often  the  upper 
respiratory  passages — viz.,  the  larynx  and  nose.  In  other  cases  the  tubercle 
bacilli  fasten  first  upon  the  digestive  tract  (the  intestines,  less  often  the  phar- 
ynx and  the  tongue).  In  many  other  cases,  however,  it  cannot  be  that  the 
tubercle  bacilli  directly  reach  the  organ  which  seems  to  be  first  affected. 
This  is  true  of  the  so-called  tuberculosis  of  serous  membranes,  of  the  tuber- 
culosis of  lymph-glands,  of  bones  and'  joints,  of  the  brain  and  of  the  genito- 
urinary tract.  Investigators  have  yet  to  determine  the  paths  by  which  the 
tubercle  bacilli  reach  the  respective  organs  in  these  cases.  The  glance  which 
we  have  just  taken  at  the  organs  most  frequently  attacked  by  tuberculosis 
shows  the  great  clinical  variety  of  tuberculous  diseases  viewed  from  this 
aspect. 

Another  reason  for  the  great  variation  in  the  course  of  tuberculosis  is 
found  in  the  fact  that  the  extension  of  the  local  tubercular  process  varies 
very  greatly  as  regards  time.  Tuberculosis  in  one  case  may  produce  the  most 
extensive  destruction  in  both  lungs  in  a  few  months  or  even  weeks,  and  in 
another  case  it  may  remain  almost  quiescent  for  years,  or  advance  only  very 
slowly.  We  do  not  know  fully  on  what  these  differences  depend,  but  much  is 
certainly  due  to  the  hygienic  influences  under  which  the  patient  lives.  In  the 
last  analysis,  however,  we  are  often  led  to  think  of  individual  differences  of 
constitution,  which  now  check  and  now  favor  the  rapid  extension  of  the 
disease. 

This  predisposition  is,  in  most  cases,  congenital,  but  sometimes  acquired. 
This  is  particularly  true  of  alcoholic  subjects,  who  often  evince  a  feeble  power 
of  resistance  to  tuberculosis,  although  originally  of  vigorous  constitution,  so 
that  the  rapidly  spreading  or  "  galloping  "  forms  of  tuberculosis  are  particu- 
larly common  in  drunkards. 

A  third  and  final  reason  for  the  differences  in  the  course  of  tuberculous 
infection  is  the  manner  of  the  further  extension  of  the  tuberculous  poison  in 
the  body.  As  we  shall  see  in  the  description  of  tuberculosis  in  single  organs, 
there  are  different  ways  in  which  tuberculosis  may  pass  from  one  organ  to 
another.  Many  contingencies  are  involved  here,  and  we  can  easily  compre- 
hend how  greatly  the  whole  clinical  course  of  the  disease  must  be  modified 
by  the  rapidity  and  the  degree  in  which  individual  organs  are  affected. 

After  these  preliminary  remarks  we  will  pass  on  to  the  description  of  the 
clinical  course  of  pulmonary  tuberculosis. 

The  onset  of  pulmonary  tuberculosis  is  quite  slow  and  gradual  in  the 
majority  of  cases.  The  patient  can  give  only  an  approximate  idea  of  the 
time  when  he  began  to  be  ill.  The  symptoms  are  referred  directly  to  the  re- 
spiratory organs.     The  cough  and  its  attendant  expectoration  are  the  chief 


286  DISEASES   OF  THE  RESPIRATORY   ORGANS 

things  which  affect  him.  Moreover,  there  is  often  pain  in  the  chest,  either  the 
pleuritic  stasis,  or  pain  in  the  sternal  region,  or  pain  between  the  shoulder 
blades.  Some  physicians  are  inclined  to  refer  these  backaches  of  incipient 
tuberculosis  to  tuberculous  disease  of  the  bronchial  lymph-nodes  (vide  supra). 
The  patient  is  also  apt  to  complain  of  shortness  of  breath,  especially  on 
exertion. 

Besides  these  symptoms,  which  point  pretty  directly  to  disease  of  the 
respiratory  organs,  there  are  often  quite  striking  general  symptoms.  The 
patient's  emaciation  is  especially  noticeable.  This  may  be  partly,  though  not 
wholly,  explained  by  his  loss  of  appetite.  Besides  the  emaciation  there  is 
a  steadily  increasing  pallor  of  the  skin.  The  patient  also  shows  a  general 
dullness,  weakness,  and  disinclination  to  work.  There  is  not  infrequently 
a  slight  rise  of  temperature  in  the  first  stages  of  the  disease,  which  causes 
subjective  feelings  of  chilliness  and  fever.  Severe  night-sweats  may  also  be 
noticed  early.  The  pulse  rate  is  almost  invariably  accelerated,  even  in  the 
absence  of  fever. 

Any  such  constitutional  disturbance  should  lead  the  physician  not  to  regard 
the  mild  thoracic  symptoms,  which  are  also  present,  as  insignificant,  but  to 
think  of  the  possibility  of  incipient  tuberculosis.  It  is  very  important  to  re- 
member that  the  pulmonary  symptoms  may  be  entirely  subordinate  to  the 
general  symptoms  mentioned,  and  that  the  patient  himself  is  apt  to  pay  little 
or  no  attention  to  them.  Incipient  phthisis  is  therefore  frequently  diag- 
nosticated as  simple  "  chlorosis  "  or  "  gastric  catarrh  "  for  a  long  time,  and 
is  treated  as  such.  An  early  and  careful  physical  examination  of  the  lungs 
and  of  the  expectoration  is  the  only  protection  against  such  an  error. 

Both  the  pulmonary  and  the  general  symptoms  assume  significance,  if  we 
have  to  do  with  a  patient  in  whom  we  suspect  a  "  tuberculous  predisposition."- 
We  very  often  meet  persons  in  whose  family,  either  in  the  parents  or  the 
brothers  and  sisters,  several  cases  of  phthisis  have  occurred.  They  are  persons 
who  are  always  pale  and  weak,  and  who  have  previously  shown  a  special  lia- 
bility to  catarrh  and  other  diseases  of  the  respiratory  organs — e.  g.,  pneu- 
monia. They  have  perhaps  had  diseases  which  our  present  theories  bring 
into  direct  relation  with  tuberculous  infection.  We  refer  to  those  quite  fre- 
quent cases  of  pulmonary  tuberculosis  in  individuals  who  have  previously  suf- 
fered from  "  scrofulous  diseases,"  such  as  chronic  swelling  of  the  lymph- 
glands,  chronic  affections  of  the  eye  or  ear,  or  fungous  diseases  of  the  bones 
and  joints,  pleurisy,  etc. 

Although  the  first  symptoms  of  pulmonary  tuberculosis  often  develop  in 
those  who  were  not  quite  well  before,  this  is  true  in  only  a  part  of  the  cases. 
We  often  see  precisely  the  same  symptoms,  both  the  pulmonary  and  the  gen- 
eral, occurring  in  persons  who  previously  seemed  quite  well  and  strong.  No 
constitution  is  perfectly  protected  against  the  disease.  We  have  even  seen  the 
herculean  athlete  of  a  circus  die  of  phthisis. 

In  distinction  from  the  slow  and  gradual  method  of  the  development  of 
tuberculosis  which  has  just  been  described,  the  first  symptoms  in  other  cases 
may  be  more  sudden.  A  definite  exposure  is  often  given  as  a  cause,  after 
which  the  first  symptoms  of  the  disease  have  speedily  developed.  It  goes 
without  saying  that  we  must  consider  these  harmful  influences — a  chilling  of 
the  body,  a  cold  draught,  overexertion,  or  marked  mental  excitement — at 


TUBERCULOSIS  OF  THE  LUNGS  287 

most,  as  exciting  causes.  When  pulmonary  tuberculosis  begins  somewhat 
abruptly,  either  the  initial  symptoms  are  from  the  start  directly  referable 
to  the  respiratory  organs  (cough,  thoracic  pain,  dyspnoea),  or  the  chesl 
symptoms  may  be  obscured  by  Hie  severity  of  the  constitutional  disturbance. 
Tims  we  recall  a  number  of  cases  in  which  young  persons  fell  sick  rather  sud- 
denly with  somewhat  severe,  febrile  constitutional  disturbance.  At  lii-t  do 
cause  of  the  fever  could  be  found,  so  that  the  diagnosis  was  doubt  fid,  or  was 
supposed  to  be  typhoid  or  some  other  disease.  Then  after  a  time  thoracic 
symptoms  developed  and  pulmonary  tuberculosis  could  be  recognized.  In 
most  cases  the  illness  would  take  a  rather  rapid  course  That  form  of  pulmo- 
nary tuberculosis  which  is  termed  "pneumonic"  (vide  infra)  also  exhibits 
a  decidedly  acute  onset. 

Those  cases  of  pulmonary  tuberculosis  which  begin  with  hemoptysis  are 
of  special  practical  importance.  Of  course,  it  must  be  understood  that  the 
tubercular  process  in  the  lung  has  existed  for  some  time  before  the  blood 
appears.  But  in  the  midst  of  apparent  health,  or  after  some  slight  constitu- 
tional disturbance,  comes  a  cough  with  bloody  expectoration.  Very  often  the 
further  symptoms  of  pulmonary  tuberculosis  follow  directly  upon  this  initial 
hemoptysis  (vide  infra) .  ■ 

In  conclusion,  those  cases  are  to  be  mentioned  in  which  the  first  signs  of 
tuberculosis  appear  not  in  the  lungs  but  in  the  larynx.  The  full  description 
of  these  cases  has  already  been  given  in  the  chapter  on  laryngeal  tuberculosis. 

The  further  course  of  pulmonary  tuberculosis  may  vary  so  much  that  it 
is  impossible  to  give  a  complete  enumeration  of  all  the  possibilities. 

In  some  cases  it  advances  rapidly.  We  can  make  out  the  extension  of  the 
disease  objectively,  almost  from  week  to  week.  At  first  the  apex  of  one  lung 
alone  is  attacked,  soon  after  the  lower  lobe  of  the  same  lung,  then  the  other 
lung,  either  at  the  apex  first  or  in  the  lower  part.  Besides  the  pulmonary 
symptoms,  there  is  quite  a  high  fever,  rapidly  increasing  emaciation,  and  gen- 
eral loss  of  strength.  Death  ensues  in  a  few  months.  We  term  such  cases 
florid  phthisis,  or  "  galloping  consumption.'" 

In  other  cases,  however,  the  disease  has  a  remarkably  chronic  course.  Its 
onset  is  very  gradual,  or  else,  after  rather  an  acute  onset,  there  is  a  compara- 
tive cessation  of  all  symptoms.  The  thoracic  symptoms  do  not  disappear,  but 
they  are  only  trifling,  and  do  not  disturb  the  patient.  Physical  examination 
of  the  lungs  does  not  show  any  extension  of  the  process  for  months.  The 
fever  which  accompanies  it  is  slight,  if  there  be  any.  The  patient  remains 
quite  well  nourished,  but  in  some  cases  there  is  a  good  deal  of  weakness. 
He  feels  better  and  worse  by  turns,  his  condition  being  greatly  influenced  by 
the  care  and  nursing  he  receives. 

Unilateral  contracting  phthisis  especially  has  this  comparatively  favor- 
able course  (vide  supra).  The  affection  remains  confined  to  one  lung  for  a 
long  time.  The  occurrence  of  contraction  shows  the  slight  tendency  of  the 
tubercular  process  to  advance,  and  with  satisfactory  care  the  patient  may  re- 
main quite  well  for  years. 

In  cases,  too,  which  have  had  severe  symptoms  for  a  long  time,  a  temporary 
standstill  of  the  affection  may  take  place,  or  an  actual  improvement  in  all  the 
symptoms.  At  other  times,  in  cases  which  have  made  no  advance  for  a  long 
time,  the  symptoms  suddenly  grow  worse. 


288  DISEASES   OF   THE   RESPIRATORY   ORGANS 

There  are  all  possible  varieties  between  the  extremes  of  florid  phthisis  and 
the  very  chronic  cases  which  last  for  years  and  decades.  If  we  recall  the  fur- 
ther modifications  which  the  course  of  the  disease  may  assume  if  complications 
arise,  we  can  appreciate  the  manifold  character  of  the  clinical  picture  of 
phthisis. 

Most  eases  with  definite  signs  of  somewhat  extensive  disease  terminate 
fatally.  Death  ensues,  either  with  the  signs  of  general  exhaustion,  or  as  a 
result  of  the  final  failure  of  respiration ;  or  it  is  due  to  the  occurrence  of 
complications,  such  as  tuberculous  meningitis,  miliary  tuberculosis,  pulmo- 
nary hemorrhage,  or  pneumothorax.  Yet,  on  the  other  hand,  if  the  tubercu- 
losis is  not  extensive,  the  disease  may  terminate  in  complete  recovery.  To 
say  how  frequent  recovery  is,  is  difficult,  for  it  is  probable  that  many  insignifi- 
cant cases  escape  diagnosis.  Furthermore,  a  distinction  should  be  drawn 
between  recovery  from  a  standpoint  of  pathological  anatomy,  meaning  com- 
plete cicatrization,  with  disappearance  of  all  tubercular  new  growth,  and  recov- 
ery from  a  clinical  standpoint  [arrest],  meaning  disappearance  of  all  symp- 
toms.    Often  apparent  recovery  proves  deceptive. 

SPECIAL   SYMPTOMS  AND   COMPLICATIONS 

1.  Lung  Symptoms. — Pain  in  the  Chest. — Extensive  destruction  of  the 
lungs  may  occur  without  any  feeling  of  pain.  Many  cases  of  phthisis  are 
painless  throughout  their  course.  In  other  cases,  however,  the  patient's  chief 
complaint  is  of  severe  pains  in  the  side  or  in  the  front  of  the  chest.  These 
are  probably  always  due  to  coexisting  affections  of  the  pleura,  such  as  pleu- 
risy, or  pleuritic  adhesions.  In  patients  who  suffer  from  severe  cough,  pains 
sometimes  arise  in  the  abdominal  muscles  and  at  the  insertion  of  the  dia- 
phragm, due  to  the  excessive  muscular  contraction.  It  has  been  above  pointed 
out  that  the  diseased  lymph-nodes  at  the  roots  of  the  lungs  may,  in  some 
cases,  be  the  cause  for  the  spontaneous  backache,  or  for  the  tenderness  on 
pressure. 

Cough. — In  the  majority  of  instances  cough  is  one  of  the  most  distressing 
symptoms  of  phthisis,  but  its  severity  varies  very  much  in  different  individuals, 
and  at  different  times  in  the  same  patient.  We  sometimes  see  cases,  particu- 
larly in  senile,  insensitive  individuals,  in  which,  in  spite  of  advancing  phthi- 
sis, cough  is  remarkably  slight,  or  entirely  absent.  In  cases  with  severe  cough, 
it  is  often  worse  at  night,  but  paroxysms  of  coughing  of  long  duration  are 
also  apt  to  come  on  in  the  morning  or  evening  hours,  which  are  painful  and 
very  distressing,  and  exhausting  for  the  patient.  The  cough  is  usually  asso- 
ciated with  a  more  or  less  abundant  expectoration,  but  sometimes  there  is 
chiefly  a  dry  cough.  The  cough  becomes  very  severe  if  the  tuberculous  affec- 
tion attacks  the  larynx  and  trachea  (see  laryngeal  tuberculosis). 

Expectoration. — The  amount  of  expectoration  differs  very  much  in  differ- 
ent cases.  It  is  most  abundant  when  there  is  extensive  formation  of  cavities 
in  the  lungs.  In  such  cases  it  is  often  evacuated  in  the  morning  by  persist- 
ent coughing.  The  consistence  of  the  great  part  of  the  sputum  is  muco- 
purulent, and  it  differs  little  from  that  of  simple  bronchitis;  in  fact,  a  large 
part  of  the  phthisical  expectoration  comes  from  the  catarrhal  inflammation 
of  the  bronchial  mucous  membrane.     Usually,  however,  the  amount  of  mucus 


TUBERCULOSIS  OF  THE   LUNGS  289 

as  compared  with  the  amount  of  pus  is  less  in  phthisical  sputum  than  in 
that  of  simple  bronchitis.  The  sputum  is  therefore  less  viscid  and  more 
fluid.  The  amount  of  mucus  in  the  expectoration  is  also  apl  to  be  greater 
in  chronic'  bronchitis  than  in  tuberculosis,  although  mucus  i-  seen  in  the 
latter.  The  expectoration  which  comes  from  cavities  is  almost  pure  pus, 
with  only  a  slight  amount  of  serum  and  mucus  intermixed.  Such  sputum 
consists  often  of  large  separate  masses  described  as  nummular,  or  coin-shaped. 
If  received  in  water,  the  uneven,  rough  surface  of  these  masses  is  often  evi- 
dent, and  suggests  their  formation  in  the  irregular  pulmonary  cavities. 

The  admixture  of  blood  with  the  sputum  is  of  great  diagnostic  and  prac- 
tical importance.  Since  no  other  disease  so  often  gives  rise  to  the  presence  of 
blood  in  the  expectoration,  coughing  of  blood  (hemoptysis)  is  almost  synony- 
mous with  consumption  among  the  laity.  Little  streaks  of  blood  in  the  expec- 
toration are  quite  frequent.  They  have  no  great  significance,  but,  of  course, 
they  may  sometimes  be  the  precursors  of  severe  hemorrhages.  Profuse  hemop- 
tysis takes  place  when  the  wall  of  a  little  pulmonary  vessel — almost  always 
a  branch  of  the  pulmonary  artery — is  infiltrated,  destroyed,  and  finally 
eroded,  by  the  tubercular  new  growth.  The  reason  why  hemoptysis  is  not 
more  frequent  is  because  the  contents  of  the  vessels  usually  undergo  throm- 
bosis. Severe  hemorrhages  very  often  have  their  origin  in  little  aneurisms 
of  the  branches  of  the  pulmonary  artery,  which  penetrate  into  the  interior 
of  the  cavities.  In  the  cases  of  fatal  hemoptysis  we  frequently  succeed  in 
finding  the  little  aneurism  and  its  point  of  rupture. 

Pulmonary  hemorrhage  occurs  in  all  stages  of  phthisis.  The  initial  hemop- 
tysis has  already  been  mentioned.  This  may  be  followed  by  other  symptoms 
of  pulmonary  tuberculosis,  or  the  hemoptysis  may  cease  without  any  imme- 
diate sequels.  Pulmonary  hemorrhage  may  also  occur  at  any  time  in  the 
further  progress  of  the  disease.  The  amount  of  blood  raised  is  variable. 
There  may  be  one  or  more  tablespoonfuls,  or  one  or  more  pints.  The  blood 
is  bright  red,  usually  quite  frothy,  but  little  clotted,  and  in  part  mixed  with 
other  constituents  of  the  sputum.  After  the  first  well-marked  hemoptysis,  the 
expectoration  usually  is  mixed  with  blood  for  several  days.  Again,  there  may 
be  repeated  hemorrhages  in  a  short  time.  Sometimes  the  hemoptysis  begins 
abruptly,  not  infrequently  at  night,  without  any  occasion.  In  other  cases,  the 
hemorrhage  is  referable  to  some  distinct  cause,  such  as  bodily  exertion,  a 
violent  paroxysm  of  coughing,  straining  at  stool,  mental  excitement,  and  the 
like.  Many  cases  of  phthisis  are  characterized  by  a  special  tendency  to  hemor- 
rhage, while  in  many  others  hemoptysis  never  occurs.  Severe  hemoptyses 
are,  of  course,  always  an  undesirable  and  dangerous  complication,  since  they 
weaken  the  patient  very  much,  and  also  depress  his  spirits.  Many  patients 
maintain  their  peculiar  careless  indifference,  which  is  almost  characteristic  of 
the  disease,  despite  the  spitting  of  blood.  The  hemoptysis  may  sometimes 
be  the  direct  cause  of  death,  but,  as  a  rule,  the  patients  survive  it.  We  have 
no  better  means  of  determining  with  certainty  the  influence  which  hemoptysis 
has  upon  the  progress  of  tuberculosis  than  by  the  bodily  temperature.  If  there 
was  no  fever  before,  and  the  hemoptysis  also  has  an  afebrile  course,  or  only 
a  very  brief  rise  of  temperature,  then  we  may  hope  in  general  that  the  patient 
may  fully  recover  from  the  hemorrhage  and  be  as  well  as  before.  If,  however, 
the  hemoptysis  is  followed  by  persistent  fever,  or  if  the  fever  which  may  have 


290 


DISEASES   OF  THE   RESPIRATORY  ORGANS 


previously  existed  becomes  higher  and  more  persistent,  we  have  every  reason 
to  suppose  that  the  tubercular  process  is  making  more  rapid  advances  subse- 
quently to  the  hemoptysis.  We  here  append  a  temperature  chart  (Fig.  50) 
illustrating  the  temporary  influence  of  a  hemoptysis  upon  the  temperature  in 


Hemoptysis. 


40.° 


39.' 


38.c 


37.° 


36.° 


IHsmsSKHNESsi  !Ui!  !i: 
ESS  iS'awAw  EkmhSuh  \mfffmwmm 


■  ■■■■■■■■■■■■■■■■WMHIMMIITWt.B.B1! 

iiHii!   IHiillMRBiaglH 


Fig.  50. — Influence  of  a  pulmonary  hemorrhage  upon  the  bodily  temperature. 
(Erlangen  Medical  Clinic.) 

a  stationary  afebrile  case  of  pulmonary  tuberculosis.  The  fact  that  the  fever 
preceded  the  hemorrhage  by  a  few  clays  is  probably  due  to  the  tuberculous  arte- 
ritis, because  of  which  material  capable  of  exciting  fever  entered  the  circula- 
tion before  the  process  had  caused  complete  destruction  and  bursting  of  the 
arterial  wall,  and  consequent  pulmonary  hemorrhage. 

A  purulent  sputum  intimately  mixed  with  blood  is  quite  frequent  and 
characteristic  in  many  cases  of  phthisis  with  extensive  formation  of  cavities. 
This  is  formed  in  the  cavities  from  the  mixture  of  the  purulent  secretion  with 
little  capillary  hemorrhages.  In  this  way  the  sputum,  which  is  often  nummu- 
lar, assumes  a  greasy  character  and  a  reddish-brown  or  chocolate  color. 

If  fetid  or  gangrenous  processes  develop  in  the  lungs,  the  sputum  becomes 
fetid.  In  some  cases  we  see  temporarily  in  phthisis  the  characteristic  sputum 
of  croupous  pneumonia,  which  comes  from  portions  of  the  lung  attacked  with 
secondary  pneumonia. 

Microscopic  examination  of  the  sputum  may  show — besides  the  ordinary 
morphological  elements,  such  as  pus  corpuscles,  red  blood  corpuscles,  and  epi- 
thelium— two  constituents  which  are  of  decided  diagnostic  importance :  elastic 
fibers  and  tubercle  bacilli. 

The  demonstration  of  elastic  fibers  in  the  expectoration  permits  us  to 
decide  with  certainty  that  there  is  a  destructive  process  in  the  lungs,  and 
thus  it  usually  is  direct  proof  of  tuberculosis.  Elastic  fibers  are  also  found 
in  pulmonary  gangrene,  and  in  cases  of  pulmonary  abscess,  as  well  as  in 
tuberculosis,  but  these  diseases  are  easily  recognized  by  the  other  peculiarities 
of  the  sputum.  The  search  for  elastic  fibers  in  the  expectoration  of  tubercu- 
lous patients  demands  a  certain  amount  of  practice.  We  are  most  sure  to  find 
them  if  we  look  in  the  sputum,  when  it  is  spread  out,  for  little  lentiform 
particles,  which  can  easily  be  discerned  with  the  naked  eye.  These  consist  of 
necrotic  shreds  of  tissue  torn  off  from  the  walls  of  cavities.  If  we  press  one 
of  these  "  kernels  "  under  a  cover-glass  we  find,  in  the  midst  of  the  granular 
detritus,  beautifully  twisted  elastic  fibers,  which  often  have  quite  a  definite 
alveolar  arrangement  (see  Fig.  51).    The  elastic  tissue  is  the  only  one  spared 


TUBERCULOSIS   OF  THE   LUNCS 


291 


in  the  general  destruction.  There  is  a  special  method  of  Looking  for  elastic 
fibers.  The  sputum  is  boiled  in  sodium  hydrate,  diluted  with  water,  and  we 
look  for  elastic  fibers  in  the  precipitate  which  then  forms.  We  are  never 
justified,  however,  in  deciding  that  pulmonary  tuberculosis  ie  absent  because 

we  do  not  find  elastic  fibers  in  the 
sputum.  Their  presence  alone  has 
real  diagnostic  significance. 


Fig.  51. — Elastic  fibers  from  the  sputum  of  a 
case  of  pulmonary  tuberculosis. 


Fig.  52. — Tubercle  bacilli  in  the  sputum. 


The  discovery  of  tubercle  bacilli  in  the  expectoration  of  phthisical  patients 
is  of  much  greater  importance,  and  often  this  alone  is  decisive  (see  Fig.  52). 
They  were  first  demonstrated  by  Koch,  but  Ehrlich  devised  the  first  simple 
method  for  their  discovery,  which  can  be  easily  employed  by  any  physician. 

The  simplest  method,  and  the  one  which  we  now  employ  almost  exclu- 
sively for  staining  the  bacilli,  is  as  follows:  Some  of  the  sputum  is  rubbed 
between  two  cover-glasses,  which  are  then  slowly  separated,  leaving  upon  each 
cover-glass  a  very  thin  layer  of  sputum.  In  order  to  fasten  this  sputum  upon 
the  cover-glass,  the  latter  is  passed  three  times  slowly  through  a  gas  flame. 
The  cover-glass  is  now  held  with  a  pair  of  forceps  and  covered  with  the 
following  staining  fluid  (carbol-fuchsin  solution),  which  was  first  proposed 
by  Ziehl  and  ISTeelsen :  Distilled  water,  100  parts ;  crystals  of  carbolic  acid, 
5  parts;  fuchsin,  1  part;  mix,  filter,  and  add  alcohol,  10  parts.  This  staining 
solution  upon  the  cover-glass  is  heated  to  boiling  for  a  short  time,  and  then 
the  staining  is  completed.  The  cover-glass  is  now  washed,  first  in  absolute  alco- 
hol, then  in  distilled  water,  then  placed  for  about  two  minutes  in  a  solution 
of  2  parts  of  methyl  blue  in  100  parts  of  a  twenty-five-per-cent  solution  of 
sulphuric  acid.  The  acid  bleaches  out  the  diffused  fuchsin  stain,  leaving  the 
tubercle  bacilli  still  colored,  while  the  pus  corpuscles  are  colored  blue.  The 
preparation  is  now  rinsed  in  water,  dried  between  two  pieces  of  filter  paper, 
and  examined  in  Canada  balsam.  The  whole  process,  when  one  has  had  a 
certain  degree  of  experience,  requires  four  or  five  minutes.  The  number  of 
bacilli  in  different  cases,  and  at  different  times  in  the  same  case,  varies  con- 
siderably. The  more  abundant  the  bacilli,  the  more  reason  have  we  to 
suppose  there  is  a  rapidly  advancing  process  of  ulceration,  but  of  course  we 


292  DISEASES   OF  THE   RESPIRATORY  ORGANS 

can  never  draw  a  broad  conclusion  as  to  the  extent  of  the  tuberculous  disease 
from  the  number  of  bacilli  in  the  sputum.  Our  only  information  on  this 
point  must  come  from  the  physical  examination,  and  other  clinical  observa- 
tions. On  the  other  hand,  the  diagnostic  significance  of  the  demonstration 
of  bacilli  with  regard  to  the  recognition  of  a  pulmonary  tuberculosis  cannot  be 
overrated.  A  positive  result  is  absolutely  decisive,  and  the  diagnosis  of  tuber- 
culosis of  the  lungs  ought  certainly  never  to  be  made  unless  the  bacilli  have 
been  demonstrated.  Very  frequently  bacilli  may  be  found  in  the  sputum  in 
early  cases,  at  a  time  when  no  other  certain  sign  of  tuberculosis  can  be  de- 
tected. On  the  other  hand,  we  scarcely  need  to  point  out  that  the  physician 
should  be  cautious  in  the  interpretation  of  negative  results.  In  all  suspicious 
cases  we  must  repeat  the  examination  of  the  sputum  over  and  over  again. 

Dyspnoea. — Many  patients  hardly  ever  complain  of  their  breathing  in  spite 
of  extensive  destruction  in  the  lungs.  A  patient  who  is  much  emaciated  mani- 
festly needs  little  oxygen,  and  the  increased  frequency  of  respiration,  which  is 
almost  constant,  can  satisfy  his  needs.  If  there  is  a  greater  demand  upon. 
the  respiration  a  subjective  feeling  of  dyspnoea  may,  of  course,  very  readily 
occur,  especially  on  a  slight  bodily  exertion.  In  many  cases,  however,  the 
patient  complains  of  a  difficulty  in  breathing  even  when  quiet,  especially  if 
pleuritic  pains  or  adhesions  between  the  surfaces  of  the  pleura  prevent  him 
from  taking  a  deep  breath;  and  in  the  final  stages  the  dyspnoea  may  be 
extreme. 

2.  Symptoms  on  Physical  Examination.1 — In  many  cases  inspection  gives 
us  that  general  impression  of  the  patient  which  we  term  the  "  phthisical 
habit."  The  special  signs  of  this  are  as  follows:  A  slender  but  often  quite  a 
tall  frame,  weak  muscular  development,  a  thin  layer  of  fat,  a  pale  and  per- 
haps very  delicate  skin  with  a  bluish  translucence,  sometimes  a  circumscribed 
"  hectic  "  flush  in  the  cheeks,  a  long  and  slender  neck,  a  long  and  flat  thorax, 
small,  thin  hands,  etc.  Of  course  this  characteristic  constitutional  habit  is 
not  equally  well  marked  in  all  cases.  The  inspection  of  the  thorax  is  of  special 
value.  The  phthisical  or  "  paralytic  "  thorax  is  generally  noticeable  from  its 
length,  but  it  is  narrow  and  flat.  Unusual  width  of  single  intercostal  spaces, 
and  acuteness  of  the  epigastric  angle,  are  associated  with  a  long  thorax. 
The  sternum  is  also  long  and  narrow,  and  the  sternal  angle — Louis'  angle — is 
sometimes  particularly  prominent.  The  supraclavicular  and  infraclavicular 
fossas  are  sunken,  the  neck  is  wasted,  and  the  shoulder  blades  stand  out  from 
the  thorax.  On  comparing  the  two  halves  of  the  thorax  we  very  often  observe 
a  distinct  drawing  in  and  flattening  (contraction)  on  the  side  most  affected. 
This  change  is  most  frequently  in  the  upper  and  anterior  portions  of  the  chest, 
but  it  is  not  rare  even  in  the  posterior  and  lower. 

The  paralytic  form  of  thorax  is  very  often  seen  in  phthisis,  but  it  may  be 
entirely  absent. 

The  respiration  is  usually  somewhat  accelerated,  and  sometimes  quite 
markedly  so  in  women  with  disease  of  the  apices.  The  feminine  type  of  high 
thoracic  breathing  is  largely  changed  to  low  thoracic  or  diaphragmatic  breath- 
ing.    A  unilateral  impairment  of  respiration  is  of  greater  importance;  in 

1  The  significance  of  the  X-ray  examination  will  be  considered  in  the  section  dealing  with  the 
diagnosis  of  pulmonary  tuberculosis. 


TUBERCULOSIS   OF   THE   LUNGS  203 

such  a  case  the  apex  in  front,  or  even  the  whole  side,  if  there  be  phthisis  of 
the  lower  lobe,  lags  in  inspiration.  The  respiration  is  sometimes  irregular, 
especially  if  l  here  be  pleuril  ic  pains. 

The  results  of  percussion  are,  of  course,  entirely  dependent  upon  the  sort 
of  anatomica]  changes  in  the  lungs,  and  hence  differ  very  greatly  in  different 
cases.  Since  the  phthisical  process  begins  in  the  apices  in  the  majority  of 
cases,  our  chief  attention  is  turned  to  the  condition  of  the  upper  portions 
of  the  lungs  on  percussion.  Slight  changes  in  percussion  may  wholly  escape 
discovery.  Only  when  the  air  contained  in  the  lung  tissue  in  the  part  affected 
is  replaced  to  a  certain  degree  by  the  tubercular  infiltration  does  the  percus- 
sion note  become  dull.  Unilateral  dullness  at  the  apex  is  therefore  one  of  the 
most  frequent  physical  signs  of  phthisis.  We  can  make  it  out  most  plainly 
in  the  upper  anterior  intercostal  spaces  first,  and  in  incipient  cases  often  in 
the  supraclavicular  fossae  only,  but  it  is  also  observed  sometimes  in  the  back 
in  the  suprascapular  fossae. 

As  the  infiltration  advances  the  dullness  becomes  more  extensive.  For  the 
accurate  determination  of  the  limits  of  dullness  in  the  upper  portions  of  the 
lungs,  we  recommend  that  percussion  should  be  practiced  in  such  a  way  as  to 
proceed  from  the  normal  resonance  of  the  lower  portions  upward  toward  the 
affected  area.  This  method  is  particularly  useful  for  the  back  of  the  chest. 
If  light  percussion  is  practiced  from  below  upward  on  both  sides  of  the  ver- 
tebral column  of  a  normal  chest,  the  percussion  note  will  be  of  the  approxi- 
mately same  clearness  and  pitch  up  to  the  apices.  If,  on  the  other  hand,  as 
is  the  rule  in  tuberculosis,  we  are  dealing  with  disease  in  the  upper  portion  of 
the  lungs  and  normal  lower  lobes,  a  decided  change  in  the  percussion  note  will 
be  heard  either  at  the  level  of  the  root  of  the  lungs  or  when  the  upper  lobes, 
are  reached.  The  note  is  dull,  or  its  pitch  is  changed,  becomes  tympanitic, 
etc.  This  method  of  percussion  for  the  demonstration  of  beginning  apical 
dullness  appears  more  advantageous  to  me  than  the  method  usually  employed, 
of  comparison  of  the  percussion  notes  on  the  two  sides.  With  simultaneous 
disease  of  both  apices,  slight  dullness  may  be  more  easily  overlooked  with  the 
methods  of  percussion  usually  employed.  Within  certain  limitations  the  ver- 
tical method  of  percussion  from  below  upward  also  gives  the  most  trustworthy 
information  as  to  the  extent  of  the  lesion  in  cases  of  advanced  tuberculosis. 
In  the  percussion  of  the  apices,  Kronig  lays  special  stress  upon  the  diag- 
nostication  of  possible  retraction  of  the  apices,  by  the  fact  that,  with  the  patient 
in  the  horizontal  posture,  the  width  of  pulmonary  resonance  is  diminished  in 
the  supraclavicular  fossae  in  front,  or  over  the  apices,  posteriorly.  This  method 
sometimes  gives  very  good  results,  but,  in  my  experience,  it  is  of  less  practical 
value  than  the  direct  demonstration  of  apical  dullness.  Often  the  dullness 
takes  a  tympanitic  quality  as  a  result  of  diminished  tension  in  the  lung,  or 
more  or  less  pulmonary  retraction.  Changes  in  tension  may  render  the  reso- 
nance, in  beginning  tuberculosis,  deeply  tympanitic  without  any  accompanying 
dullness. 

The  formation  of  cavities  in  tuberculosis  has  a  great  influence  on  the  per- 
cussion note.  The  dullness  on  percussion  may  thus  become  decidedly  less,  the 
degree  of  resonance  depending,  of  course,  upon  the  fullness  of  the  cavity  and 
the  character  of  the  surrounding  tissue.  We  often  find  a  decided  tympanitic 
resonance  or  a  combination  of  dullness  and  tympany  over  a  cavity.    The  dif- 


294  DISEASES   OF  THE   RESPIRATORY  ORGANS 

ferent  modifications  of  the  percussion  note  in  cavities  are  given  below.  The 
"  cracked-pot  resonance,"  or  buckram  sound,  is  met  with  in  percussing  over 
cavities,  but  we  also  find  it  in  many  other  pathological  conditions,  and  in 
children  not  infrequently  when  the  lung  is  normal. 

Auscultation  also  gives  no  special  pathognomonic  signs  of  phthisis.  Vary- 
ing with  the  character  and  extent  of  the  tuberculous  changes,  abnormal  re- 
spiratory sounds  and  adventitious  sounds  are  heard  in  place  of  the  normal 
vesicular  murmur.  With  slighter  changes  the  vesicular  breathing  is  merely 
modified;  it  seems  remarkably  diminished  or  interrupted  ["  cog-wheel  "J,  or 
sometimes  exaggerated,  with  jDrolonged  expiration.  When  the  infiltration  of 
the  lungs  increases,  we  find  bronchial  respiration  in  place  of  the  vesicular 
breathing;  but,  on  the  other  hand,  the  formation  of  a  cavity  is  a  frequent 
cause  of  bronchial  respiration. 

Various  sorts  of  moist  rales  are  among  the  most  frequent  and  diagnostically 
important  of  the  auscultatory  signs  of  phthisis.  They  are  caused  by  the  col- 
lection of  secretion  in  the  bronchi,  or  in  pulmonary  cavities.  The  more  abun- 
dant and  liquid  the  secretion  is  which  is  set  in  motion  by  the  air  current  which 
traverses  it,  the  more  abundant  and  moister  the  rales.  The  larger  the  space  is 
in  which  they  develop,  the  coarser  they  are.  Besides  the  true  moist  rales, 
there  are  also  dry  bronchitic  rales  (sibilant  or  sonorous)  occasionally  to  be 
heard  in  portions  of  the  tuberculous  lung.  In  general,  we  may  say  that  the 
extent  of  the  tuberculous  disease  in  the  lungs  can  be  determined  by  no  symp- 
tom so  surely  as  by  the  auscultatory  signs  relating  to  the  respiration,  and  the 
adventitious  sounds  which  may  be  present. 

Physical  Diagnosis  oe  Incipient  Phthisis. — The  importance  of  the 
diagnosis  of  early  phthisis  is  so  great  that  we  will  briefly  sketch  its  most  im- 
portant physical  signs.  Now  that  the  examination  of  the  sputum  for  tubercle 
bacilli  plays  by  far  the  most  prominent  part  in  the  recognition  of  incipient 
tuberculosis,  and  is  the  only  decisive  evidence,  the  physical  signs  of  this  con- 
dition have  lost  much  of  their  former  importance.  Despite  this,  the  determi- 
nation of  the  seat  and  extent  of  the  early  process  is  extremely  desirable.  We 
will  mention  the  following  symptoms:  1.  Constant  and  evident  diminution 
of  the  respiratory  murmur  at  one  apex,  especially  if  it  is  associated  with 
marked  deficiency  of  the  respiratory  movement  on  the  affected  side.  In  some 
cases  the  respiratory  murmur  on  the  diseased  side  is  not  weaker,  but  it  has 
a  more  indefinite  and  harsher  character ;  or,  again,  it  may  be  rude,  sharp,  and 
"  puerile."  2.  Markedly  interrupted  respiration  at  one  apex.  3.  A  prolonged 
expiratory  murmur,  which  has  a  harsh  character.  4.  The  discovery  of  dry 
rhonchi  or  moist  rales  at  one  apex  is  most  important,  since  we  know  by  expe- 
rience that  "  apex  catarrhs  "  are,  almost  invariably,  tuberculous.  5.  Definite 
dullness,  apparent  on  repeated  examinations,  or  tympanitic  dullness  or  tym- 
pany at  one  apex.  6.  Evident  contraction  at  one  apex,  as  revealed  by  inspec- 
tion or  percussion  above  the  clavicles.  7.  Some  authors  lay  stress  upon  a  sys- 
tolic murmur  in  the  subclavian  artery,  especially  loud  on  expiration.  This 
is  said  to  occur  in  the  beginning  of  phthisis,  if  the  caliber  of  the  vessel  is  nar- 
rowed by  processes  of  contraction  in  the  neighboring  apex.  The  symptom  has 
no  practical  significance,  however,  since  similar  vascular  murmurs  are  occa- 
sionally heard  over  normal  apices. 

The  chief  rule  in  the  diagnosis  of  incipient  phthisis  must  be  held  to  be 


TUBERCULOSIS  OF  THE   LUNGS  295 

this — not  to  give  a  definite  opinion  until  repeated  examinations  have  been 
made.  The  other  portions  of  the  lungs  are  to  be  carefully  examined  as  well 
as  the  apices,  since  in  not  very  rare  cases  tuberculosis  may  begin  in  the  lower 
lobes.     We  must  always  consider  other  circumstances   (heredity,  constitution, 

general  symptoms  of  the  disease,  fever,  expectoration,  etc.),  as  well  as  the 
physical  signs  presented  by  the  patient.  These  as  well  as  the  specific,  biological 
reactions  and  the  extremely  valuable  aid  to  diagnosis  rendered  by  the  X-ra;  -. 
will  be  considered  below. 

Diagnosis  of  Cavities. — The  positive  diagnosis  of  pulmonary  cavities  by 
means  of  physical  examination  is  often  very  difficult.  x\nyone  who  will  com- 
pare the  discoveries  at  autopsies  with  the  results  of  previous  physical  exami- 
nation of  consumptives  will  be  in  a  position  to  confirm  the  truth  of  this  state- 
ment. We  may  mention  as  the  chief  symptoms  of  a  cavity:  1.  Loud  bronchial 
respiration,  perhaps  of  an  amphoric  character,  in  places  where  the  percussion 
note  is  only  slightly  or  not  at  all  dull,  but  perhaps  tympanitic.  Such  a  con- 
dition means  that  the  bronchial  respiration  is  not  due  to  an  infiltration  of 
lung  tissue.  Bronchial  respiration,  however,  may,  of  course,  be  heard  over 
cavities  which  are  surrounded  by  thickened  lung  tissue,  and  hence  give  dull- 
ness on  percussion.  Pure  amphoric  respiration  is  very  characteristic  of  a 
cavity,  particularly  if  there  is  a  clear,  metallic  quality  to  the  sound;  but  this 
sort  of  respiratory  murmur  is  heard  only  when  the  cavity  is  comparatively 
large,  of  regular  shape,  and  with  smooth  walls.  Under  these  circumstances 
the  moist  rales,  if  there  are  any,  also  have  a  clearly  metallic  sound  (tinkle), 
and  the  percussion  resonance  may  also  be  distinctly  metallic.  This  last  should 
be  demonstrated  by  rod  percussion  with  simultaneous  auscultation.  In  many 
cases  of  this  sort  the  differential  diagnosis,  between  a  large  cavity  and  a  saccu- 
lated pneumothorax  (see  page  364),  is  very  difficult.  2.  The  so-called  meta- 
morphosing respiration,  which  begins  as  vesicular  and  suddenly  becomes  bron- 
chial, is  heard  especially  over  cavities,  and  hence  has  a  diagnostic  value.  3. 
The  different  kinds  of  "  changes  in  the  percussion  note "  over  cavities  are 
important  signs.  The  most  frequent  and  of  greatest  practical  importance  is 
Wintrich's  change  of  note.  This  is  when  the  tympanitic  resonance,  which  is 
obtained  over  the  cavity,  becomes,  on  opening  the  mouth,  more  decidedly  tym- 
panitic, louder,  and  especially  much  higher.  The  respiratory  change  of  pitch 
of  Friedreich  usually  consists  of  a  higher  pitch  on  inspiration,  but  here  there 
are  numerous  variations.  Gerhardt's  change  of  pitch  (Weil)  consists  in  a 
change  of  the  tympanitic  resonance  when  the  patient  changes  his  position,  the 
pitch  usually  being  higher  when  the  patient  sits  up  than  when  he  is  lying 
down.  4.  Loud,  bubbling  rales  are  one  of  the  most  frequent  signs  of  a  cavity. 
They  are  definite  indications  of  the  occurrence  of  rales  in  a  larger  space  than 
is  normally  present  in  the  apices  of  the  lungs.  If  we  have  coarse  and  metallic 
rales  in  the  apices  of  the  lung,  there  is  considerable  probability  of  the  exist- 
ence of  a  cavity,  inasmuch  as  the  normal  apices  cannot  produce  such  sounds. 
5.  Finally,  we  would  point  out  that  large  cavities  not  infrequently  appear  in 
X-ray  pictures  in  the  form  of  distinct,  sharply  circumscribed,  lighter  areas. 

In  addition  to  the  physical  signs,  the  nature  of  the  sputum  must  be  con- 
sidered.   As  a  rule,  a  profuse,  purulent  clumpy  ("nummular")  expectoration 
indicates  cavity  formation.     In  febrile  cases  of  phthisis  with  remarkably  little 
expectoration,  large  cavities  can,  as  a  rule,  be  excluded. 
19 


296  DISEASES   OF  THE  RESPIRATORY   ORGANS 

Contraction  of  the  Lungs  [Fibroid  Phthisis]. — Unilateral  contrac- 
tion of  the  lungs,  much  more  frequent  on  the  left  than  on  the  right,  is  a  form 
of  tuberculosis  which  is  made  apparent  both  by  special  physical  signs  and  also 
by  certain  clinical  peculiarities.  It  is  usually  recognized  at  once  by  inspection 
of  the  thorax,  one  side  of  the  thorax  being  remarkably  retracted.  The  upper 
anterior  portions  of  the  thorax,  and,  in  all  cases  of  a  high  degree  of  disease, 
the  lower  lateral  and  posterior  portions,  are  much  less  expanded  than  the  cor- 
responding parts  on  the  other  healthy  side.  The  fossae  and  intercostal  spaces 
on  the  affected  side  are  deeper,  the  shoulder  blade  is  drawn  nearer  the  vertebral 
column,  and  the  latter  is  even  sometimes  drawn  over  to  the  contracted  side 
(scoliosis).  The  resonance  is  diminished  to  a  greater  or  less  degree  over  the 
affected  side,  which  either  lags  behind  or  remains  almost  wholly  at  rest  on 
respiration.  The  respiratory  murmur  is  quite  loud  and  bronchial;  and  we 
also  hear  many  rales,  which  are  usually  bubbling.  Exceptionally  the  rales  are 
few  and  the  respiratory  murmur  feeble  and  indistinct.  Anatomically,  we 
have  to  do  with  a  marked  jjrocess  of  contraction  of  the  interstitial  connective 
tissue  in  the  lungs,  which  is  almost  always  associated  with  extensive  formation 
of  cavities,  partly  of  an  ulcerative,  partly  of  a  bronchiectatic  character.  The 
pleura  is  almost  invariably  involved  in  the  process,  but  with  the  exception  of 
the  cases  that  have  begun  with  a  pleurisy  with  effusion  this  is  only  secondary. 
The  pleura  is  also  thickened  and  contracted.  If  the  pleuritic  thickening  is 
marked,  the  respiratory  murmur  and  the  vocal  fremitus  are  decidedly  weakened. 

The  influence  of  the  contraction  on  the  neighboring  organs  is  very  decided, 
and  usually  it  is  easy  to  discover.  The  heart  especially,  whose  external  peri- 
cardium is  in  most  cases  very  adherent  to  the  pleura,  is  drawn  well  over  to  the 
side  of  the  contraction.  The  apex  beat  and  the  cardiac  dullness  are  corre- 
spondingly displaced.  With  left-sided  contraction  the  heart  may  be  drawn 
over  to  the  line  of  the  left  axilla,  and  with  right-sided  contraction  it  may  be 
drawn  to  the  median  line,  or  even  to  the  right  of  the  sternum.  With  contrac- 
tion of  the  left  upper  lobe  the  anterior  surface  of  the  heart  comes  into  imme- 
diate contact  with  the  anterior  chest  wall  over  a  larger  area  than  normal.  We 
therefore  see  the  motions  of  the  heart  over  an  abnormal  extent,  and  we  can 
often  feel  very  plainly  in  the  second  left  intercostal  space  the  pulsation  and  the 
closure  of  the  valves  in  diastole  of  the  pulmonary  artery.  The  upward  trac- 
tion of  the  diaphragm  may  be  recognized  by  the  position  of  the  liver,  or,  in 
left-sided  contraction,  by  the  increase  of  the  "  semilunar  "  tympanitic  space 
on  the  left.  We  usually  find  the  sound  lung  on  the  other  side  quite  emphy- 
sematous, as  shown  by  the  downward  displacement  of  the  lower  boundary  of 
the  lung,  and  also  by  the  drawing  over  of  the  anterior  median  edge  of  the 
lung  to  the  contracted  side.  In  a  part  of  the  cases  we  can  make  out  by  per- 
cussion the  development  of  consecutive  dilatation  and  hypertrophy  of  the  right 
ventricle. 

These  are  the  chief  physical  signs  of  the  so-called  unilateral  form  of 
chronic  pulmonary  contraction.  We  would  add  here  a  few  clinical  remarks. 
These  cases  often,  but  of  course  not  always,  run  a  very  chronic  course,  lasting 
for  years.  The  general  condition  and  the  nutrition  of  the  patient  may  thus 
remain  comparatively  undisturbed  for  a  long  time.  The  patient  looks  some- 
what pale  and  cyanotic,  yet  he  is  so  well  nourished  as  to  present  a  very  marked 
contrast  to  the  appearance  of  the  ordinary  cases  of  phthisis.     The  appetite 


TUBERCULOSIS   OF  THE   LUNGS  297 

remains  good,  the  fever  is  entirely  absent,  or  else  a  slighl  degree  of  fever  may 
be  ;il  times  discovered  by  careful  examination.  The  cough  and  expectoration, 
too,  though  often  quite  troublesome,  are  at  other  times  very  Blight,  especially 

when  the  patient  has  good  care  and  nourishment.  We  need  not  wonder,  then, 
that  formerly  many  physicians  did  not  consider  thai  these  case.-  had  any- 
thing to  do  with  phthisis — "consumption";  and  yet  we  are  convinced  by 
many  clinical  and  anatomical  observations  that,  serologically,  they  are  in  by 
far  the  greatest  part  tuberculous.  They  represent  a  very  slow  form  of  tuber- 
culosis, which  has  time  to  develop  interstitial  processes  which  lead  to  contrac- 
tion— that  is,  to  local  healing.  If  such  cases  come  to  autopsy,  their  tubercu- 
lous character  is  usually  definitely  confirmed.  We  find  undoubted  tuberculous 
lesions  in  the  other  lung  and  also  in  the  remaining  organs — e.g.,  the  intes- 
tines. Sudden  changes  for  the  worse  are  always  possible  in  "pulmonary  con- 
traction," even  in  those  cases  which  seem  favorable;  the  other  lung  may  be- 
come highly  tuberculous,  a  miliary  tuberculosis  or  a  tuberculous  meningitis 
may  develop,  etc.  On  the  whole,  however,  the  slow  course  of  this  form  of 
chronic  tuberculosis  is  characteristic  and  of  great  practical  significance,  and  its 
prognosis  is  therefore  comparatively  favorable. 

We  cannot  deny  that  a  nontuberculous  unilateral  contraction  of  the  lung 
may  occur.  As  a  result  of  bronchitis  (particularly  in  cases  due  to  the  inhala- 
tion of  dust),  and  also  after  pleurisy,  processes  of  contraction  develop,  which 
are  associated  with  the  formation  of  bronchiectasis,  and  certainly  have  nothing 
to  do  with  tuberculosis.  In  rare  cases  also  croupous  pneumonia  is  followed  by 
unilateral  contraction  of  the  lung ;  and  finally  there  is  a  rare  and  by  no  means 
satisfactorily  investigated  form  of  unilateral  chronic  interstitial  pneumonia, 
with  contraction,  often  associated  with  the  formation  of  bronchiectasis.  The 
differential  diagnosis  of  these  conditions  from  tuberculous  contraction  rests 
in  part  u]3on  the  clinical  history,  which  should  be  carefully  taken,  but  mainly 
upon  the  absence  of  tubercle  bacilli  in  the  expectoration. 

In  conclusion,  we  must  mention  that  there  are  very  many  transitional 
forms  between  pulmonary  contraction  and  the  other  varieties  of  pulmonary 
tuberculosis.  We  find  more  or  less  extensive  processes  of  contraction  in  one 
apex  in  most  cases  of  phthisis. 

Disseminated  Pulmonary  Tuberculosis. — There  is  a  form  of  pulmo- 
nary tuberculosis  which  it  is  very  hard  to  make  out  on  physical  examination. 
In  this  we  have  to  do  with  numerous  peribronchial  nodules  disseminated  over 
the  whole  lung.  As  there  is  still  a  good  deal  of  normal  tissue,  containing  air, 
between  these  nodules,  percussion  affords  no  dullness,  and  auscultation  gives  at 
most  diffuse  rhonchi ;  hence  this  form  is  often  confused  with  chronic  bronchitis 
or  pulmonary  emphysema.  The  diagnosis  can  seldom  be  made  from  the  physi- 
cal signs,  but  only  from  the  other  symptoms,  such  as  fever,  emaciation,  strik- 
ing pallor  of  the  skin,  and  the  sputum.  X-ray  examination  may  give  impor- 
tant information  as  to  the  condition  of  the  lungs. 

The  disseminated  form  of  phthisis  sometimes  runs  a  chronic  course,  but 
usually  it  is  quite  rapid.  It  occurs  in  elderly  people,  and  also  in  children. 
Many  forms  of  "  disseminated,  coarse  granular  "  tuberculosis  are  transitional 
forms  between  this  and  genuine  acute  miliary  tuberculosis  (q.v.). 

Pneumonic  Form  of  Pulmonary  Tuberculosis. — A  special  clinical  in- 
terest attaches  to  that  form   of  pulmonary  tuberculosis  termed  pneumonic, 


298  DISEASES   OF   THE   RESPIRATORY   ORGANS 

which  we  have  already  briefly  mentioned.  The  disease  begins  in  a  decidedly 
acute  manner  with  dyspnoea,  frequent  cough,  and  pain  in  the  side.  Sometimes 
we  observe  even  a  distinct  initial  chill.  The  expectoration  is  scanty,  viscid, 
mucous,  and  often  reddish  or  hemorrhagic.  It  sometimes  also  has  a  peculiar 
greenish  color.  Even  after  a  few  days  of  illness  we  find,  on  examination,  the 
well-marked  signs  of  lobar  infiltration.  There  is  first  pneumonic  resonance, 
then  a  dull  tympany,  with  fine  moist  rales  and  bronchial  breathing.  In  most 
cases,  but  not  all,  a  lower  lobe  is  involved.  The  disease  is  almost  invariably 
regarded  at  first  as  a  croupous  pneumonia,  but  the  expected  crisis  does  not 
appear.  The  fever  remains  high,  the  infiltration  does  not  undergo  resolution, 
the  rales  become  coarser,  the  patient  looks  pale  and  wretched.  Now,  suspicion 
of  tuberculosis  being  aroused,  the  sputum  is  carefully  examined,  and  soon, 
although  perhaps  not  at  the  first  examination,  tubercle  bacilli  are  found. 
Nearly  all  cases  of  this  sort  take  a  rapid  and  unfavorable  course.  They  may 
be  called  galloping  consumption.  Upon  autopsy  we  find  diffuse  tuberculous  in- 
filtration, and  usually  incipient  cavity  formation  in  numerous  places.  Other 
portions  of  the  lungs  than  that  first  and  most  violently  attacked  ordinarily 
present  considerable  tuberculous  change.  In  tbese  instances  it  is  evident  that 
we  have  to  do  with  an  acute  infection  of  a  large  portion  of  the  lung  with 
tubercle  bacilli,  which  of  themselves  exert  a  powerful  inflammatory  action, 
with  unusual  virulence.  In  some  cases  there  may  also  be  a  mixed  infection, 
due  to  the  pheumococcus. 

We  have  seen  a  few  cases  in  which  the  pneumonic  form  of  tuberculosis  fol- 
lowed a  severe  hemoptysis.  In  these  instances  the  aspirated  blood  probably 
led  to  the  rapid  spread  of  the  infection. 

3.  General  Symptoms  in  Pulmonary  Tuberculosis. — In  the  description  of 
the  general  course  of  pulmonary  tuberculosis  we  have  already  mentioned  the 
value  of  the  constitutional  symptoms  in  diagnosis  and  prognosis. 

Fever. — Only  a  few  cases  of  phthisis  run  their  course  entirely  without  fever, 
but  it  may  be  absent  for  a  time,  even  for  weeks  and  months;  and  indeed,  in 

cases  with  a  very  slow  and  favorable 
course    (e.  g.,   where   there   is  uni- 


37.° 


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(HHSfflnnnMn 

lateral  contraction),  there  may  be 
no  fever  at  all  for  years.  The  more 
carefully  we  measure  the  tempera- 
ture the  more  often  shall  we  find 
slight  elevations  of  the  same,  even 
when  the  patient  is  feeling  well. 
In  normal  individuals  the  axillary 
temperature  hardly  ever  rises  above 
98.6°  to  99°  F.  (37°  to  37.2°  C), 
and  generally  it  is  somewhat  lower 
than  98.6°  P.  (37°  C).  A  persistent 
temperature   above    98.6°    P.    (37° 

Fig.  53.— Subfebrile  state  in  chronic  pulmonary      q  j      an(j   especially   frequent    eleva- 
tuberculosis.  ^    ^    ^^    ^    ^^    R     ^go 

to  38°  C. )  should  be  considered  as  decidedly  pathological.  Such  slight  elevations 
of  temperature  (so-called  subfebrile  state)  often  persist  for  a  long  time,  or  at 
least  occur  occasionally  in  numerous  cases  of  tuberculosis  (see  Fig.  53).    Ele- 


TUBERCULOSIS    OF   THE    LU.VIS 


299 


to, 


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Fig.  54. — Hectic  fever  in  chronic  pulmonary 
tuberculosis. 


vations  of  temperature  to  loo.  I"  or  101°  F.  (38°  to  38.5°  <'.).  especially  when 
observed  in  the  evening,  indicate  increased  activity  of  the  tubercular  process. 

Very  often,  particularly  in  the  more  rapid  <asc-,  there  is  considerable  ele- 
vation of  temperature,  and  the  varieties  and  course  of  the  fever  are  more  or 
less  characteristic.  We  should  first  mention  the  "  hectic  fever"  (see  Fig.  51 ) 
which  is  often  observed.  For  months 
the  temperature  chart  may  present  a 
uniform  appearance  with  a  morning 
temperature  approaching  or  reaching 
the  normal,  while  there  is  a  regular 
elevation  every  evening  to  102°  or  104° 
F.  (39°  to  40°  C).  In  general,  the 
higher  the  evening  exacerbations  the 
more  unfavorable  the  case.  In  some 
cases  the  temperature  rises  in  the 
morning  and  drops  in  the  evening. 
This  is  the  so-called  inverted  type, 
and  is  usually  an  unfavorable  symp- 
tom. In  other  cases  the  tempera- 
ture chart  is  quite  irregular;  longer 
or  shorter  periods  of  persistent  ele- 
vation   alternate    with    periods    when 

there  is  no  fever.  Particularly  toward  the  end  of  the  disease,  as  the 
bodily  weakness  increases,  the  previously  regular,  intermitting  temperature 
grows  irregular.  At  this  time  the  intermissions  often  become  more  marked, 
and  not  infrequently  collapse  temperatures — 95°  to  93.2°  F.  (35°  to  34°  C.)  — 
are  observed.  Again,  the  fever  may  for  limited  periods  take  on  a  more  con- 
tinuous character,  probably  in  connection  with  exacerbations  of  the  tubercular 
process.  In  some  few  cases  with  acute  onset  (vide  supra)  we  have  also  seen, 
in  the  beginning  of  the  disease,  a  tolerably  high  and  approximately  continuous 
fever,  passing  gradually  into  the  ordinary  febris  hectica.  The  cause  of  the 
fever  in  pulmonary  tuberculosis  is  not  yet  settled.  The  special  question  is 
whether  the  tubercular  process  causes  the  fever  of  itself  (by  production  of 
toxins),  or  whether  the  fever  is  due  to  the  secondary  inflammatory  processes, 
such  as  the  absorption  of  septic  and  toxic  material  from  the  decomposing  con- 
tents of  the  bronchi  and  the  pulmonary  cavities.  The  practical  importance  of 
the  fever  in  pulmonary  tuberculosis  is  very  great.  The  emaciation  and  weak- 
ness of  the  patient  are  caused  mainly  by  fever  (vide  infra),  as  are  many  sub- 
jective symptoms,  including  headache,  chilliness,  and  perspiration.  It  is  im- 
portant to  remember  that  in  observations  of  the  fever  we  possess  one  of  the 
most  positive  means  of  forming  an  opinion  as  to  the  course  of  pulmonary 
tuberculosis.  In  cases  which  are  either  completely  stationary  or  very  chronic 
there  is  no  fever  at  all.  The  subfebrile  condition  shows  a  slow,  but  still  con- 
tinuous, advance  of  the  disease.  Continuous  hectic  fever  is  an  unfavorable 
sign,  and  indicates  a  comparatively  rapid  march  of  the  disease — the  more 
rapid,  the  higher  the  evening  temperature.  In  the  florid  or  galloping  forms 
we  find  tolerably  high  fever,  at  times  continuous  and  at  times  remittent.  Sub- 
normal temperatures  are  almost  always  of  bad  omen. 

All  changes  in  the  general  course  of  the  disease  for  better  or  worse  stamp 


300  DISEASES   OF  THE   RESPIRATORY   ORGANS 

themselves  clearly  on  the  temperature  chart.  The  onset  of  complications  and 
secondary,  disease  is  often  first  indicated  by  the  thermometer.  Whether  an 
attack  of  hemoptysis  passes  over  without  permanent  damage,  or  whether  it  is 
followed  by  an  aggravation  of  the  disease,  can  usually  be  told  by  the  tem- 
perature sooner  than  in  any  other  way  (vide  supra,  page  290).  Thus  we  see 
that  the  persistent  and  careful  observation  of  the  temperature  in  consumption 
deserves  to  rank  as  one  of  the  most  important  means  of  estimating  the  status 
and  course  of  the  illness. 

Emaciation. — The  great  emaciation  of  the  patient  is  very  striking  in  most 
cases  of  phthisis.  The  muscular  system  and  the  fatty  tissue  are  affected  in 
equal  degree.  The  soft  parts  of  the  thorax  are  often  especially  involved. 
The  emaciation  is  due  in  part  to  the  patient's  loss-  of  appetite,  and  to  the 
small  amount  of  food  which  he  takes  in  consequence  thereof,  but  the  chief 
cause  lies  in  the  persistent  fever  and  the  increased  metamorphosis  of  tissue. 
Quite  a  high  degree  of  emaciation,  however,  may  appear  in  the  beginning  of 
the  disease  with  no  fever.  This  we  are  wont  to  ascribe  to  the  "  general  ill- 
ness," but  the  special  cause  of  it  is  unknown.  Under  favorable  external  con- 
ditions phthisical  patients  may  make  quite  a  decided  gain  in  weight,  especially 
at  the  times  when  they  are  free  from  fever.  In  very  chronic  cases,  which  run 
their  course  from  the  first  without  fever,  the  nutrition  of  the  patient  may 
remain  good  for  a  long  time.  Toward  the  end  of  the  disease  emaciation  some- 
times reaches  its  highest  degree,  and  many  phthisical  patients  die  "  wasted 
to  a  skeleton  "  in  the  true  sense  of  the  word. 

Anamiia — Color  of  the  Stein. — In  most  cases  anaemia  appears  in  the  course 
of  the  disease,  to  be  recognized  by  the  pale  and  sallow  color  of  the  skin  and  of 
the  visible  mucous  membranes.  The  anaemia  only  rarely  reaches  that  degree  of 
peculiar  waxy  pallor  that  is  found  in  idiopathic  pernicious  anaemia.  If  the 
pallor  is  extreme,  however,  there  is  usually  some  special  reason,  such  as  profuse 
hemoptysis  or  the  complication  of  amyloid  degeneration.  The  existence  of  the 
anaemia  is  also  the  reason  why  the  phthisical  patient  does  not  look  cyanotic 
in  spite  of  the  respiratory  disturbance.  In  the  more  chronic  forms,  where 
the  general  nutrition  suffers  less,  we  often  see  a  cyanotic  coloring  of  the  lips 
and  cheeks.  Sometimes  the  skin  of  phthisical  patients  assumes  a  dirty,  dusky 
hue.  We  have  already  spoken  of  the  circumscribed  "  hectic  flush  of  the 
cheeks  "  seen  with  the  fever. 

General  Weakness — Night-sweats — Nervous  Disturbances. — We  need  not 
say  that  the  general  emaciation  and  anaemia  are  accompanied  by  a  marked 
decline  in  the  patient's  strength.  He  finally  becomes  so  helpless  that  he  can 
scarcely  move  alone  in  the  bed. 

The  tendency  which  very  many  patients  have  to  severe  night-sweats  is  uni- 
versally acknowledged  but  not  wholly  explained.  It  may  have  some  connection 
with  the  fall  from  the  evening  febrile  temperature  to  the  morning  remission, 
and  perhaps  it  is  due  to  the  greater  accumulation  of  carbonic  acid  in  the  blood 
from  the  disturbance  of  respiration. 

The  disease  has  remarkably  little  influence  upon  the  higher  nervous  func- 
tions, especially  those  of  the  mind.  Most  patients  have  a  perfectly  clear  in- 
tellect to  their  latest  breath.  We  all  know  the  contented,  hopeful,  sanguine 
disposition  of  many  patients,  who  do  not  recognize  their  own  danger  until 
the  last  stages  of  the  disease.     Occasionally  the  anaemia  and  the  general  dis- 


TUBERCULOSIS   OF   THE    LINGS  301 

turbance  of  the  nutrition  of  the  brain  lead  to  mental  alterations,  such  as  eon- 
fusion,  distraction,  or  melancholic  conditions. 

We  find,  more  frequently,  disturbances  in  the  peripheral  nerves  and  mus- 
cles. Among  these  are  neuralgic  pains,  and  pains  of  an  indefinite  character, 
which  have  their  seat  in  the  legs,  or  sometimes  in  the  arms,  especially  in  the 
ulnar  region  and  the  sciatic  nerve.  These  may  be  very  distressing.  .Marked 
hyperaesthesia  of  the  skin  and  deeper  parts  is  also  not  uncommon.  The  cause 
of  such  disturbances  is  probably  often  to  be  looked  for  in  the  degenerative 
changes  in  the  peripheral  nerves  (Vierordt  and.  others).  Well-marked  mul- 
tiple neuritis  has  been  repeatedly  observed  in  tuberculous  patients  (see 
Vol.  II). 

We  very  often  see  an  increased  reaction  upon  direct  mechanical  irritation 
in  the  emaciated  muscles,  and  great  liveliness  of  the  so-called  idiomuscular 
contractions,  which  is  shown,  for  example,  on  percussing  the  pectoral  muscles 
on  the  anterior  wall  of  the  chest.  The  phenomena  grouped,  under  the  name  of 
tendon  reflexes  are  also  much  increased  in  phthisis. 

4.  Symptoms  and  Complications  on  the  Part  of  Other  Organs. — 1.  Pleura. 
— In  pulmonary  tuberculosis  the  pleura  is  also  involved,  as  a  rule.  The  affec- 
tion is  almost  always  the  result  of  a  direct  extension  of  the  process  from  the 
lung  to  the  pleura.  At  the  autopsy,  we  find  in  the  pleura  a  few  or  many 
miliary  tubercles,  besides  the  simple  inflammatory  process — tuberculous 
pleurisy. 

In  many  cases,  in  which  we  have  to  do  only  with  an  adhesive  pleurisy  and 
with  pleuritic  contraction,  we  can  merely  suspect  the  disease  of  the  pleura,  but 
it  cannot  be  directly  made  out  and  differentiated  clinically  from  the  pulmonary 
affection.  In  other  cases  we  can  diagnosticate  a  dry  pleurisy  in  phthisis  from 
the  occurrence  of  the  pleuritic  friction  rub.  The  symptoms  of  pleurisy  become 
more  marked  if  there  is  a  pleuritic  effusion,  which  is  usually  readily  discovered 
by  a  physical  examination.  The  patient's  pain  and  dyspnoea  are  usually  much 
increased  by  such  a  complication.  Besides  a  simple  serofibrinous  effusion  we 
quite  frequently  find  purulent  and  even  hemorrhagic  effusions  in  tuberculosis 
of  the  pleura. 

The  formation  of  pneumothorax  is  an  important  complication  in  the  pleura 
in  phthisis.  It  is  due  to  the  rupture  of  a  superficial  pulmonary  cavity  into  the 
pleural  cavity,  and  the  entrance  of  air  into  the  latter.  The  different  forms  of 
pneumothorax  and  its  symptoms  will  be  described,  under  diseases  of  the  pleura. 

2.  Larynx,  Trachea,  and  Pharynx — Buccal  Cavity. — The  symptoms  of  lar- 
yngeal tuberculosis  and  their  relation  to  pulmonary  tuberculosis  have  already 
been  given  under  diseases  of  the  larynx  (see  page  178).  We  saw  there  that, 
although  there  is  a  primary  laryngeal  tuberculosis,  most  cases  are  secondary  in 
their  development  to  a  pulmonary  tuberculosis. 

The  same  holds  true  in  regard  to  the  much  rarer  tuberculosis  of  the  phar- 
ynx. In  some  cases  this  may  be  of  primary  origin,  but  it  is  usually  a  result 
of  reinoculation  with  tuberculosis  by  means  of  the  sputum,  or  of  a  direct 
extension  of  the  tubercular  process  from  the  larynx  to  the  pharynx.  Tuber- 
cular ulcers  of  the  pharynx  are  found  most  frequently  on  the  soft  palate,  on 
the  tonsils,  on  the  root  of  the  tongue,  and  on  the  boundary  between  the 
pharj'nx  and  the  larynx;  they  are  rare  in  other  parts  of  the  pharynx.  In 
exceptional  cases  tuberculous  affections  are  seen  in  the  mouth — on  the  tongue. 


302  DISEASES   OF  THE   RESPIRATORY  ORGANS 

The  local  discomforts  which  all  these  ulcers  cause  is  usually  very  considerable. 
Disseminated  miliary  tubercles,  too,  have  been  repeatedly  seen  in  the  mucous 
membrane  of  the  pharynx.  Pronounced  thrush  formation  sometimes  develops 
in  the  pharynx  of  patients  who  are  very  ill. 

3.  Stomach  and  Intestinal  Canal — Peritoneum. — Tubercular  ulcers  in  the 
mucous  membrane  of  the  stomach  are  exceedingly  rare,  but  we  very  often 
notice  some  symptoms  on  the  part  of  the  stomach.  Loss  of  appetite  is  a  par- 
ticularly common  symptom  in  phthisis.  Vomiting  occurs  often  in  phthisical 
patients,  especially  when  the  larynx  is  involved.  It  is  usually  brought  on  by 
paroxysms  of  coughing.  Less  frequently  the  cause  of  the  vomiting  is  gastric 
catarrh,  occasioned  by  the  irritation  of  the  sputa  which  have  been  swallowed; 
but  in  some  cases  the  gastric  symptoms  depend  upon  the  general  condition — 
e.  g.,  the  anaemia. 

Although  the  tubercle  bacilli  swallowed  with  the  sputum  hardly  ever  infect 
the  stomach,  probably  from  the  acid  reaction  of  its  contents,  they  very  often 
attack  the  intestinal  canal.  In  the  majority  of  the  cases  of  phthisis  we  find 
tubercular  ulcers,  either  singly  or  in  considerable  numbers,  in  the  vicinity  of 
Bauhin's  valves  [the  ileocecal  valve],  in  the  lower  part  of  the  ileum,  and  the 
upper  part  of  the  large  intestine. 

Intestinal  tuberculosis  (q.  v.)  does  not  always  cause  very  marked  clinical 
symptoms,  but,  as  a  rule,  we  find  diarrhea  in  patients  with  tubercular  ulcers  of 
the  intestine.  They  may  have  three  or  four  stools  in  the  twenty-four  hours, 
and  even  more,  but  the  stools  have  nothing  characteristic.  We  rarely  see 
a  slight  admixture  of  pus  or  blood  in  them.  Tubercle  bacilli  have  been  repeat- 
edly discovered  in  the  dejections,  but  the  search  for  them  is  rather  difficult. 
We  must  call  attention,  however,  to  the  fact  that  many  patients  have  diarrhea 
during  life  in  whom  we  find  at  the  autopsy  no  intestinal  tuberculosis,  but 
only  a  simple  intestinal  catarrh.  Severe  diarrhea  of  a  persistent  and  refrac- 
tory character  may  also  occur  in  association  with  amyloid  degeneration  of  the 
intestine,  which  is  not  infrequently  seen  in  connection  with  other  amyloid 
changes.  Sometimes  tubercular  ulcerations  of  the  intestine  are  found  at 
autopsy  which,  during  life,  had  caused  no  diarrhea. 

In  cases  of  severe  intestinal  tuberculosis  we  sometimes  meet  with  meteor- 
ism.  With  deep  ulcers,  extending  to  the  peritoneum,  we  often  find  marked 
tenderness  of  the  abdomen. 

The  peritoneum  may  be  affected  by  the  tubercular  ulcers  of  the  intestine 
in  a  twofold  manner.  Genuine  peritonitis  from  perforation,  with  a  purulent 
or  even  a  sanious  exudation,  is  quite  rare,  and  is  excited  by  the  rupture  of 
an  ulcer  and  the  entrance  of  the  contents  of  the  intestine  into  the  abdominal 
cavity.  An  infection  of  the  peritoneum  with  the  tuberculous  poison  is  more 
frequent.  This  may  arise  from  deep-seated  ulcers,  which  do  not  reach  actual 
perforation,  so  that  we  have  a  peritoneal  tuberculosis  or  a  tuberculous  perito- 
nitis. During  life  peritonitis  from  perforation  and  that  from  tuberculosis  are 
not  always  to  be  distinguished.  We  must  also  mention  that  simple  ascitic 
fluid  is  sometimes  found  in  the  abdominal  cavity  in  phthisis,  which  may  lead 
to  a  false  diagnosis  of  peritoneal  tuberculosis. 

Another  way  in  which  we  have  a  peritoneal  tuberculosis  in  the  course  of 
phthisis  is  from  the  extension  of  the  process  in  a  tuberculous  pleurisy,  through 
the  diaphragm  to  the  peritoneum. 


TUBERCULOSIS   OF  THE   LUNGS  303 

4.  Liver  and  Spleen. — We  very  often  find  a  few  or  even  many  tubercles  in 
the  liver  in  phthisis,  but  they  have  no  clinical  significance.  Tin-  liver  i-: 
almost  always  infected  with  the  tuberculous  poison  from  tubercular  ulcers  in 
the  intestines,  from  which  the  poison  passes  to  the  branches  of  the  portal  vein 
and  then  to  the  liver.  Fatty  liver  and  amyloid  or  lardaceous  liver  are  more 
important  clinical  changes.  We  can  sometimes  recognize  tin.'  former  by  mak- 
ing out  on  physical  examination  the  increase  in  the  size  of  the  organ,  and  by 
feeling  its  characteristic  blunt  lower  edge.  Moreover,  we  must  empha.-iy 
the  fact  that,  in  our  experience,  fatty  infiltration  of  the  liver  is  found  much 
more  rarely  at  the  autopsy  of  consumptive  subjects  than  the  statements  of 
many  earlier  authors  would  lead  one  to  expect.  Still,  the  occasional  finding 
of  a  pronounced  fatty  liver  in  an  otherwise  extremely  emaciated  phthisical 
body  is  a  very  striking  though  not  yet  fully  explained  circumstance.  It 
would  almost  appear  as  if  the  fat  had  migrated  from  the  tissues  to  the  liver, 
and  remained  there  in  part  in  a  nonoxidized  state. 

Amyloid  degeneration  of  the  liver  appears  almost  always  in  association 
with  amyloid  change  in  other  organs  (kidneys,  spleen,  intestine).  If  the 
amyloid  degeneration  is  advanced,  the  liver  is  considerably  enlarged,  and  it  is 
usually  possible  to  feel  distinctly  its  sharp  and  resistant  edge;  and,  not  infre- 
quently also,  its  firm  upper  surface. 

Miliary  tubercles  or  single  large  tubercular  nodules  in  the  spleen  have  a 
pathological  interest  only.  Great  splenic  enlargement  is  found  in  amyloid 
degeneration. 

5.  Kidneys,  Urinary  Passages,  and  Sexual  Organs. — The  presence  of  mil- 
iary tubercles  in  the  kidneys  is  the  first  change  in  them  to  be  mentioned,  but 
it  has  no  clinical  significance.  Extensive  tuberculosis  of  the  genito-urinary 
apparatus,  however,  may  produce  marked  symptoms,  such  as  pyuria.  Genito- 
urinary tuberculosis  will  be  discussed  in  a  later  part  of  this  work.  In  regard 
to  the  symptoms  of  amyloid  kidney,  which  may  develop  in  the  course  of 
phthisis  in  connection  with  amyloid  disease  in  other  organs,  we  will  refer  to 
the  section  on  renal  diseases. 

Genuine  cases  of  nephritis,  both  acute  and  chronic,  are  also  found  quite 
frequently  in  phthisis,  often  combined  with  amyloid  disease.  We  have  also 
observed  chronic,  hemorrhagic  nephritis.  The  extent  to  which  the  kidneys 
are  affected  cannot  escape  notice  if  the  urine  is  carefully  examined.  The 
development  of  nephritis  is  probably  always  referable  to  the  excretion  of  toxic 
material,  arising  from  the  disease  in  the  lung. 

6.  Circulatory  Organs — Blood. — The  rate  of  the  pulse  is  often  increased  in 
consumption.  This  increase  in  frequency  may  be  merely  proportional  to  the 
fever,  if  any  exists.  It  is  also  usually  seen  and  it  may  be  considerable  when 
there  is  no  fever.  A  persistently  rapid  pulse,  when  the  temperature  is  little,, 
if  at  all,  elevated,  may  therefore  be  an  important  diagnostic  sign  of  pulmonary 
(and  all  other)  tuberculous  diseases.  The  increase  of  the  pulse,  which  readily 
comes  on  from  comparatively  trifling  external  causes,  is  especially  noteworthy. 
It  may  be  seen  after  slight  physical  exertion,  or  upon  mental  excitement,  as 
during  the  physician's  visit. 

Anatomical  changes  in  the  heart  are  rare,  except  that  it  is  often  remark- 
ably small  and  flaccid.  Moderate  fatty  degeneration  of  the  heart,  slight 
endocarditis  of  the  valves,  or  occasional  tubercles  in  the  heart,  cause  no  symp- 


304  DISEASES   OF  THE   RESPIRATORY   ORGANS 

toms.  The  occurrence  of  tuberculous  pericarditis,  however,  is  important. 
This  almost  always  arises  from  the  extension  of  the  tubercular  process  from 
the  adjacent  pleura,  but  in  exceptional  cases  pericarditis  has  been  seen  as  a 
result  of  rupture  of  a  tuberculous  lymph-gland  or  a  pulmonary  cavity  into  the 
pericardium.  In  many  cases  of  tuberculosis  the  blood  shows  a  simple  anaemia. 
As  a  rule,  the  number  of  red  blood  cells  is  not  lowered  as  much  as  is  the  per- 
centage of  hemoglobin.  A  moderate  polynuclear  leucocytosis,  with  a  lowered 
proportion  of  lymphocytes,  is  often  found  in  advanced  tuberculosis  with 
fever.  In  cases  with  severe,  persistent  dyspnoea  (compensatory?)  increase  in 
the  red  blood  cells  and  hemoglobin  is  sometimes  observed. 

7.  Lymph-glands. — The  lymph-glands  are  a  favorite  seat  for  tuberculous 
changes.  We  have  stated  above  that  the  so-called  scrofulous,  cheesy  lymph- 
glands,  which  are  seen  chiefly  in  the  neck  and  the  axillae,  are  affected  with 
tubercle  in  the  majority  of  cases.  The  tuberculous  infection  probably  develops 
here  from  slight  injuries  and  excoriations  of  the  skin,  by  which  the  bacilli 
enter  the  body  and  reach  the  neighboring  glands  by  means  of  the  lymph  cur- 
rent. In  other  cases  the  infection  comes  perhaps  from  the  mucous  membrane 
of  the  pharynx.  In  tuberculosis  of  internal  organs,  too,  we  very  often  find  the 
corresponding  lymph-glands  enlarged  and  more  or  less  cheesy.  The  bronchial 
lymph-glands  are  swollen  as  a  result  of  pulmonary  tuberculosis,  the  mesenteric 
and  retroperitoneal  glands  as  a  result  of  intestinal  tuberculosis.  The  tuber- 
culosis of  the  bronchial  lymph-glands  is  of  especial  importance  in  children. 
Indeed,  the  tuberculous  virus  which  has  gained  access  to  the  lungs  may  appar- 
ently reach  the  bronchial  glands  by  means  of  the  lymph-channels,  passing 
through  without  affecting  the  lungs  themselves,  and  occasion  a  tuberculous  dis- 
ease of  the  glands.  Bronchial  glands,  thus  diseased,  may  involve  the  lungs 
by  direct  or  indirect  (via  the  lymph-channels)  infection.  Eecently,  as  above 
mentioned  (page  277),  there  has  been  a  tendency  to  refer  primary  tuberculous 
disease,  even  in  adults  (in  some  cases,  at  least),  to  the  bronchial  lymph-nodes. 

Pressure  from  the  enlarged  glands  may  affect  the  air-passages,  the  branches 
•of  the  pulmonary  artery,  the  veins,  the  recurrent  nerve  (paralysis  of  the 
vocal  cords),  and  even  the  aorta.  Perforation  of  the  cheesy  bronchial  glands 
into  the  oesophagus,  the  blood  vessels,  etc.,  has  also  been  observed.  Tubercu- 
losis of  the  bronchial  glands  does  not  present  any  definite  type  of  disease, 
however.  Very  doubtful,  too,  is  the  interpretation  of  any  statements  con- 
cerning painful  points  in  the  back,  or  certain  painful  sensations  felt  in  conse- 
quence of  pressure  upon  the  bronchial  lymph-glands  by  means  of  a  bougie 
in  the  oesophagus.  X-ray  examination  (see  Plate  II)  gives  by  far  the  most 
certain  clew  to  the  diagnosis  of  tuberculosis  of  the  bronchial  glands,  if  the 
plates  are  examined  without  bias  by  experienced  men.  The  author  himself 
observed  a  noteworthy  case  of  tuberculosis  of  the  bronchial'  glands,  with 
compression  of  one  vagus  nerve  in  a  patient  who,  during  life,  for  weeks 
coughed  up  large  amounts  of  a  purely  seromucous  expectoration  containing  no 
bacilli. 

8.  Nervous  System. — We  have  already  mentioned  various  nervous  symp- 
toms in  the  description  of  the  general  symptoms.  We  must  also  add  that 
tuberculous  meningitis  is  seen  at  the  termination  of  phthisis  (see  Vol.  II), 
and  that  large  solitary  tubercles  may  occasionally  develop  in  the  central  nerv- 
ous system. 


TUBERCULOSIS   OF  THE   LUNGS  305 

9.  Skin. — We  have  spoken  of  the  great  tendency  which  many  patients  have 
to  severe  sweats,  especially  at  night.  The  frequent  appearance  of  pityria-j- 
versicolor,  especially  on  the  skin  over  the  thorax,  is  also  worthy  of  note.  We 
■often  see  moderate  cedema  of  the  legs  and  ankles,  which  is  due  to  weakness 
of  the  heart.  More  marked  oedema  of  one  leg  sometimes  arises  from  throm- 
bosis of  the  femoral  vein.  We  must  also  mention  here,  in  conclusion,  the 
specific  tuberculous  disease  of  the  skin,  lupus,  and,  in  addition,  the  so-called 
•cutaneous  tuberculides.  The  manner  of  infection  is  very  evident  in  some  cases. 
Thus,  for  example,  in  a  woman  who  had  for  a  long  time  washed  the  soiled 
handkerchiefs  of  a  very  sick  consumptive,  I  observed  a  tuberculous  skin  lesion 
of  the  nature  of  the  so-called  "  post-mortem  tubercle,"  formerly  so  commonly 
seen  among  pathologists.  In  this  case  the  source  of  infection  was  very  evi- 
dently the  sputum.  The  details  of  the  different  types  of  tuberculous  skin  dis- 
ease are  to  be  found  in  special  works  on  the  subject. 

DIAGNOSIS 

The  diagnosis  of  pulmonary  tuberculosis  has  become  absolutely  certain, 
since  the  discovery  of  the  tubercle  bacilli,  by  the  demonstration  of  their  pres- 
ence in  the  sputum  (vide  supra).  In  all  incipient  cases,  in  which  the  other 
symptoms  of  the  disease  have  not  yet  made  themselves  manifest,  but  the  sus- 
picion of  incipient  phthisis  has  been  aroused  by  a  persistent  cough,  by  marked 
pallor  and  emaciation,  by  slight  hoarseness,  by  an  evening  rise  of  temperature, 
by  the  appearance  of  night-sweats,  by  the  presence  of  a  hereditary  predisposi- 
tion, and  similar  symptoms,  the  finding  of  tubercle  bacilli  in  the  sputum  is 
often  the  sole  deciding  factor.  If  no  sputum  can  be  obtained,  the  exhibition 
of  sodium  iodid  may  stimulate  expectoration.  Still,  it  must  not  be  forgot- 
ten that  the  examination  for  bacilli  is  decisive  only  when  its  result  is  posi- 
tive, and  that  the  greatest  attention  should  be  given  also  to  all  the  other 
symptoms.  To  form  an  opinion  as  to  the  severity  of  a  particular  case,  and  as 
to  its  exact  distribution  and  the  variety  of  the  tubercular  process,  is  at  pres- 
ent possible  only  by  means  of  a  consideration  of  the  other  symptoms,  and  in 
particular  of  the  results  of  physical  examination.  The  latter,  therefore,  has 
lost  none  of  its  importance  by  the  discovery  of  the  tubercle  bacilli.  Con- 
fusion between  phthisis  and  other  diseases  is  twofold.  Where  the  constitu- 
tional symptoms  are  predominant,  and  there  are  no  marked  pulmonary  symp- 
toms, an  existing  tuberculosis  may  be  overlooked.  In  the  beginning,  espe- 
cially, many  cases  of  phthisis  are  considered  to  be  merely  anaemia,  chronic 
gastric  catarrh,  or  simple  bronchitis.  If  a  continuous  or  intermitting  fever- 
appears  in  an  early  stage  of  phthisis,  before  any  marked  pulmonary  symptoms 
have  developed,  the  disease  may  be  mistaken  for  malaria  or  the  like.  On 
the  other  hand,  it  is  by  no  means  rare  to  consider  patients  phthisical  who  are 
suffering  from  some  entirely  different  affection.  Severe  latent  diseases  of 
the  stomach,  or  certain  general  diseases,  such  as  anaemia,  diabetes,  or  chronic 
nephritis,  may  be  mistaken  for  phthisis.  Other  pulmonary  affections,  too, 
may  be  confounded  with  tuberculosis,  especially  chronic  bronchitis,  emphy- 
sema, bronchiectasis,  fetid  and  gangrenous  processes,  and  carcinoma  of  the 
lungs.  A  careful,  unprejudiced,  and  complete  examination  of  the  patient  is 
the  only  possible  protection  against  such  errors.     It  is  very  important  for  the 


306  DISEASES   OF   THE   RESPIRATORY   ORGANS 

physician  to  know  that  there  is  such  a  thing  as  hypochondriacal  phthiseo- 
phobia.  Some  nervous  individuals  are  tormented  by  a  constant  dread  of 
becoming  consumptive.  Such  persons  complain  of  thoracic  pain,  dry  cough, 
weakness,  and  other  imaginary  sjanptoms,  which  might  readily  mislead  the 
physician  into  supposing  that  they  actually  have  incipient  pulmonary  tuber- 
culosis. A  mistake  is  especially  apt  to  be  made  if  the  patient  claims  to  have 
suffered  from  hemojrtysis.  The  experienced  physician  will  usually  be  struck 
by  the  fact  that  the  "  hemoptysis  "  is  said  to  have  recurred  in  slight  amounts 
almost  daily,  and  has  lasted  for  weeks.  A  thorough  examination  usually  dis- 
closes the  nasopharynx  or  the  gums  as  the  source  of  the  bleeding  (compare 
with  remarks  on  the  so-called  hysterical  hemoptysis  in  Yol.  II  of  this  work). 
Of  course,  the  correct  interpretation  of  such  conditions  is  usually  no  difficult 
matter  to  the  experienced  physician,  who  is  guided  by  the  general  impression 
of  "  nervousness,"  and  by  the  complete  absence  of  any  objective  physical  signs. 

In  this  connection  we  ought,  furthermore,  to  express  our  opinion  of  the 
diagnostic  value  of  Koch's  tuberculin  {vide  infra).  Koch  made  the  impor- 
tant discovery  that  tuberculous  patients,  particularly  those  suffering  with 
pulmonary  tuberculosis,  exhibit  a  particular  "  reaction "  after  the  injection 
of  small  amounts  of  tuberculin  (gm.  0.001  to  0.002  of  Koch's  preparation). 
When  this  reaction  occurs  there  develops,  some  four  or  five  hours  after  the 
injection,  a  fever  of  102°  to  104°  F.  (39°  to  40°  C),  associated  with  chilliness, 
headache,  pain  in  the  limbs,  nausea,  and  languor.  This  constitutional  reac- 
tion passes  off  after  some  twelve  or  fifteen  hours.  If  the  tubercular  process 
is  located  in  the  skin,  trachea,  or  some  other  part  where  it  is  accessible  to- 
direct  observation,  a  very  decided  local  reaction  may  usually  be  observed  be- 
sides the  constitutional  disturbance.  The  tuberculous  tissue  becomes  swollen, 
red,  and  finally  in  part  necrotic.  In  patients  with  tuberculosis  of  the  internal 
organs,  also,  this  local  reaction  probably  takes  place,  but  of  course  it  cannot 
be  actually  seen,  although  it  may,  perhaps,  be  inferred  because  of  the  secondary 
phenomena.  Thus,  in  pulmonary  tuberculosis  there  may  be  an  increase  in 
the  cough  and  expectoration.  On  the  other  hand,  if  an  injection  of  tubercu- 
lin is  made  in  a  person  who  is  healthy,  or  who  is  suffering  from  some  disease 
other  than  tuberculosis,  then,  according  to  Koch,  there  will  be  no  reaction 
at  all  to  small  doses.  To  obtain  any  reaction  in  persons  who  are  healthy,  or, 
at  any  rate,  not  tuberculous,  the  dose  of  Koch's  preparation  must  be  increased 
to  the  amount  of  gm.  0.01. 

These  statements  of  Koch  are,  in  general,  certainly  true,  but  subject  to 
several  exceptions.  Other  observers  as  well  as  the  present  author  have  occasion- 
ally found  that  healthy  persons,  or  persons  without  any  demonstrable  focus 
of  tuberculosis,  have  reacted  to  doses  of  1  or  2  mgm.  of  tuberculin ;  while,  on 
the  other  hand,  patients  with  indubitable  pulmonary  tuberculosis  have  shown 
no  distinct  reaction  even  to  considerable  doses  of  tuberculin.  Consequently, 
the  result  of  an  injection  of  tuberculin  can  never  be  completely  decisive  from 
a  diagnostic  point  of  view,  and  in  practice,  therefore,  the  employment  of 
tuberculin  for  diagnosis  has  been  adopted  by  comparatively  few.1  Still,  it 
would  be  a  mistake  to  discard  this  means  of  diagnosis  completely.     In  doubt- 

1  In  veterinary  practice,  the  tuberculin  test  is  employed  with  very  excellent  results  in  the 
diagnosis  of  bovine  tuberculosis. 


TUBERCULOSIS   OF  THE   LUNGS 


307 


ful  cases  the  injection  of  from  1  to  2  tngm.  of  tuberculin  is  of  real  impor- 
tance, and  the  result  of  the  test  is  certainly  a  valuable  item  in  summing  up 
such  a  case.     It  is  presupposed  that  the  patient's  temperature  is  carefully 

taken  for  two  to  three  days  (and  every  two  hours,  if  possible)  before  the 
tuberculin  injection  is  given.  If  the  temperature  has  been  entirely  norma], 
the  injection  of  even  a  small  dose  of  tuberculin  (0.5  mgm.  or  less)  will  be 
followed  by  a  distinct,  if  slight  (1°  to  2°  F.  [0.5°  to  1°  C.])3  elevation  of  tem- 
perature. But  it  is  just  the  fact  that  the  tuberculin  test  can  only  be  employed 
in  patients  free  from  fever  that  diminishes  its  practical  importance.  For  often 
it  is  precisely  in  patients  suffering  from  fever  that  we  wish  to  learn  if  there 
is  a  hidden  focus  of  tuberculosis. 

Very  interesting,  too,  are  the  observations  recently  made,  in  which  the 
inoculation  of  tuberculin  was  also  found  to  have  a  local  effect  differing  accord- 
ing to  whether  the  in- 
dividual is  suffering 
from  tuberculosis  or 
not.  According  to  Pir- 
quet,  if  a  drop  of  a 
twenty- five-per-cent,  or 
even  weaker,  solution  of 
tuberculin  be  introduced 
into  the  skin  through  a 
pin-point  hole  or  a  su- 
perficial scratch,  when 
tuberculosis  is  present 
in  an  individual,  a  dis- 
tinct cutaneous  reac- 
tion, consisting  of  more 
or  less  hyperemia  and 
swelling  (see  Fig.  55), 
will  appear  within 
twenty-four  to  forty- 
eight  hours  at  the  site 
of  the  vaccination.  In 
the  absence  of  tubercu- 
losis there  is  no  such 
reaction  whatever.  Cal- 
mette  and  Wolf -Eisner 
perform  the  test  by 
dropping  a  single  drop 
of  a  one-per-cent  solu- 
tion of  tuberculin  into 
the  conjunctival  sac  of 
the  eye.  An  ofttimes 
rather  intense  inflam- 
matory redness  of  the 
conjunctiva  (ophthalmic  reaction)  appears  after  twenty-four  hours  in  cases  of 
tuberculosis,  and  is  absent  in  healthy  individuals.  This  reaction  has  not  been 
widely  employed  in  medical  practice,  because  very  disagreeable  inflammations 


Fig.  55. — Pirquet  skin  reaction  (personal  observation),  a,  Re- 
action at  the  site  of  the  tuberculin  inoculation,  b,  Control 
scratch  without  tuberculin  inoculation. 


308  DISEASES   OF   THE   RESPIRATORY   ORGANS 

of  the  eye  have  occasionally  been  observed  after  its  use.  Its  diagnostic  value 
is  also  limited,  because  it  is  occasionally  absent  in  undoubted  cases  of  tubercu- 
losis and  present  in  individuals  in  whom  tuberculosis  is  not  even  suspected.. 
Although  the  practical  diagnostic  value  of  both  the  above-mentioned  tests  can- 
not, as  yet,  be  rated  very  highly,  they  are  of  great  theoretical  interest,  and 
certainly  deserve  thorough  further  study. 

Finally,  we  would  also  refer  to  the  great  diagnostic  value  of  X-ray  exami- 
nation (see  Plate  II)  in  pulmonary  tuberculosis,  especially  in  the  estimation 
of  doubtful  and  of  incipient  cases.  When  careful  technic  is  employed,  tuber- 
cular infiltrations  of  the  lungs  give  very  distinct  shadows,  but  a  trained  eye 
is  certainly  just  as  essential  for  their  interpretation  as  is  a  trained  ear  for 
the  proper  detection  of  differences  in  the  percussion  note.  Numerous  obser- 
vations in  recent  years  have  proved  to  me  that  all  tubercular  infiltrations  are 
easily  recognized  in  the  X-ray  pictures,  and  usually  correspond  exactly  with 
the  changes  in  percussion;  occasionally,  however,  they  may  even  stand  out. 
prominently  where  percussion  has  revealed  only  doubtful  changes  or  even 
none  at  all.  X-ray  examination  is,  at  any  rate,  an  extremely  valuable  pro- 
cedure in  the  establishment  of  a  diagnosis.  The  fact  is  also  very  important, 
that  tuberculous  bronchial  lymph-nodes  that  can  be  demonstrated  in  no  other 
way  often  appear  very  distinctly  in  X-ray  pictures  (P.  Krause  and  others). 
Their  presence  should  put  us  on  our  guard,  even  though  the  lungs  are  other- 
wise normal.  On  the  other  hand,  when  the  possibility  of  incipient  tubercu- 
losis is  being  considered,  there  is  nothing  that  gives  one  such  ease  of  mind 
with  respect  to  the  normal  state  of  the  lungs  as  the  demonstration  of  a  com- 
pletely uniform  clearness  in  the  X-ray  picture.  Naturally,  it  must  be  con- 
ceded that  under  some  circumstances  beginning  tuberculous  changes  in  the 
apices  (so-called  "apical  catarrh")  can  be  demonstrated  by  auscultation 
when  it  does  not  cast  any  distinct  X-ray  shadow.  The  so-called  Williams's 
sign  (early  limitation  or  absence  of  diaphragmatic  movements  on  the  diseased 
side)  is  not  of  great  importance,  inasmuch  as  it  is  but  rarely  observed.  When 
not  due  to  pleuritic  changes,  it  appears  to  be  due  to  a  lesion  of  the  phrenic 
nerve  at  the  apex  of  the  lung. 

At  the  conclusion  of  these  remarks  on  diagnosis,  I  would  point  out  that 
the  diagnosis  of  incipient  tuberculosis  should  never  be  based  on  a  single 
symptom,  but  on  the  study  of  the  whole  case.  After  several  days'  careful 
observation  of  the  temperature,  the  pulse,  physical  signs,  sputum,  X-ray 
picture,  and  perhaps  the  tuberculin  reaction,  a  correct  opinion  can  usually  be 
arrived  at. 

PROGNOSIS 

It  is  very  difficult  to  make  a  general  statement  as  to  the  prognosis  of  pul- 
monary tuberculosis.  There  is  no  doubt  that  tuberculous  foci  in  the  lungs, 
if  of  limited  extent,  may  become  completely  healed,  at  least  from  a  clinical 
point  of  view.  Indeed,  such  recovery  probably  takes  place  oftener  than  many 
suppose;  at  least,  it  is  not  very  exceptional  to  find  at  the  autopsy  of  elderly 
persons  cicatricial  contractions  in  the  apices  of  the  lungs  which  may,  without 
doubt,  be  regarded  as  healed  tuberculosis.  In  many  of  these  cases  the  previ- 
ous tuberculosis  had  never  come  to  the  knowledge  of  any  physician.  At  the 
present  day  the  discovery  of  tubercle  bacilli  in  the  sputum  has  rendered  the 


PLATE    IJ 


Fig.  1. — Radiogram  of  an  Advanced  Case  of 
Pulmonary  Tuberculosis.  Extensive  in- 
volvement of  the  left  lung  and,  to  a  lesser  de- 
gree, of  the  right. 


Fig.  2. — Radiogram  of  a  Case  of  Marked 
Tuberculous  Disease  of  the  Left  Lung. 
Large  cavity  at  c.  Slighter  involvement  of 
the  right  lung. 


Fig.  3. — Radiogram  of  a  Case  of  Beginning  Pulmonary  Tuberculosis. 
Both  sides  show  distinct  shadows  in  the  neighborhood  of  the  bronchial  glands. 


TUBERCULOSIS  OF   THE    LUNGS  309 

diagnosis  of  even    very   limited    tubercular   processes   an   easy   matter,   and, 
consequently,  cases  of  recovery   from  pulmonar}   tuberculosis  are  now    re< 
nized  much  more  often  than  formerly. 

Nevertheless,  the  prognosis  of  pulmonary  tuberculosis  musl  alwa 
garded  even  now  us  very  serious,  and  when  the  disease  has  made  any  great 
progress  the  prognosis  is  decidedly  unfavorable.  Many  cum--:  of  apparent 
recovery  exhibit  merely  a  temporary  improvement,  to  grow  worse  again,  and 
the  assertion  that  treatment  is  absolutely  hopeless  in  almosl  all  cases  in  which 
the  disease  has  reached  an  advanced  stage  is,  unfortunately,  too  well  estab- 
lished to  require  elaborate  argument. 

There  is,  however,  one  fact  of  extreme  importance  which  should  never  be 
disregarded  in  the  prognosis  of  pulmonary  tuberculosis.  There  is  a  great 
difference  in  the  duration  of  the  disease.  It  is  possible  for  the  process  to 
go  on  for  years,  while  the  patient  feels  tolerably  well,  and  yet  the  disease 
smolders.  From  this  point  of  view  cases  may  be  distinguished  as  "  benign," 
compared  with  those  of  rapid  progress,  and  this  prognostic  distinction  has 
the  greatest  importance  in  practice,  although  it  is  often  very  difficult  to  recog- 
nize. Many  a  consumptive,  when  first  examined,  gives  one  the  impression 
that  he  cannot  live  a  fortnight  longer,  and  yet  the  disease  lasts  many  months, 
with  improvement  in  most  of  the  symptoms  and  general  alleviation  of  the 
patient's  condition.  Again,  one  believes  the  disease  to  be  incipient,  encour- 
ages the  family,  and  the  patient  dies  in  a  few  weeks  of  galloping  consumption. 

Certain  complications  may  occur  which  it  is  impossible  to  foresee,  such  as 
pulmonary  hemorrhage,  pneumothorax,  tuberculous  meningitis,  and  miliary 
tuberculosis.  Apart  from  these,  however,  there  are  certain  conditions  which 
lead  us  to  expect  a  comparatively  favorable  course  for  the  disease:  such  are  a 
vigorous  constitution  unimpaired  by  bad  habits,  of  which  drinking  is  par- 
ticularly unfavorable ;  a  good  weight ;  freedom  from  hereditary  taint ;  limited 
extent  of  the  local  process,  and  moderate  age  [experience  has  shown  that  all 
cases  of  tuberculosis  beginning  in  individuals,  say,  over  thirty,  give  a  better 
prognosis,  in  general,  than  do  those  beginning  in  earlier  life]  ;  the  absence 
of  complications;  and,  finally,  the  persistent  absence  of  fever.  This  last 
factor  is  so  important  that  we  must  lay  special  stress  upon  it.  If  there  is 
no  fever  whatever  in  a  case  of  pulmonary  tuberculosis,  the  patient  is  at  that 
time  in  a  condition  in  which  the  disease  is  quiescent;  and  a  decided  improve- 
ment, perhaps  even  cure,  may  be  expected  if  appropriate  means  are  employed. 
On  the  other  hand,  whenever  fever  appears  we  know  that  the  disease  is  not 
quiescent,  but  is  actively  advancing  with  more  or  less  rapidity.  The  impor- 
tant points  about  the  temperature  in  this  regard  have  been  already  emphasized 
(see  page  298).  It  is  self-evident,  also,  that  the  worldly  circumstances  of 
the  patient,  as  well  as  the  factors  which  we  have  just  alluded  to,  are  of  great 
prognostic  importance.  On  these,  for  instance,  depends  the  possibility  of 
proper  care,  of  abundant  nourishment,  and,  it  may  be,  of  a  change  of  climate. 

TREATMENT 

1.  Prophylaxis. — The  question  of  what  prophylactic  measures  may  effec- 
tually prevent  the  extension  of  the  disease  has  entered  upon  a  new  stage  since 
our  definite  knowledge  as  to  the  infectious  nature  of  tuberculosis.     We  can 
20 


310  DISEASES  OF  THE  RESPIRATORY  ORGANS 

no  longer  doubt  the  contagious  character  of  phthisis,  in  support  of  which 
isolated  examples  were  previously  brought  forward.  Even  if,  according  to 
all  experience,  the  danger  of  contagion  is  not  very  great,  still,  it  is  foolish 
to  ignore  it  entirely.  We  must  therefore  call  the  attention  of  the  relatives 
of  phthisical  patients  to  the  possibility  of  this  danger,  and  we  should  not 
permit  the  children  of  such  patients  to  be  uselessly  exposed  to  it.  We  should 
take  satisfactory  precautions  for  isolation,  and  also  for  disinfection  of  the 
sputum.  Suitable  sputum  cups  should  be  employed,  and  care  should  also 
be  taken  to  prevent  the  dissemination  of  the  expectoration,  either  in  its  fresh 
state  or  after  it  has  become  dry.  The  future  will  teach  us  whether  much  evil 
may  not  be  averted  by  such  measures. 

The  "  prophylaxis  "  till  now  employed  was  almost  exclusively  confined  to 
hardening  and  strengthening  the  threatened  individual  as  much  as  possible. 
We  should  try  to  strengthen  the  bodies  of  children  of  a  weak  habit,  with 
"  scrofulous  "  symptoms,  and  children  from  families  in  which  cases  of  tuber- 
culosis have  already  occurred,  and  thus  to  arm  them  against  the  enemy  that 
threatens  them.  Good  food,  fresh  air,  and  a  diminution  of  the  sensitiveness 
of  the  body  by  cold  sponging  and  cold  baths — these  are  factors  whose  favorable 
influence  is  generally  recognized,  but  should  also  not  be  overestimated. 

The  removal  of  certain  foci  of  tuberculous  disease,  already  existing,  from 
the  body  may  prove  of  great  prophylactic  importance.  We  refer  to  the  timely 
treatment  or  extirpation  of  scrofulous — that  is,  tuberculous — swellings  of  the 
lymph-glands,  healing  or  resection  of  tuberculous  bones  and  joints,  etc.  Al- 
though in  individual  cases  we  can,  of  course,  never  know  whether  the  part 
removed  is  the  sole  focus  of  disease  in  the  body,  still,  we  are  undoubtedly  justi- 
fied in  trying  to  remove  at  least  one  possible  source  of  some  later  general 
infection.  A  fuller  discussion  of  this  important  point  must  be  left  to  the 
works  on  surgery. 

2.  Therapeusis. — Physicians  have  often  thought  that  they  had  discovered 
a  specific  remedy  for  tuberculosis,  but  apparently  they  have  thus  far  been 
mistaken.  Formerly,  the  inhalation  of  antiseptic  substances,  such  as  carbolic 
acid,  benzoate  of  sodium,  lignosulphite,  and  iodoform,  was  recommended,  but 
this  practice  is  now  almost  entirely  given  up.  Arsenic  was  for  a  time  much 
used,  best  given  in  pills  containing  ^  gr.  (gm.  0.003)  repeated  several  times 
a  day;  but  this  practice,  again,  has  not  held  its  own.  Arsenic  may  be  tried 
in  incipient  cases,  particularly  those  associated  with  marked  anaemia,  but  great 
curative  influence  is  not  to  be  expected  from  it.  Creosote  has  won  far  more 
advocates.  Continued  for  a  considerable  time  in  large  doses  (15  to  30  gr. 
[gm.  1  to  2]  or  more,  in  the  course  of  twenty-four  hours),  it  is  regarded  by 
many  physicians  as  an  excellent  remedy  in  incipient  and  even  in  advanced 
pulmonary  consumption.  It  is  best  prescribed  in  gelatin  capsules,  or  in  a 
mixture  of  1  part  of  creosote  to  2  parts  of  the  tincture  of  gentian,  of  which 
20  to  80  drops  may  be  given  three  times  a  day  in  a  considerable  amount  of 
milk,  or  in  wine.  This  remedy  is  usually  fairly  well  borne,  and  the  patients 
are  pleased  with  the  improvement  it  causes  in  their  appetite  and  general 
condition.  Of  late,  guaiacol,  the  active  ingredient  of  creosote,  has  been  gen- 
erally used  instead  of  the  drug  itself,  especially  since  carbonate  of  guaiacol 
has  been  brought  forward,  a  preparation  which  has  very  little  of  the  disagree- 
able odor  and  taste  of  creosote  itself.     Carbonate  of  guaiacol  is  administered 


TUBERCULOSIS  OF  THE  LUNGS  311 

in  powders  containing  aboui  8  gr.  (gm.  0.5),  in  daily  doses  at  firsl  of  25  gr. 
(gm.  1.5),  gradually  increasing  to  30  or  L5  gr.  (gm.  2  to  3).  Dyspeptic 
disturbance  sometimes  follows  the  use  even  of  guaiacol,  but  still  this  remedy 
is,  in  general,  better  borne  and  more  readily  taken  than  creosote.  Thio- 
col  (potassium  sulphoguaiacolate)  is  another  creosote  preparation  worthy 
of  trial.  It  is  taken  in  the  form  of  powders,  gr.  vijss.  to  xv  (gm.  0.5  to 
1.0),  several  times  a  day,  or  in  the  form  of  a  proprietary  solution  known 
as  sirolin.  The  following  mixture  is  often  employed  in  my  clinic:  Potas- 
sium sulphoguaiacolate,  20  parts;  syrupus  aurantii,  20  parts;  distilled  water, 
200  parts.  One  half  to  one  tablespoonful  of  this  is  to  be  taken  three 
times  a  day.  As  to  the  specific  and  therapeutic  use  of  creosote  and  its  nu- 
merous derivatives  (in  addition  to  those  above  mentioned,  creosotal,  sulpho- 
sote,  eosote,  and  many  others),  in  pulmonary  tuberculosis,  it  is  nol 
to  form  a  decided  opinion.  It  is  certain  that  many  patients  praise  these 
remedies,  and  improve  considerably  while  using  them;  but,  on  the  other 
hand,  the  indiscriminate  laudation  of  many  authors  is  decidedly  unjustifiable. 
When  the  disease  is  slowly  progressing  with  persistent  subfebrile  tempera- 
tures, the  author  has  scarcely  ever  felt  sure  of  any  distinct  influence  exerted 
by  guaiacol  or  creosote  upon  the  temperature  and  the  disease.  Nevertheless, 
it  is  often  advisable  in  practice  to  make  trial  of  these  remedies,  particularly 
of  the  carbonate  of  guaiacol.  The  remedy  must  be  employed  for  months  and, 
if  possible,  in  increasing  doses.  Among  the  remedies  which  are  recommended 
as  having  a  specific  influence,  we  will  also  mention  cinnamic  acid,  which  is 
contained  in  Peruvian  balsam.  This  has  been  employed  extensively  by  Lan- 
derer  in  the  treatment  of  various  tuberculous  diseases,  and  particularly  in 
pulmonary  tuberculosis.  He  gives  it  in  the  form  of  small  intravenous  injec- 
tions of  a  five-per-cent  emulsion,  made  up  of  the  sweet  oil  of  almonds  and 
the  yolk  of  egg.  The  results  obtained  by  Landerer,  in  the  institute  of 
Krahenbad,  in  the  Black  Forest,  appear  very  favorable,  but  as  yet  they  lack 
confirmation.     The  method  has  not  yet  been  generally  adopted. 

On  the  basis  of  our  present  general  bacteriological  knowledge,  an  entirely 
different  scientific  significance  belongs  to  the  ever-increasing  efforts  of  recent 
years  to  discover  a  true,  specific  curative  agent  for  tuberculosis.  At  the  end 
of  1890  great  interest  was  excited,  as  is  well  known,  by  the  statement  of  E. 
Koch  that  he  had  extracted  from  pure  cultures  of  tubercle  bacilli,  by  means 
of  glycerin,  a  substance  called  tuberculin,  by  which  he  was  able  to  heal  tuber- 
cular processes  both  in  animals  and  men.  This  assertion  aroused  the  thought- 
less enthusiasm  which  is  unfortunately  so  common  with  regard  to  therapeutic 
questions,  and  which  indeed  in  this  case  was  rendered  excusable  by  the  high 
authority  of  the  discoverer.  In  fact,  within  a  few  weeks  after  the  remedy 
was  made  known,  numerous  reports  were  published  of  cures  due  to  tuberculin. 
But  the  longer  the  experiments  were  pursued  the  more  evident  it  became 
that  these  extravagant  opinions  were  not  substantiated,  and  there  set  in  a 
revulsion  of  sentiment  which  has  led  to  many  adverse  criticisms,  perhaps 
equally  unjustifiable  with  the  early  praise.  It  is  absolutely  impossible  to 
speak  of  tuberculin  as  an  established  remedy  for  tuberculosis.  In  many 
patients  there  does  indeed  appear  a  decided  improvement  under  treatment, 
but  these  cases  are  such  as  were  favorable  anyway,  and  therefore  they  may 
owe  their  improvement  to  the  general  symptomatic  treatment  and  regimen 


312  DISEASES   OF  THE   RESPIRATORY   ORGANS 

which  they  have  also  enjoyed.  At  any  rate,  tuberculin  has  done  no  harm  in 
such  cases.  Then,  again,  we  have  seen  numerous  cases  of  rather  severe  disease, 
in  which  it  was  not  possible  to  notice  any  distinct  influence  of  the  tuberculin 
upon  the  general  course  of  the  illness.  Perhaps  the  condition  of  the  patient 
improved  or  remained  unchanged;  or,  again,  it  grew  worse.  Yet,  whatever 
the  change,  it  was  such  as  might  have  occurred  independently.  Finally,  there 
are,  in  the  third  place,  cases  which  have  been  seen  by  the  author  as  well  as 
other  observers,  in  which  there  was  such  a  decided  change  for  the  worse  shortly 
after  the  commencement  of  treatment,  that  one  might  really  suppose  that 
the  remedy  had  exerted  an  actually  harmful  influence.  We  refer  especially  to 
cases  in  which  the  patient,  previously  without  fever,  exhibited  after  the  injec- 
tion a  persistent  elevation  of  temperature,  with  a  more  rapid  advance  of  the 
local  process  in  the  lungs. 

Consequently,  we  may  say  that,  in  all  advanced  cases,  we  can  expect  noth- 
ing from  tuberculin.  In  incipient  cases  we  may  make  trial  of  it,  but  we 
should  be  extremely  careful  in  our  dosage,  so  as  to  avoid  any  chance  of  doing 
injury.  Koch's  rule  at  first  was  that  the  physician  should  begin  with  injec- 
tion of  gm.  0.001,  and  gradually  increase.  In  this  way  was  discovered  the 
interesting  fact  that  the  necessary  dose  for  the  production  of  the  "  reaction  " 
(vide  supra,  page  306)  became  greater  and  greater.  Many  patients  would 
finally  bear  the  injection  of  100  mgm.  of  tuberculin  without  any  reaction  at 
all.  At  first  it  was  regarded  as  the  object  of  treatment  to  reach  this  point  of 
tolerance,  but  the  practice  is  now  abandoned.  One  should  begin  with  very 
small  doses,  about  0.25  to  0.5  mgm.,  and  increase  so  slowly  and  b„  such  minute 
gradations  as  to  avoid  any  marked  reaction.  By  such  a  method  we  can 
almost  entirely  exclude  any  harmful  effect,  and  it  may  not  be  impossible  that 
some  of.  the  patients  who  have  had  a  favorable  result  actually  owe  their 
improvement  to  the  tuberculin,  but  it  is  extremely  difficult  to  make  sure  of  this. 
It  would  require  the  continuous  observation  of  many  patients  for  years  to 
enable  one  to  form  a  reliable  opinion  with  regard  to  this  question.  Still,  it 
cannot  be  denied  that  more  and  more  observers  have  recently  spoken  in  favor 
of  tuberculin.  In  addition  to  "  old  tuberculin,"  various  other  tuberculin 
preparations  (new  tuberculin,  Spengler's  bovine  tuberculin,  etc.)  and  cura- 
tive sera  have  been  presented.  We  are,  however,  far  from  any  conclusion  as 
to  their  value.  Yet,  when  everything  is  considered,  including  other  bacterio- 
logical facts,  we  seem  to  be  standing  on  the  threshold  of  a  future  in  which 
the  remarkable  effects  of  bacterial  products  will  be  made  to  exert  a  curative 
influence  on  the  infectious  diseases  in  general,  and,  especially,  on  tuberculosis. 
•  Meanwhile,  therefore,  we  physicians  must  continue  to  lay  the  greatest 
stress  in  the  treatment  of  tuberculosis  upon  those  methods  which  are  termed 
in  the  widest  sense  hygienic  and  constitutional.  It  is  undeniable  that,  by 
the  correct  and  faithful  employment  of  such  methods,  many  very  satisfactory 
successes  may  be  obtained. 

The  hygienic  and  constitutional  method  of  treating  consumption  has  for 
its  object  the  greatest  possible  promotion  of  the  natural  powers  of  healing. 
We  aim  at  this,  in  the  first  place,  by  avoiding  as  much  as  possible  all  influ- 
ences which  might  cause  a  further  extension  of  the  disease,  and  by  reenforc- 
ing,  so  far  as  we  can,  all  influences  which  increase  the  resisting  powers  of 
the  individual,  and  the  processes  of  spontaneous  cure.     The  factors  which 


TUBERCULOSIS  OF  THE   LUNGS  313 

arc  of  most  importance  in  this  connection  are,  first,  diet;  second,  v<-ri  ;  and 
third,  the  uninterrupted  enjoyment  of  good  air.  To  obtain  these  three 
therapeutic  factors  all  at  once  requires  the  renunciation  by  the  patieni  of 
his  calling,  and  his  usual  mode  of  life.  The  treatment  of  tuberculosis,  there 
fore,  should  begin  with  the  demand  that  the  patient,  for  as  long  a  time  as 
possible,  should  devote  himself  exclusively  to  the  care  of  bis  health.  The 
next  point  is  the  choice  of  the  place  in  which  the  "cure  "  shall  be  carried  on. 
In  many  cases  the  proper  management  of  the  patieni  may  be  pursued  under 
the  ordinary  surroundings  of  home.  Often,  however,  this  is  uol  the  case,  he- 
cause  the  last  two,  or  even  all  three,  of  the  essentials  named  cannot  be  pro- 
vided at  home.  It,  therefore,  is  the  duty  of  the  physician  in  every  i  ml  i  vidua  I 
case  to  determine  bow  the  desiderata  are  best  to  be  obtained.  According  to 
the  patient's  means  we  consider  respectively  a  residence  in  the  country  (if 
possible,  in  a  picturesque  and  wooded  region);  a  special  health  resort;  or, 
finally,  a  suitable  sanitarium.  From  a  therapeutic  standpoint,  there  is  no 
doubt  that  treatment  in  a  specially  adapted  sanitarium  is  chiefly  to  be  recom- 
mended. In  this  all  the  requirements  for  recovery  can  best  be  carried  out, 
and  the  patient  constantly  remain  under  medical  observation.  In  most  cases 
it  is  only  external  considerations,  for  instance,  pecuniary,  which  keep  the 
patient  from  a  sanitarium.  It  is  a  true  philanthropy,  therefore,  which  has  of 
late  led  everywhere  to  efforts  to  render  the  benefits  of  institutional  treatment 
accessible  to  the  less  wealthy  classes.  The  requirements  for  proper  treat- 
ment are  also  partially  fulfilled  in  the  so-called  public  health  resorts  for 
pulmonary  consumptives.  These  resorts,  however,  have  the  disadvantage  that 
the  patient  is  left  far  more  to  his  own  resources,  and  is  consequently  apt  to  be> 
incautious,  and  hence  jeopardize  his  recovery.  A  public  health  resort  would, 
therefore,  be  especially  chosen  for  patients  who  have  already  been  in  an  insti- 
tution, and  have  learned  what  mode  of  life  is  proper  for  them;  or  for  those 
who  have  already  so  far  recovered  that  they  may  be  allowed  a  certain  degree 
of  freedom. 

With  regard  to  the  minutiae  in  carrying  out  the  above-enumerated  essen- 
tials of  treatment,  we  would  add  as  follows:  1.  Diet.  This  should  be  as 
nourishing  and  abundant  as  possible.  Meat,  milk,  eggs,  farinaceous  foods, 
and  butter  are  chiefly  to  be  recommended,  care  being  taken  that  the  body 
should  receive  a  sufficient  amount  of  carbohydrates  and  fats,  as  well  as  an 
abundance  of  albumen.  Many  special  "  cures  "  for  pulmonary  consumption 
have  a  value,  in  so  far  as  they  lead  to  the  ingestion  of  an  abundant  amount  of 
easily  assimilated  nourishment.  Such  are  cures  with  milk,  koumiss,  or  kefir. 
It  has  even  been  proposed  to  introduce  large  amounts  of  such  nourishment 
as  milk  and  pulverized  meat  into  the  stomach  by  means  of  a  stomach  tube, 
and  thus  accomplish  "overfeeding."  This  method  has  not  become  very 
popular,  although  it  may  be  indicated  in  some  cases.  It  is  very  important 
to  see  that  the  patient  has  a  diet  that  is  not  only  abundant,  but  also  palatable 
and  varied.  If  pure  milk  is  not  readily  taken,  we  may  try  the  addition  of 
coffee,  tea,  common  salt,  or  brandy.  With  regard  to  the  prescription  of  alco- 
hol we  recommend,  unhesitatingly,  moderate  amounts  of  beer,  and  par- 
ticularly such  beer  as  is  rich  in  extractive  matter;  and  perhaps  also  extract 
of  malt,  and  porter.  Small  amounts  of  good  wine  may  contribute  to  the 
improvement  of  the  appetite  and  the  general  condition.     On  the  other  hand, 


314  DISEASES  OF  THE  RESPIRATORY  ORGANS 

we  think  it  useless  and,  in  some  circumstances,  harmful,  to  order  large  amounts 
of  the  stronger  alcoholic  beverages,  such  as  port  wine  and  brandy,  as  pre- 
scribed in  many  sanitariums.  Artificial  foods,  such  as  various  preparations 
of  meat,  somatose,  neutrose,  hygiama,  and  the  like,  should  be  used  merely  as 
makeshifts.  The  employment  of  cod-liver  oil  to  the  amount  of  2  to  4 
tablespoonfuls  a  day  is  sometimes  not  inappropriate,  if  it  is  well  borne.  2. 
The  two  other  factors  of  cure — rest,  and  the  continuous  enjoyment  of  good  air 
— are  best  fulfilled  by  the  fresh-air  treatment,  which  is  of  late  gaining  in  im- 
portance and  popularity.  The  patients  spend  the  greatest  part  of  the  day  lying 
in  the  open  air  on  comfortable  reclining  chairs.  At  the  same  time  they  avoid 
any  unnecessary  bodily  exertion,  any  great  demands  upon  respiration,  and 
any  irritation  of  the  respiratory  passages.  Gain  in  bodily  weight  is  pro- 
moted. The  limitation  of  the  diseased  process  in  the  lungs  is  favored.  Of 
course,  in  such  matters  also  the  individual  should  be  considered,  for  moder- 
ate exercise  in  the  open  air  is  certainly  for  many  patients  not  harmful,  but 
rather  beneficial.  This  applies  only  to  phthisical  patients  who  have  no  fever. 
As  soon  as  there  is  even  the  slightest  elevation  of  temperature,  complete  rest 
is  the  only  correct  procedure.  Often  the  methodical  carrying  out  of  the  open- 
air  treatment  under  suitable  conditions  demands  the  resources  of  a  sani- 
tarium, but  we  may  find  in  a  garden  or  on  a  veranda  a  sunny  spot,  screened 
from  the  wind,  where  the  patient  may  lie  comfortably  and  pass  the  entire  day 
till  near  sunset  in  the  open  air.  In  case  of  necessity  the  patient  must  content 
himself  with  a  place  by  an  open  window.  The  advantages  of  the  climatic 
health  resorts  (vide  infra)  consist  principally  in  the  fact  that  they  render 
possible  a  continuous  enjoyment  of  the  open  air,  even  during  the  colder  part 
of  the  year.  It  has  been  maintained  that  climatic  factors,  particularly  eleva- 
tion, exercise  a  specific  influence  upon  the  healing  of  pulmonary  tuberculosis; 
but  this  has  not  yet  been  proved. 

The  best-known  sanatoria  for  pulmonary  diseases  are  Gorbersdorf  in 
Silesia,  St.  Blasien,  Wehrawald,  and  Schomberg  in  the  Black  Forest,  Reibolds- 
griin  in  Hohenhonnef  on  the  Rhine,  Andreasberg  in  the  Hartz  Mountains, 
Davos  and  Arosa  in  Switzerland,  Gardone,  Gries,  etc.  Of  the  public  health 
resorts  which  are  particularly  suitable  for  consumptives,  we  would  name  for 
summer  use  the  acidulated,  alkaline,  and  chlorid-of-sodium  waters  of  Ems, 
Obersalzbrun,  and  Reinerz;  the  chlorid-of-sodium  waters  in  Reichenhall, 
Salzungen,  and  Soden;  the  mud  springs  in  Lippspringe,  Inselbad,  and 
Weissenburg  in  Switzerland.  For  summer  climate,  the  following  are  to  be 
recommended:  Beatenberg,  Heiden,  Engelberg  in  Switzerland;  Badenweiler, 
St.  Blasien,  Rippolclsau  in  the  Black  Forest,  and  many  others.  For  the  colder 
portion  of  the  year  we  have,  in  their  lofty  situation,  Davos,  Arosa,  and 
others.  The  more  vigorous  the  constitution  of  the  patient,  the  more  proper 
it  is  to  recommend  him  to  go  to  a  great  elevation  in  the  winter ;  while  delicate 
subjects  are  usually  better  suited  in  the  southern  resorts.  Of  course  only  the 
very  distant  health  resorts  in  Algiers,  Egypt,  Malta,  and  the  much-praised 
Madeira,  can  furnish  a  certain  guarantee  of  constant  mild  weather.  The 
Sicilian  health  resorts  (Catania  and  Palermo),  and  also  Ajaccio,  afford  favor- 
able climatic  conditions;  while  the  health  resorts  of  the  Riviera,  Meran, 
Gries,  Arco,  Gardone,  Lugano,  Pallanza,  and  Montreux,  are  much  more  uncer- 
tain in  this  respect,  and  therefore  are  to  be  used  merely  as  stopping  places  by 


TUBERCULOSIS   OF   THE    LINOS  315 

the  way  during  the  spring  and  autumn  months.    We  would  also  here  state  that, 
in  incipient  cases  that  have  become  stationary,  a  residence  by  the  sea,  or  a  long 

sea,  voyage,  may  sometimes  be  of  greal  help. 

We  cannot  go  into  a  full  description  here  of  all  the  health  resorts  men- 
tioned. Wo  cannot  omit,  however,  calling  special  attention  to  the  £ad  that 
we  should  always  ask  ourselves,  in  choosing  a  health  resort,  whether  the  ex- 
pense and  inconvenience  thus  imposed  upon  the  patienl  can  be  balanced  by 
the  possible  benefit.  The  earlier  the  stage  of  the  disease  and  the  better  the 
general  condition  of  the  patient,  the  more  will  his  physician  be  justified  in 
urging  him  to  make  every  sacrifice  in  order  to  regain  his  health.  We  must 
particularly  insist  with  the  patient  that  no  cure  of  tuberculosis  can  be  accom- 
plished by  a  single  visit  to  any  health  resort,  but  that  recovery  must  be  achieved 
by  living  continuously  for  years  in  accordance  with  all  the  demands  of  hygiene. 
On  the  other  hand,  it  is  wrong,  both  from  a  medical  and  from  a  humane  -land- 
point,  to  send  away  consumptives  in  the  last  stages  of  their  disease,  to  perish 
far  from  home  and  friends.  Consumptives  with  fever  should  never  be  sent 
from  home,  unless  they  find  refuge  in  a  real  sanitarium  where  they  may 
enjoy  the  constant  observation  and  treatment  of  a  physician. 

[Our  own  health  resorts  for  consumptives  are  too  well  known  to  demand  ex- 
tensive consideration  here.  The  prime  object  is  to  secure  for  the  patient  a 
pure  air,  with  such  climatic  conditions  that  he  can  pass  the  largest  amount  of 
time  out  of  doors,  at  the  same  time  that  within  doors  his  comfort  is  provided 
for,  and  a  sufficiency  of  suitable  and  well-cooked  foods  is  attainable.  In 
Colorado,  New  Mexico,  and  California  large  numbers  of  former  consumptives 
are  leading  active  lives.  Florida,  Aiken,  Thomasville,  Asheville,  and  some 
other  southern  resorts,  are  good  winter  asylums  for  many  cases,  but  patients 
should  not  return  to  New  England  before  June  1st.  An  outdoor  life  in  the 
Maine  or  Adirondack  woods  during  the  warmer  months  is  highly  to  be  recom- 
mended for  early  and  otherwise  suitable  cases.  Saranac,  N.  Y.,  affords  every 
comfort  during  the  colder  months,  combined  with  the  very  best  medical 
attendance,  and  many  people  do  well  there.  A  relative  disadvantage  under 
which  nearly  all  American  health  resorts  labor,  as  compared  with  those  of 
Europe,  consists  in  the  greater  difficulty  in  providing  occupation  and  thus 
securing  a  mental  attitude  most  favorable  to  recovery.  In  general,  the  north- 
ern seaboard  is  much  less  favorable  than  the  interior,  and  early  cases  often  do 
well  during  the  winter  removed  from  the  dampness  of  the  coast,  with  its 
alternations  of  freezing  and  thawing.  A  change  of  climate  is  a  very  impor- 
tant step,  and  should  receive  the  most  careful  consideration  of  the  physician — 
the  circumstances  of  the  patient,  the  stage  and  character  of  his  disease,  his 
tastes,  etc.,  being  carefully  weighed  before  a  decision  is  reached.] 

Finally,  the  employment  of  hydrotherapy  should  be  mentioned  in  the 
hygienic  treatment  of  tuberculosis.  Although  this  cannot  exert  any  specific 
influence  on  the  disease,  and  therefore  must  not  be  prized  too  highly,  yet  it  is 
often  beneficial  in  the  form  of  cold  sponging  or  brief  cool  douching  and  the 
like;  and  the  stimulation  of  the  skin  has  a  favorable  influence  upon  the  gen- 
eral health.  In  severe  febrile  cases  we  may  order  sponging  and  rubbing  in 
bed  with  cold  water,  brandy,  aromatic  vinegar,  and,  in  addition,  chest  packs, 
compresses,  and  the  like.  Also  for  the  relief  of  symptoms  (vide  infra),  such 
as  pain,  fever,  and  perspiration,  we  may  often  employ  sponging,  cold  or  warm 


316  DISEASES   OF  THE   RESPIRATORY  ORGANS 

compresses,  and  the  wet  pack  ("  Priessnitz").  I  not  infrequently  employ 
inunctions  of  soft  soap  for  tuberculosis,  similar  to  those  used  for  a  long  time 
in  the  treatment  of  tuberculous  pleurisy  and  of  swollen  lymph-glands. 

The  symptomatic  treatment  of  phthisis  is  directed  in  the  first  place  against 
the  pulmonary  symptoms.  We  use  much  the  same  remedies  to  help  the  cough 
as  in  chronic  bronchitis.  We  try  inhalations  x  with  a  solution  of  common  salt, 
or  of  the  alkaline  carbonates,  or,  if  there  is  much  secretion,  with  solutions 
of  tannin  and  the  balsams,  such  as  turpentine,  or  balsam  of  Peru.  When 
there  is  severe,  spasmodic  cough,  inhalations  with  narcotic  solutions  some- 
times give  some  relief,  such  as  cherry-laurel  water,  opium,  or  bromid  of 
potassium. 

Morphin  stands  first  among  the  drugs  employed  to  check  the  cough.  We 
should  be  cautious  and  sparing  in  its  use  at  first,  but  it  is  an  indispensable 
remedy  in  severe  and  hopeless  cases.  It  relieves  the  irritation  of  coughing, 
the  pain  and  the  oppression  in  the  chest,  and  at  least  gives  the  patient  for  a 
time  the  desired  sleep.  In  chronic  cases,  with  moderately  severe  symptoms, 
we  may  use  for  a  long  time  the  milder  narcotics  with  advantage,  particularly 
codein  (powders  of  gr.  ss.  to  j  [gm.  0.03  to  0.05],  or  phosphate  of  codein, 
gr.  vijss.  [gm.  0.5],  aq.  amyd.  amar.,  5v  [20  c.c],  dose  15  to  20  drops)  ; 
also  the  two  morphin  derivatives,  heroin  (gr.  TV  to  ^  [gm.  0.006  to  0.012] 
carefully  given),  and  dionin  (gr.  0.25  to  0.5  [gm.  0.01  to  0.03]  a  dose). 
Under  some  circumstances,  we  also  employ  the  extract  of  hyoscyamus  (for 
example,  extracti  lryoscyami,  1  part;  aquae  laurocerasi,  20  parts;  15  to  20 
drops  of  the  mixture  every  two  hours),  the  extract  of  belladonna  2  (in  0.5  to  1 
gr.  [gm.  0.03  to  0.05]  powders),  etc.  It  is  important  that  the  patient  should 
learn  to  suppress  his  inclination  to  cough,  at  least  up  to  a  certain  point.  Sips 
of  cold  water  often  quiet  the  cough,  as  may  also  a  "  cough  drop  "  held  in  the 
mouth,  or  a  pastille  containing  the  salts  found  in  Ems  mineral  water. 

If  the  patient  complains  of  difficulty  in  loosening  the  expectoration,  we 
prescribe  expectorants,  the  action  of  which  often  fails  to  meet  our  desires, 
but  which  cannot  be  dispensed  with  in  practice.  The  expectorants  most  fre- 
quently used  are  carbonate  of  ammonia,  ipecacuanha,  apomorphin,  and  senega. 
We  very  often  combine  expectorants  with  narcotics,  as  in  Dover's  powder. 

If  severe  pain  in  the  chest  comes  on,  we  often  use  local  applications : 
mustard  plasters,  warm  poultices  and  cold  compresses,  painting  with  iodin, 
or  embrocations  of  chloroform.  Narcotics,  such  as  morphin,  are  indispen- 
sable in  severe  dyspnoea,  which  usually  occurs  only  in  the  last  stages  of  the 
disease  or  as  a  result  of  pneumothorax. 

The  treatment  of  hemoptysis  is  important.  As  a  slight  admixture  of 
blood  in  the  expectoration  often  precedes  a  severe  hemopytsis,  such  an  appear- 
ance always  suggests  caution.  When  there  is  any  hemoptysis,  absolute  rest 
in  bed  is  necessary.  We  should  avoid  any  careful  examination  of  the  lungs, 
especially  any  severe  percussion.  We  should  lay  a  flat  and  not  too  heavy 
ice  bag  over  the  lung  on  the  side  from  which  we  suspect  the  hemorrhage; 
the  cold  is  usually  well  borne,  but  sometimes  it  aggravates  the  cough,  and 
must  then  be  omitted.     We  would  also  recommend  swallowing  bits  of  cracked 

1  For  details  as  to  dosage,  see  Appendix  III,  "  Formulae,"  in  Vol.  II  of  this  work. 

2  Ext.  belladon.,  U.  S.  P.,  is  four  times  stronger  than  the  German  preparation. 


TUBERCULOSIS  OF  THE   LUX  OS  317 

ice.  Narcotics,  such  as  morphin,  arc  the  most  suitable  interna]  remedies, 
since  they  aid  the  cessation  of  the  hemorrhage  by  suppressing  the  attacks  of 
coughing.  The  more  trouhlesome  the  cough  the  more  necessary  is  it,  there- 
fore, to  administer  morphin  in  solution,  by  the  mouth  or  even  subcutaneously. 
Of  remedies  to  check  the  blood  we  should  name,  first,  extract  of  ergot  or 
ergotin,  winch  may  be  given  by  the  mouth,  or,  still  better,  subcutaneously, 
in  doses  of  2  to  8  gr.  (gm.  0.1  to  0.5)  several  times  a  day.  Of  the  individual 
ergotin  preparations,  that  to  be  most  recommended,  especially  for  subcutaneous 
use,  is  cornutin.  citricum  (Merck).  [Any  preparation  of  ergot  will  raise  the 
tension  in  the  pulmonary  artery,  and  is  therefore  to  be  avoided.  Inhalation 
of  nitrite  of  amyl  has  recently  been  recommended.  Its  physiological  action 
is,  of  course,  the  opposite.  Purgation  is  advisable — e.  g.,  an  ounce  of  Epsom 
salts.]  The  subcutaneous  injection  of  sterilized  solutions  of  gelatin  has  been 
widely  praised.  Eemarkable  observations  have  recently  been  made  on  the 
hemostatic  effect  of  serum  injections.  We  may  also  try  the  fluid  extract  of 
hydrastis,  with  equal  parts  of  an  elixir,  giving  30  to  40  drops  of  the  mixture 
several  times  a  day ;  also,  acetate  of  lead  and  atropin.  The  influence  of  these 
remedies,  particularly  those  last  named,  is,  however,  quite  uncertain.  The 
inhalation  of  a  one-  to  two-per-cent  solution  of  perchlorid  of  iron  usually 
excites  cough,  and  is  therefore  more  harmful  than  beneficial.  A  very  popular 
remedy  among  the  laity,  and  one  almost  always  at  hand,  is  common  salt, 
of  which  several  teaspoonfuls  may  he  given  in  water.  When  the  hemorrhage 
recurs  frequently,  it  is  also  advisable  to  "  tie  off  "  the  limbs — that  is,  to  apply 
bandages  rather  firmly  around  the  middle  of  the  upper  arms  and  the  thighs. 
This  causes  venous  congestion,  and  hinders  the  return  of  blood  to  the  lungs. 
When  pulmonary  hemorrhage  has  occurred,  the  diet  should  consist  at  first  of 
nothing  but  cold  milk,  eggs,  and  similar  food.  Hot  food,  alcohol,  and  large 
amounts  of  meat  are  to  he  forbidden.  It  is  a  good  thing  to  give  acids,  such 
as  lemonade,  or  aromatic  sulphuric  acid,  well  diluted. 

Even  when  the  bleeding  has  ceased  we  must  keep  the  patient  several  days  in 
bed,  and  for  a  longer  time  be  extremely  cautious,  since  the  hemorrhage  is  apt 
to  be  repeated. 

The  hectic  fever  of  consumption  is  remarkably  little  influenced  by  anti- 
pyretic drugs.  It  often  is  entirely  useless,  or  even,  on  account  of  its  evil  effect 
upon  the  stomach,  actually  harmful  to  give  large  doses  of  antipyretics  to  fever- 
ish consumptives,  for  long  periods  of  time,  particularly  as  the  fever  often  of 
itself  has  deep  morning  remissions.  The  prescription  of  antipyretics  is  only 
justified  when  they  make  the  patient  feel  better.  The  continuous  use  of 
pyramidon  (gr.  4  [gm.  0.25]),  three  times  a  day,  is  particularly  worthy  of 
trial.  Antipyrm/ quinin,  and  other  similar  drugs  may  also  be  employed.  On 
the  other  hand,  it  is  very  appropriate  to  give  a  cold  sponging  and  rubbing  to 
the  whole  body  or  chest,  with  water  or  alcohol,  especially  in  the  evening  when 
the  fever  is  high.  The  sponging  is  almost  always  well  borne,  and  makes  the 
patient  feel  brighter  and  easier.  The  cold  pack  may  also  be  tried  occa- 
sionally. 

Cold  sponging  often  diminishes  the  troublesome  sweats  in  phthisis,  but  if 
this  does  not  check  them,  we  may  often  prescribe  atropin  to  advantage,  gr. 
Tib"  to  jfc  (gin.  0.0005  to  0.001)  at  night,  but  its  action  does  not  usually  last 
very  long.     Lately  agaricin  in  TV  to  {-gr.  pills  (gm.  0.005  to  0.01)  has  been 


318  DISEASES  OF  THE   RESPIRATORY   ORGANS 

recommended  for  the  night-sweats  in  phthisis ;  also  picrotoxin,  of  which  gr. 
■J  to  -J  (gm.  0.008  to  0.01)  is  given  in  pill  or  solution  at  bedtime,  and  lately 
camphoric  acid,  gr.  20  to  30  (gm.  1.5  to  2)  in  wafers.  Dusting  the  body 
with  a  powder  of  5  parts  of  salicylic  acid  to  95  of  French  chalk  is  also  good. 
Sage  tea  is  a  favorite  remedy  for  night-sweats — 2  or  3  cups  of  it  cold  at 
night — and  so  are  milk  and  cognac. 

If  there  is  loss  of  appetite,  small  doses  of  quinin,  compound  tincture  of 
cinchona,  wine  of  cinchona,  and  other  bitter  remedies,  such  as  tinctura  amara 
(P.  G.),  are  sometimes  of  service.  It  is  also  frequently  a  good  thing  to  pre- 
scribe a  little  muriatic  acid,  5  to  10  drops  of  the  dilute  acid,  with  the  meals. 
It  is  often  very  hard  to  check  diarrhea  in  phthisis.  Opium,  combined  with 
tannin  or  acetate  of  lead,  is  most  effective.  This  subject  will  be  discussed  more 
fully  in  the  chapter  on  intestinal  tuberculosis. 

We  often  prescribe  preparations  of  iron,  combined  sometimes  with  quinin 
or  arsenic  (vide  supra),  in  the  beginning  of  the  disease  to  improve  the  general 
condition  and  the  anaemia,  but,  as  experience  shows,  iron  is  contraindicated 
in  patients  who  are  feverish  or  who  have  a  tendency  to  hemoptysis. 

The  treatment  of  the  diseases  complicating  phthisis  is  to  be  found  in  the 
appropriate  chapters. 


CHAPTEE   VII 

ACUTE    GENERAL    MILIARY   TUBERCULOSIS 

iEtiology. — Acute  miliary  tuberculosis  is  a  form  of  tuberculosis  which  we 
are  justified  in  describing  particularly  because  of  its  anatomical  relations  and 
its  peculiar  clinical  history.  The  disease  is  characterized  anatomically  by  the 
extremely  abundant  development  of  miliary  tubercles  in  a  comparatively  short 
time  in  many  organs  of  the  body.  We  cannot  liken  this  process  to  anything 
but  an  overwhelming  of  the  body  with  tubercle  bacilli,  which  in  some  way 
reach  the  different  organs  simultaneously,  and  in  them  give  rise  to  the  erup- 
tion of  tubercles.  Buhl  advanced  the  hypothesis  a  long  time  ago,  that  a  cheesy 
focus  could  be  found  somewhere  in  the  body  in  every  case  of  acute  miliary 
tuberculosis,  and  that  the  general  infection  of  the  body  resulted  from  the 
absorption  of  these  cheesy  masses  by  the  blood.  Later  investigations,  how- 
ever, have  given  us  a  much  more  definite  explanation  of  the  nature  and  man- 
ner of  this  general  infection.  Ponfick  found,  in  some  cases  of  acute  miliary 
tuberculosis,  an  extensive  tuberculosis  of  the  thoracic  duct  with  breaking  down 
of  the  tubercular  new  growth.  It  is  easy  to  see  how,  in  this  way,  a  large 
amount  of  tuberculous  material  could  be  brought  directly  into  the  circulation, 
from  the  free  communication  of  the  lymph  duct  with  the  subclavian  vein,  and 
thus  be  "  disseminated  "  through  the  different  organs  in  a  short  time.  Still 
more  frequently,  however,  the  tuberculosis  of  the  large  venous  trunks,  dis- 
covered by  Weigert,  especially  the  pulmonary  veins,  seems  to  be  the  starting- 
point  for  an  acute  general  miliary  tuberculosis.  Usually  there  are  tuberculous 
lymph-glands,  or  sometimes  other  foci  of  tuberculous  disease,  which  involve  the 
wall  of  a  neighboring  vein,  gradually  break  through  it,  and  project  into  its 
lumen.    If  caseation  and  ulceration  result  in  this  spot,  the  infectious  material 


ACUTE   GENERAL-  MILIARY  TUBERCULOSIS  319 

is  of  course  constantly  washed  off  by  the  blood  current  and  carried  away,  and 
thus  it  reaches  the  other  organs. 

Since  such  a  tuberculous  focus — e.g.,  a  tuberculous  bronchial  gland — may 
remain  for  a  long  time  entirely  withoul   symptoms,  we  can   understand  how 

miliary  tuberculosis  may  break  out  in  an  acute'  form  in  persons  who  previously 
seemed  perfectly  well.  In  other  cases  the  patient  has  already  suffered  from 
some  tuberculous  affection,  and  suddenly  the  conditions  occur  somewhere  in 
the  body  which  lead  to  the  development  of  miliary  tuberculosis.  Thus  we 
sometimes  see  it  break  out  in  a  patient  who  lias  ordinary  phthisis,  but  acute 
miliary  tuberculosis  is  one  of  the  rarities  in  advanced  phthisis.  If  we  find, 
at  the  autopsy  of  a  case  of  acute  general  miliary  tuberculosis,  old  phthisical 
changes  in  the  lungs,  which  is  by  no  means  very  common,  they  consist  of  old, 
partly  cicatrized  foci,  pigment  indurations,  etc.  We  see  miliary  tuberculosis 
rather  frequently  as  a  sequel  to  pleuritic  effusion.  We  have  already  called  at- 
tention to  the  fact  that  in  such  cases  the  pleurisy  itself  is  a  tuberculous  disease. 
Miliary  tuberculosis  is  also  seen  in  persons  with  old  tuberculous  affections  of 
the  bones  and  joints,  such  as  coxitis  and  vertebral  caries,  with  tuberculous 
swellings  of  the  lymph-glands,  as  in  the  neck  and  the  axilla?,  or  with  tubercu- 
losis of  the  genito-urinary  organs,  etc.  In  such  cases,  of  course,  the  tuberculous 
affection  which  is  discovered  during  life  is  not  always  the  source  of  the  gen- 
eral miliary  tuberculosis,  but  the  discovery  of  the  existence  of  such  an  affection 
is  of  the  greatest  significance  in  diagnosis,  as  in  this  way  our  attention  is 
strongly  directed  to  the  possibility  of  a  general  tuberculous  affection. 

In  some  cases  an  outbreak  of  miliary  tuberculosis  has  been  seen  to  follow 
other  acute  diseases,  such  as  typhoid  or  measles. 

Pathological  Anatomy. — Except  for  the  presence  of  an  old  tuberculous  af- 
fection in  some  organ,  and  except  for  the  tuberculosis  of  a  vein  or  of  the 
thoracic  duct,  which  are  usually  demonstrable,  and  which  have  been  described 
above,  the  anatomical  lesion  in  acute  miliary  tuberculosis  consists  in  the  dis- 
semination of  miliary  tubercles  through  a  large  number  of  the  organs  of  the 
body.  The  lungs,  the  liver,  and  the  spleen  are  constantly  affected;  almost  as 
constantly  the  kidneys,  the  thyroid  gland,  the  marrow  of  the  bones,  the  heart, 
and  the  choroid;  less  constantly,  but  still  quite  frequently,  the  serous  mem- 
branes and  the  meninges.  The  miliary  nodules  may  be  found  in  large  numbers 
in  all  the  organs  mentioned.  They  may  in  part  be  easily  recognized  by  the 
naked  eye,  and  in  the  lungs  they  may  be  very  plainly  perceived  by  the  touch. 
In  many  organs,  however,  especially  in  the  liver  and  often  in  the  spleen,  they 
are  hard  to  recognize  with  the  naked  eye,  but  they  are  easily  discovered  by 
the  microscope.  In  regard  to  the  histological  structure  of  miliary  tubercles, 
and  the  discovery  of  tubercle  bacilli  in  them,  we  must  refer  to  what  has  been 
said  in  the  chapter  on  pulmonary  tuberculosis,  but  we  must  also  mention  that, 
in  some  of  the  more  chronic  cases,  some  of  the  nodules  may  grow  to  be  large 
tuberculous  foci,  from  the  size  of  a  lentil  to  that  of  a  pea.  Less  developed  cases 
of  miliary  tuberculosis  are  also  found,  in  which  only  a  limited  number  of 
organs  are  attacked,  and  these  with  less  severity. 

Clinical  History. — The  clinical  symptoms  of  miliary  tuberculosis  depend 
upon  two  factors,  the  first  being  the  general  infection  of  the  body,  and  the 
second  the  local  tuberculous  affection  of  certain  organs.  Although  in  many 
organs  miliary  tuberculosis  is  entirely  without  symptoms,  as  in  the  liver,  the 


320  DISEASES  OF  THE  RESPIRATORY  ORGANS 

kidneys,  the  heart,  and  the  marrow  of  the  bones,  in  two  organs — the  lungs, 
and  more  especially  the  brain — it  leads  to  the  most  marked  local  symptoms. 
The  miliary  tuberculosis  of  the  choroid,  discovered  by  Cohnheim  and  Manz,  is 
also  without  symptoms,  but  it  can  be  made  out  with  the  ophthalmoscope,  and 
it  is  therefore  of  great  diagnostic  value. 

Miliary  tuberculosis  affords  quite  different  pictures,  according  to  the  pre- 
dominance of  one  or  the  other  of  the  groups  of  symptoms  mentioned.  We 
distinguish  the  four  following  forms : 

1.  Miliary  Tuberculosis,  with  Predominant  Symptoms  of  General  Infec* 
Hon:  the  so-called  Typhoidal  Form. — This  form  may  in  part  greatly  resemble 
typhoid  fever.  The  patient,  who  previously  seemed  quite  well,  or  in  whom 
some  local  manifestation  of  tuberculosis  was  suspected,  falls  ill  with  gradually 
increasing  general  symptoms,  dullness,  loss  of  appetite,  headache,  and  fever. 
Since  there  is  no  local  affection  to  be  discovered  to  explain  the  symptoms,  the 
disease  at  first  may  well  be  taken  for  typhoid.  The  general  condition  grows 
worse  constantly,  the  fever  is  high  and  continually  rises,  and  cerebral  symp- 
toms appear.  In  some  cases  an  exanthematous  eruption,  like  roseola,  may 
increase  the  resemblance  to  typhoid.  With  careful  observation,  however, 
symptoms  are  almost  always  detected  later  in  the  disease  which  are,  to  a  cer- 
tain degree,  characteristic  of  miliary  tuberculosis,  and  are  due  to  the  existence 
of  that  disease  either  in  the  lungs  or  in  the  brain.  The  patient's  complexion 
assumes  a  peculiar  pallor,  and  with  it  a  definite  cyanotic  hue.  The  respiration 
becomes  remarkably  deep,  and  there  is  dyspnoea;  or  signs  of  a  tuberculous 
meningitis  arise,  such  as  rigidity  of  the  neck,  loss  of  consciousness,  disturb- 
ances in  the  innervation  of  the  ocular  muscles,  etc.,  and  death  follows  with 
these  symptoms.  These  cases  last  from  ten  days  to  three  weeks,  reckoning 
from  the  beginning  of  the  severe  symptoms. 

2.  Miliary  Tuberculosis,  with  Predominant  Pulmonary  Symptoms. — These 
cases,  too,  may  begin  quite  suddenly,  almost  like  an  acute  croupous  pneumonia, 
or  they  may  develop  gradually  with  quite  a  long  prodromal  stage.  From  the 
onset  the  symptoms  point  especially  to  disease  of  the  lungs  or  the  pleura.  The 
patient  complains  of  a  stitch  in  the  side,  cough,  and  dyspnoea.  The  expectora- 
tion may  bear  a  decided  resemblance  to  that  of  pneumonia.  Such  cases,  espe- 
cially if  they  begin  abruptly,  are  at  first  often  erroneously  regarded  as  croupous 
pneumonia,  particularly  if  we  find  fine  rales,  almost  like  crepitant  rales,  over 
certain  portions  of  the  lungs.  But  the  expected  crisis  does  not  occur :  the  fever 
continues ;  the  dyspnoea,  general  weakness,  and  anaemia  of  the  patient  increase ; 
the  physical  signs  of  pulmonary  disease  (diffuse  bronchitic  rales)  become  more 
and  more  extensive.  The  patient's  face  is  pale,  cyanotic,  and  anxious.  Death 
ensues  with  all  the  signs  of  impaired  respiration.  The  course  is  usually  some- 
what more  protracted  than  in  the  typhoidal  form,  lasting  for  three  or  four 
weeks  and  more. 

3.  Miliary  Tuberculosis,  with  Predominant  Cerebral  Symptoms,  due  to 
Tuberculous  Meningitis. — Tuberculosis  of  the  meninges  does  not  belong  among 
the  regular  lesions  of  general  miliary  tuberculosis.  It  develops  in  about  half 
the  cases,  according  to  our  estimation;  but  where  it  occurs  it  almost  always 
gives  the  whole  case  the  characteristic  imprint  of  tuberculous  meningitis,  by 
which  the  other  symptoms  are  entirely  concealed.  The  predominant  symp- 
toms are  headache,  fever,  stupor  increasing  to  deep  coma,  rigidity  of  the  back 


ACUTE   GENERAL   MILIARY  TUBERCULOSIS  321 

and  neck,  and  disturbances  in  the  innervation  of  the  ocular  muscles.  In  such 
cases  the  tuberculous  meningitis  may  alone  be  diagnosticated,  and  not  the  uni- 
versal miliary  tuberculosis.  In  fact,  all  the  other  signs  of  general  miliary 
tuberculosis  are  not  infrequently  obscured  by  meningeal  symptoms,  and  yet 
we  have  repeatedly  observed,  even  in  the  deepest  coma  of  the  patient,  a  pecul- 
iarly deep  and  hurried  respiration,  which  was  the  only  noticeable  sign  referable 
to  the  miliary  tuberculosis  in  the  lungs. 

The  symptoms  of  tuberculous  meningitis  in  many  cases  predominate  in  this 
type  of  the  disease  from  the  onset,  but  in  other  cases  they  come  on  during  the 
attack  and  form  its  final  period.  The  duration  of  the  disease  varies  ac- 
cordingly. 

4.  Miliary  Tuberculosis  ivith  a  Protracted  Course  and  Indefinite  Symp- 
toms for  a  Long  Time — Intermitting  Form. — Besides  the  forms  already  men- 
tioned, cases  occur  which  usually  take  quite  a  protracted  course,  lasting  for 
eight  or  ten  weeks,  and  having  such  indefinite  symptoms  that  an  absolute 
diagnosis  is  for  a  long  time,  or  even  throughout  the  disease,  quite  impossible. 
The  patient  complains  of  a  number  of  general  symptoms,  such  as  headache 
and  dullness,  and  also  of  thoracic  symptoms,  for  which,  however,  we  can  find 
on  examination  no  sufficient  basis.  There  is  almost  always  fever,  usually  not 
very  high,  and  with  a  very  irregular  course;  but  we  have  seen  a  regular  daily 
rise  of  temperature  for  a  time  in  some  cases,  and  attacks  of  fever  with  quite  a 
severe  chill,  so  that  at  first  we  thought  of  an  irregular  malarial  intermittent 
fever — the  intermitting  form.  Later  on  the  symptoms  gradually  increase. 
The  apparently  inexplicable  loss  of  strength,  and  the  patient's  anaemia  and 
emaciation,  are  marked,  and  they  are  important  in  diagnosis.  Finally,  either 
severe  pulmonary  symptoms  or  the  signs  of  tuberculous  meningitis  set  in,  and 
to  these  the  patient  succumbs. 

We  must  mention  particularly  that  the  four  forms  of  miliary  tuber- 
culosis just  described  are  only  the  types  of  the  disease.  In  individual 
cases  we  often  meet  with  variations  and  transitional  forms  between  these 
types. 

Single  Symptoms. — 1.  General  Symptoms. — In  all  cases  of  acute  miliary 
tuberculosis  the  general  condition  of  the  patient  is  very  serious.  Most  pa- 
tients have  a  subjective  feeling  of  severe  illness,  although  they  make  little 
special  complaint  of  it  from  the  painless  character  of  the  disease.  As  the 
disease  increases  there  is  often  a  marked  feeling  of  anxiety  and  oppression 
besides  the  dyspnoea.  There  is,  especially  in  the  face,  quite  a  peculiar  pallor, 
characteristic  of  the  disease,  and  associated  with  a  marked  cyanosis  of  the  lips 
and  cheeks. 

2.  Fever. — Acute  miliary  tuberculosis  almost  always  runs  its  course  with  a 
more  or  less  high  fever,  a  course  without  fever  having  been  observed  in  only  a 
few  instances.  It  often  happens,  in  more  protracted  cases,  that  the  temper- 
ature may  be  nearly  normal  for  a  time,  or  only  slightly  elevated.  There  is 
nothing  characteristic  or  typical  in  the  course  of  the  fever.  In  the  cases  with 
typhoidal  symptoms  the  fever  is  usually  quite  high,  between  103°  and  105°  F. 
(39JJ0  to  40.5°  C),  so  that  the  temperature  curve  may  be  exactly  like  that 
of  typhoid.  In  other  cases  the  fever  is  irregular  and  is  broken  by  many  remis- 
sions, remitting  or  intermitting  quite  regularly  for  some  time.  Death  ensues 
with  a  moderately  high  temperature  or  in  collapse.    In  cases  with  tuberculous 


322  DISEASES  OF  THE  RESPIRATORY  ORGANS 

meningitis  there  is  also  a  marked  rise  of  temperature  at  the  close,  up  to  108°  F. 
(42°  C.)  and  over. 

3.  Respiratory  Apparatus. — It  goes  without  saying  that  physical  exami- 
nation of  the  lungs  may  give  no  definite  results.  Almost  all  positive  evidence 
is  often  wanting,  and  the  contrast  between  the  labored  breathing  and  dyspnoea 
and  the  insignificance  of  the  physical  signs  in  the  lungs  is  an  important  feature 
in  diagnosis.  Auscultation,  as  a  rule,  gives  the  signs  of  an  intense  bronchial 
catarrh;  we  hear  rhonchi  or  numerous  fine  and  medium  moist  rales  all  over 
both  lungs.  The  respiratory  murmur  itself  is  usually  higher  in  pitch  than 
normal,  and  in  many  cases  it  is  obscure,  rough,  or  harsh.  In  our  cases  there 
was  occasionally  heard,  over  a  circumscribed  area  of  the  lung,  a  wholly  pe- 
culiar, sharp,  "  lapping  "  sound  on  inspiration.  In  quite  a  large  number  of 
cases  peculiar  fine  crepitant  rales  are  to  be  heard  over  some  areas  of  the  lungs ; 
these,  in  our  experience,  are  pathognomonic  of  miliary  pulmonary  tuberculosis. 
On  percussion  there  are  often  no  distinct  objective  changes  to  be  found.  With 
careful  percussion,  however,  the  abnormally  deep  note  of  the  relaxed  portions 
of  the  lungs,  or  a  slight  dullness  over  other  areas,  becomes  very  noticeable.  "We 
consider  this  varying  quality  of  the  pulmonary  resonance  (difference  in  pitch 
and  the  like)  over  different  portions  of  the  lungs  of  special  diagnostic  im- 
portance. 

In  some  cases  circumscribed  pneumonic  infiltration  has  been  observed  in  the 
lungs  in  acute  miliary  tuberculosis,  which,  as  we  have  said,  may  give  rise  to  a 
confusion  between  miliary  tuberculosis  and  croupous  pneumonia,  from  the 
presence  of  marked  dullness,  crepitant  rales,  and  bronchial  respiration. 

We  must  mention,  finally,  that  in  some  of  the  cases  physical  examination 
of  the  lungs  shows  old  changes  in  them,  a  phthisical  affection  of  the  apex,  a 
former  pleurisy,  and  the  like.  Positive  evidence  of  such  old  tuberculous  affec- 
tions may  be  of  great  diagnostic  value  in  doubtful  cases. 

Dyspnoea  has  been  repeatedly  mentioned  among  the  pulmonary  symptoms. 
The  respiration  is  usually  very  much  accelerated,  especially  during  the  more 
advanced  stage  of  the  disease,  so  that  we  see  in  adults  forty,  sixty,  and  even 
seventy  respirations  a  minute.  The  respiration  is  also  very  deep,  and  is  some- 
times noisy.  As  a  rule,  there  is  cough,  but  it  is  usually  troublesome  only  in 
the  cases  with  severe  bronchitis.  It  is  often  very  slight.  The  expectoration  is 
usually  scanty,  and  it  is  not  characteristic.  Special  mention  must  be  made  of 
the  fact  that  tubercle  bacilli  are  absent  in  it,  unless  old  ulcerated  tuberculous 
foci  are  present  at  the  same  time  in  the  lungs. 

4.  Circulatory  Apparatus. — The  pulse  is  frequent,  about  100  to  120  a 
minute,  often  weak  and  small,  and  sometimes  irregular,  especially  if  tubercu- 
lous meningitis  coexists.  The  miliary  tubercles,  which  postmortem  are  almost 
always  to  be  found  in  the  heart,  especially  in  the  endocardium,  cause  no  symp- 
toms. In  uncomplicated,  acute,  miliary  tuberculosis  there  is  little  if  any 
increase  in  the  number  of  white  corpuscles  in  the  blood.  The  presence  of 
tubercle  bacilli  in  the  blood  will  be  mentioned  below. 

5.  Digestive  Apparatus. — Vomiting  is  frequent  at  the  onset  of  the  disease. 
The  bowels  are  usually  constipated,  but  in  many  cases  there  is  a  moderate 
diarrhea.  The  loss  of  appetite,  the  thirst,  and  the  dry  tongue  are  due  to  the 
general  disease  and  the  fever.  The  spleen  is  usually  somewhat,  but  not  very 
much,  enlarged. 


ACUTE   GENERAL   MILIARY   TUBERCULOSIS  323 

6.  Nervous  System. — In  many  cases  in  which  the  pulmonary  symptoms  pre- 
dominate the  intellect  remains  quite  clear  until  the  last,  bul  in  other  < 
cerebral  symptoms,  such  as  headache,  dizziness,  stupor,  and  delirium,  come  on 
quite  early,  and  are  part  of  the  general  infection.  As  has  already  been  said, 
the  nervous  symptoms  in  the  cases  combined  with  tuberculous  meningitis  be- 
come quite  prominent,  but  in  individual  instances  it  may  be  hard  to  decide 
whether  they  are  due  to  such  a  complication,  or  are  merely  severe  general 
symptoms. 

7.  Eyes. — The  ophthalmoscopic  examination  of  the  retina  is  of  special  di- 
agnostic importance,  since  the  diagnosis  may  be  made  absolutely  certain  by 
finding  miliary  tubercles  in  the  choroid.  A  negative  result,  however,  is  never 
decisive  against  the  diagnosis,  since  the  tubercles  are  sometimes  absent,  or  at 
least  are  very  few  in  number.  Their  discovery  is  almost  always  difficult,  and 
demands  much  practice  in  the  method  of  examination.  In  cases  with  tuber- 
culous meningitis  we  sometimes  find  an  optic  neuritis. 

Diagnosis. — The  diagnosis  of  acute  general  miliary  tuberculosis  is  ordi- 
narily not  very  simple.  It  quite  often  happens  that  at  the  autopsy  a  miliary 
tuberculosis  is  found  which  was  not  even  suspected  during  life.  It  must  be 
confessed  that  frequently,  in  such  cases,  we  might  very  well  have  thought  of 
acute  tuberculosis.  If,  therefore,  the  possibility  of  acute  miliary  tuberculosis  is 
brought  to  our  attention  during  the  patient's  life,  we  can  occasionally  make  an 
absolute  diagnosis. 

The  severe  constitutional  disturbance,  usually  associated  with  fever,  is  most 
important,  and  for  this  no  local  cause  can  be  found.  Then  come  the  pulmo- 
nary symptoms,  especially  the  peculiar  dyspnoea,  for  which  there  is  also  no 
adequate  corresponding  physical  change  to  be  discovered.  Besides  the  dysp- 
noea, a  peculiar,  cyanotic  pallor  is  very  characteristic.  It  gives  decided 
support  to  our  suspicion  if  we  can  make  out  a  distinct  predisposition  to  tuber- 
culosis, either  hereditary  or  constitutional,  or  the  history  of  a  previous  tuber- 
culous affection,  especially  pleurisy,  and  also  chronic  affections  of  the  bones, 
and  the  like;  or  if  any  form  of  local  tuberculous  disease,  as  of  the  lymph- 
glands,  a  pulmonary  apex,  the  pleura,  etc.,  be  present. 

On  these  factors  rests  the  differential  diagnosis  between  the  "  typhoid " 
form  of  miliary  tuberculosis  and  typhoid  fever.  Marked  roseola  and  consid- 
erable enlargement  of  the  spleen  are  distinct  arguments  for  typhoid,  although 
they  sometimes  occur  in  miliary  tuberculosis,  and  so  are  the  intestinal  symp- 
toms of  typhoid,  such  as  meteorism,  the  characteristic,  loose  yellow  stools,  and 
possibly  intestinal  hemorrhage;  but  we  must  not  forget  that  both  the  roseola 
and  the  intestinal  symptoms  may  be  absent  in  typhoid.  The  course  of  the 
fever  must  always  be  considered  in  the  differential  diagnosis.  It  is  much 
more  frequently  irregular  and  atypical  in  tuberculosis  than  in  typhoid.  Of 
course,  the  temperature  curve  is  not  an  absolutely  decisive  factor.  The  pro- 
portionately slight  acceleration  of  the  pulse  in  typhoid  is  worthy  of  note.  The 
blood  does  not  afford  any  indubitable  signs  of  distinction  between  the  two, 
since  in  neither  disease  is  there  a  decided  leucocytosis.  If,  however,  the  num- 
ber of  leucocytes  is  conspicuously  small,  5,000  or  less,  typhoid  is  strongly 
suggested.  The  Gruber-Widal  serum  reaction  or  the  direct  demonstration  of 
the  typhoid  bacilli  in  the  blood  or  in  the  dejecta  (see  page  25)  is  very 
important  in  the  differential  diagnosis;  if  positive,  these  tests  are  decisive. 


324  DISEASES  OF  THE  RESPIRATORY  ORGANS 

On  the  other  hand,  of  course,  the  absolute  demonstration  of  miliary  tubercu- 
losis in  the  choroid  is  unequivocal  evidence  in  favor  of  miliary  tuberculosis. 
Weichselbaum  and  others  have  been  able  to  demonstrate  tubercle  bacilli  in 
the  blood  in  a  few  cases.  In  general,  however,  this  is  difficult,  and  not  always 
possible.  [Ordinary  and  also  distilled  water  sometimes  contain  acid-fast 
bacilli  which  may  be  mistaken  for  tubercle  bacilli  and  cause  errors  in  exam- 
ining blood  and  feces.]  In  all  doubtful  cases  the  sputum  must  be  very  care- 
fully searched  for  tubercle  bacilli. 

In  many  cases  the  onset  of  meningeal  symptoms  may  aid  the  diagnosis. 
Of  course,  if  the  patient  is  not  seen  until  the  last  stages  of  meningitis,  espe- 
cially when  there  is  an  incomplete  history,  the  diagnosis  is  often  very  difficult. 
In  this  case,  if  the  fluid  obtained  by  lumbar  puncture  is  found  to  contain 
tubercle  bacilli,  the  diagnosis  may  be  settled  (compare  the  chapter  on  Tuber- 
culous Meningitis  in  Vol.  II). 

Acute  tuberculosis  is  often  confounded  with  severe  bronchitis,  especially  in 
old  persons  who  are  considered  emphysematous.  The  very  bad  general  con- 
dition, the  pallor,  the  rapid  loss  of  strength,  and  the  fever  will,  when  kept  in 
mind,  call  our  attention  to  acute  tuberculosis,  and  render  the  diagnosis  pos- 
sible. We  have  already  indicated  the  possibility  of  confusion  at  the  onset 
between  miliary  tuberculosis  and  croupous  pneumonia. 

Prognosis. — The  cases  described  in  literature  as  "  cured  miliary  tuber- 
culosis "  are  so  uncertain  in  their  diagnosis  that  they  cannot  be  regarded 
as  convincing.  We  must  therefore  consider  the  prognosis  is  absolutely 
fatal.  The  differences  in  the  course  of  the  disease  have  been  already  men- 
tioned. 

Treatment. — Although  drugs  are  absolutely  powerless,  still,  the  case  in 
hand  must  always  receive  treatment,  especially  if  the  diagnosis  cannot  be  made 
with  absolute  certainty.  Our  prescriptions  are  purely  symptomatic.  The  cases 
with  a  typhoidal  course  are  to  be  treated  just  like  typhoid,  with  baths,  stimu- 
lants, etc.  Tepid  baths,  and  also  local  applications  to  the  chest,  expectorants, 
and  narcotics,  are  indicated  when  the  thoracic  symptoms  predominate.  If 
meningeal  symptoms  set  in,  we  may  try  ice,  perhaps  local  bloodletting,  iodo- 
form salve,  or  mercurial  ointment  externally,  and  iodid  of  potassium  in- 
ternally. 


CHAPTEE    VIII 

GANGRENE    OF    THE    LUNGS 

^Etiology. — The  sole  cause  of  pulmonary  gangrene — that  is,  the  death 
and  putrid  decomposition  of  the  lung  tissue — is  the  entrance  of  the  bacteria  of 
putrefaction  into  the  lungs.  The  opportunity  for  inhaling  them  is  certainly 
very  great,  but  the  normal  organism  apparently  possesses  the  property  of  nul- 
lifying them  and  making  them  powerless.  Under  certain  conditions,  how- 
ever, they  take  root  in  the  lung  and  cause  the  death  of  the  pulmonary  paren- 
chyma, which  then,  as  a  result  of  the  presence  of  these  specific  bacteria  of 
putrefaction,  succumbs  to  that  peculiar  form  of  putrid  decomposition  known 
as  "moist  gangrene." 


GANGRENE  OF  THE   LUNGS  325 

The  factor  which  most  frequently  gives  rise  to  the  development  of  pulmo- 
nary gangrene  is  the  entrance  of  organic  foreign  substances,  especially  bite  of 
food,  into  the  lungs.  The  bacteria  of  putrefaction  either  enter  the  lungs  with 
the  foreign  substance,  or  they  settle  there  later  and  set  up  a  putrid  decompo- 
sition, first  in  that  portion  of  the  lungs,  and  then  in  the  neighboring  lung 
tissue.  The  entrance  of  organic  foreign  substances  into  the  lungs  occurs  in  dif- 
ferent ways.  It  often  happens  from  swallowing  the  wrong  way,  or  from  an  ac- 
cidental inhalation.  In  this  way  pulmonary  gangrene  may  arise  in  previously 
healthy  people,  but  it  occurs  especially  in  patients  who  are  very  low,  very 
stupid,  and  soporose,  and  also  in  the  insane,  in  patients  who  cannot  swallow 
or  cough  well,  and  in  patients  with  paralysis  of  deglutition,  as  in  bulbar  paral- 
ysis. Bits  of  food  may  also  reach  the  lungs  from  eructations  and  vomiting. 
Thus  are  explained  the  cases  of  pulmonary  gangrene  which  occur  in  patients 
with  cancer  of  the  stomach,  and,  still  more  frequently,  with  cancer  of  the 
cesophagus.  Putrid  organic  material  may  also  reach  the  lungs  from  ulcerative 
and  ichorous  processes  in  the  mouth,  the  pharynx,  and  the  larynx.  In  cancer 
of  the  tongue,  the  pharynx,  and  the  larynx,  in  other  ulcerative  processes,  and 
in  injuries  or  wounds  from  operations  in  the  mouth  and  pharynx  that  have 
become  septic,  pulmonary  gangrene  may  develop  quite  readily.  Finally,  septic 
foci  in  the  vicinity  may  extend  to  the  lungs  or  perforate  into  a  bronchus.  In 
this  way  pulmonary  gangrene  may  arise  from  the  perforation  through  the 
pleura  into  the  lungs  of  an  ulcerated  cancer  of  the  stomach  or  a  gastric  ulcer, 
or  from  the  perforation  of  tuberculous  bronchial  lymph-glands  into  the 
cesophagus  with  the  formation  of  an  cesophago-bronchial  fistula,  etc. 

In  some  cases  the  cause  of  the  pulmonary  gangrene  cannot  be  made  out, 
since  the  entrance  of  a  foreign  substance  has  perhaps  been  wholly  unnoticed, 
as  may  happen  in  children,  or  during  sleep.  We  had  a  grown-up  young 
woman  under  observation  for  a  long  time  with  pulmonary  gangrene,  and  one 
day  she  coughed  up  several  fragments  of  chicken  bones,  but  she  could  give 
no  account  of  how  they  entered  the  lungs. 

Experience  teaches  us  that  pulmonary  gangrene  is  more  apt  to  develop  in 
persons  with  impaired  nutrition,  in  old,  marantic  individuals  and  drunkards, 
than  in  those  who  are  healthy.  The  tendency  of  patients  with  diabetes  mellitus 
to  pulmonary  gangrene  is  remarkable. 

Pulmonary  gangrene  often  develops  secondarily  to  some  other  pulmonary 
affection.  We  have  already  spoken  of  the  relations  between  it  and  fetid  bron- 
chitis. Fetid  bronchitis,  on  the  one  hand,  often  leads  to  pulmonary  gangrene 
through  an  extension  of  the  process  to  the  alveoli;  and,  on  the  other  hand, 
when  there  is  a  gangrenous  focus  in  the  lungs,  the  bronchi  are  often  infected 
to  a  wide  extent  by  the  putrid  secretion  coming  from  it,  and  then  there  arises 
fetid  bronchitis.  Both  diseases  often  run  into  each  other  without  any  sharp 
boundary;  but  gangrene  may  develop  secondarily  in  other  affections  of  the 
lungs.  A  new  infection  with  putrid  material,  however,  is  always  requisite, 
and  the  affection  of  the  lungs  that  already  exists  furnishes  merely  a  favorable 
soil.  This  is  the  only  explanation  of  the  process  when  croupous  pneumonia 
"  runs  into  gangrene,"  or  when  gangrene  develops  in  catarrhal  pneumonia,  in 
bronchiectasis,  or  in  phthisis. 

Although  the  agents  of  putrefaction  enter  the  lungs  through  the  bronchi  in 
most  of  the  modes  of  origin  of  pulmonary  gangrene  that  have  been  mentioned, 
21 


326  DISEASES   OF   THE   RESPIRATORY  ORGANS 

they  may  also  be  transported  into  the  lungs  by  the  blood  current.  We  call 
these  forms  embolic  gangrene.  We  find  such  gangrenous  nodules  in  the  lungs 
in  connection  with  extensive  gangrenous  bedsores,  puerperal  processes,  suppu- 
rative caries  of  the  bones,  etc.  In  these  cases  the  putrid  material  enters  a  vein 
from  the  seat  of  the  primary  process  and  is  brought  to  the  lungs,  and  here 
we  find,  as  a  result  of  the  putrid  character  of  the  embolus,  not  a  simple  in- 
farction, but  an  embolic  gangrene. 

Pathological  Anatomy. — We  more  frequently  find  pulmonary  gangrene  in 
the  lower  lobes  than  in  the  upper,  corresponding  to  its  mode  of  origin.  Either 
both  lungs  are  affected  or  only  one,  and  the  right  somewhat  more  frequently 
than  the  left.  We  distinguish  a  diffuse  and  circumscribed  form,  according  to 
the  extent  of  the  gangrene.  Embolic  gangrene  belongs  to  the  latter  form,  and 
its  nodules,  by  preference,  lie  near  the  pleural  surface. 

We  can  easily  recognize  the  anatomical  changes  in  gangrene.  The  lung 
tissue  is  changed  to  a  discolored,  dirty,  greenish-gray  mass,  which  gradually 
and  progressively  becomes  dissolved,  forming  a  most  foul-smelling  ichor.  We 
find,  left  in  it,  necrotic  fragments  of  tissue  and  vessels.  Gangrenous  cavities,, 
with  irregular,  ragged  walls,  are  formed  from  the  partial  expectoration  of  the 
softened  gangrenous  nodule.  The  lung  tissue  in  the  vicinity  of  the  gangrenous 
spot  is  to  a  greater  or  less  extent  inflamed,  partly  in  the  form  of  catarrhal 
pneumonia,  partly  in  the  form  of  circumscribed  croupous  pneumonia.  The 
inflamed  parts  in  the  vicinity  are  gradually  involved  in  the  gangrene,  so  long 
as  the  process  extends,  but  finally  a  suppurating  line  of  demarcation  may  be 
formed  about  the  gangrene,  the  whole  gangrenous  fragment  is  in  a  measure 
sequestrated,  encapsuled,  and  gradually  expelled,  and  so  healing  becomes  pos- 
sible. We  have  already  stated  that  fetid  bronchitis  may  arise  from  a  gan- 
grenous nodule. 

Whenever  a  gangrenous  nodule  reaches  the  pleura,  a  purulent  and  usually 
a  sanious  pleurisy  follows  from  direct  infection.  Pneumothorax  may  arise 
from  perforation  of  a  gangrenous  cavity. 

Clinical  History. — The  symptoms  of  gangrene  depend  for  the  most  part 
upon  the  local  affection  in  the  lung.  The  condition  of  the  expectoration  is. 
characteristic,  and  it  alone  may  decide  the  diagnosis. 

In  many  ways  the  expectoration  greatly  resembles  that  of  fetid  bronchitis,, 
and  indeed  a  great  part  of  it  does  not  come  directly  from  the  gangrenous 
nodule,  but  is  the  secretion  of  the  diseased  bronchi.  The  penetrating  stench 
of  the  sputum,  a  most  repulsive,  putrid  odor,  is  very  striking.  The  patient's 
breath  and  cough  also  have  this  stench,  which  infects  the  whole  vicinity.  The 
amount  of  the  sputum  is  usually  large;  it  may  reach  8  or  16  ounces  (200  to 
500  c.c.)  in  twenty-four  hours.  If  the  sputum  is  collected  in  a  glass  it  forms 
three  layers,  like  the  sputum  of  fetid  bronchitis — an  upper  layer,  muco- 
purulent, greasy,  consisting  in  part  of  nummular  sputa,  and  covered  with 
much  froth;  a  middle  serous  layer,  in  which  some  firm  masses  from  the  upper 
layer  float;  and  a  lower  layer,  almost  wholly  of  pus,  but  greasy  and  greenish- 
yellow,  which  usually  contains  many  large  and  small  plugs  and  shreds  of  tis- 
sue. We  find  in  these  plugs,  on  microscopic  examination,  beautifully  twisted 
needles  of  the  fat  acids  (see  Fig.  40,  page  203)  imbedded  in  countless  bac- 
teria, fat-drops,  and  detritus,  and  often  collected  in  large  bundles ;  but  besides 
these  we  find  in  the  sputum  the  constituents  of  the  parenchyma  of  the  lungs,, 


GANGRENE  OF   THE   LUNGS  327 

and  this  alone  is  the  decisive  factor  in  distinguishing  between  pulmonary 
gangrene  and  simple  fetid  bronchitis. 

Traube's  statement  that  in  pulmonary  gangrene  the  expectoration  contains 
few,  if  any,  elastic  fibers,  because  the  elastic  tissue  itself  is  destroyed  by  gan- 
grene, is  not  correct ;  or,  at  any  rate,  it  is  too  sweeping.  We  have  almost  in- 
variably found  in  the  expectoration  an  abundance  of  elastic  tissue,  as  well  as 
other  fragments  of  the  parenchyma,  pigment  granules,  and  the  like.  Yet 
there  is  a  probability,  no  doubt,  that  in  pulmonary  gangrene  the  elastic  tissue 
is  for  the  most  part  destroyed.  Filehne  succeeded  in  extracting  from  the 
sputum  of  pulmonary  gangrene,  by  means  of  glycerin,  a  ferment  which  in 
alkaline  solution  completely  dissolved  elastic  tissue  in  a  few  days.  The 
sputum  always  contains  in  enormous  numbers  bacteria  of  various  kinds,  both 
cocci  and  bacilli.  Which  of  these  are  the  special  cause  of  the  gangrene  has 
not  yet  been  definitely  settled.  The  chemical  examination  of  the  sputum 
shows  the  presence  of  those  substances  which  may  always  be  found  in  the 
putrefaction  of  organic  matter — tyrosin,  leucin,  ammonia,  sulphureted 
hydrogen,  butyric  acid,-  valerianic  acid,  caprylic  acid,  etc.  The  fresh  sputum 
usually  has  an  alkaline  reaction,  but  on  standing  it  becomes  acid. 

Many  cases  of  gangrene  lead  to  erosion  of  the  vessels  and  severe  hemopty- 
sis.    Slight  admixtures  of  blood  in  the  sputum  are  not  infrequent. 

The  other  symptoms  on  the  part  of  the  lungs  are  not  especially  character- 
istic of  gangrene.  Most  patients  complain  of  cough,  pain  in  the  side,  and 
more  or  less  severe  dyspnoea.  Physical  examination,  as  a  rule,  permits  us  to 
make  out  the  seat  of  the  nodule,  but  not  always,  since  the  physical  signs,  of 
course,  depend  upon  the  situation  and  extent  of  the  gangrene.  Small  nodules, 
situated  centrally,  often  give  no  objective  evidence  of.  their  presence.  Every 
extensive  infiltration,  however,  must  cause  dullness  on  percussion.  Over  the 
area  of  dullness  we  hear  bronchial  respiration,  and  usually  quite  numerous 
moist  rales.  If  a  gangrenous  cavity  is  formed,  the  physical  examination  may 
show  plain  symptoms  of  a  cavity — tympanitic  resonance  on  percussion,  am- 
phoric respiration,  coarse  moist  rales,  etc. 

The  physical  signs  are  sometimes  due  to  the  accompanying  pleurisy;  the 
dullness  is  more  complete,  the  respiratory  murmur  and  the  vocal  fremitus  are 
diminished,  and  the  adjacent  organs  are  displaced  by  the  abundant  effusion; 
but  an  absolute  diagnosis  of  an  accompanying  pleurisy  is  often  to  be  made 
only  by  an  exploratory  puncture.  We  have  already  spoken  of  the  occasional 
development  of  pneumothorax. 

In  many  cases  there  is  fever,  of  quite  an  irregular  character  and  of  very 
varying  intensity.  In  the  cases  in  which  the  gangrenous  nodule  is  seques- 
trated, and  the  secretion  can  be  freely  emptied  through  the  bronchi,  so  that 
there  is  no  absorption  of  septic  material  into  the  blood,  fever  may  be  entirely 
absent. 

We  often  see  gastric  and  intestinal  symptoms  in  pulmonary  gangrene,  the 
disturbance  being  without  doubt  due  to  swallowing  some  of  the  fetid  sputum. 
Many  patients  complain  of  loss  of  appetite,  and  sometimes  of  vomiting  or 
diarrhea.  In  severe  acute  cases  there  is  sometimes  a  well-marked  typhoidal 
state,  with  such  symptoms  as  stupor,  delirium,  and  great  cardiac  weakness. 
This  condition  is  probably  caused  by  the  absorption  of  septic  material  into  the 
blood.     Rheumatic  pains  in  the  muscles  and  joints  are  seen  in  this  disease, 


328  DISEASES  OF  THE  RESPIRATORY  ORGANS 

just  as  in  fetid  bronchitis.  Finally,  it  should  be  remarked  that  the  appear- 
ance of  secondary  abscesses  in  the  brain  (see  Vol.  II)  has  been  repeatedly 
observed  in  piilmonary  gangrene.  This  fact  must  be  borne  in  mind  when, 
in  the  course  of  pulmonary  gangrene,  marked  brain  symptoms  are  developed, 
especially  if  we  have  not  only  such  general  symptoms  as  coma,  but  also  such 
local  symptoms  as  hemiplegia  and  other  forms  of  paralysis,  and  convulsions. 

The  general  course  of  the  disease  shows  very  great  variations.  In  all  cases 
in  which  the  pulmonary  gangrene  is  secondary  to  some  other  affection,  the 
course  and  the  general  type  of  the  disease  depend  very  largely  upon  the  pri- 
mary attack,  but  the  cases  of  idiopathic  gangrene  also  present  great  varia- 
tions. The  onset  of  the  disease  is  either  quite  gradual  and  slow,  or  quite  acute, 
and  associated  with  fever  and  thoracic  symptoms.  The  stinking  expectoration 
and  the  bad  odor  from  the  patient's  mouth  first  direct  the  attention  to  the 
existence  of  putrid  processes  in  the  lungs.  The  disease  is  usually  very  chronic, 
lasting  for  months  or  even  years.  Many  remissions  and  intermissions  occur. 
"With  proper  care  and  treatment  we  may  see  a  decided  improvement,  and  often 
apparently  a  complete  cessation  of  the  disease.  The  bad  odor  ceases,  the 
expectoration  diminishes  or  disappears  entirely,  and  the  patient's  strength 
and  nutrition  become  almost  normal;  but  relapses  may  occur  after  long 
intervals.  When  the  affection  is  of  slight  extent  we  may  even  see  a  complete 
recovery. 

Pulmonary  gangrene  always  takes  a  worse  course  in  previously  weak  and 
marantic  persons,  and  an  unfavorable  termination  may  follow  in  a  compara- 
tively short  time.  Death  ensues  either  from  a  general  loss  of  strength,  as  a 
result  of  the  disease,  or  from  complications,  such  as  pulmonary  hemorrhage, 
ichorous  pleurisy,  pneumothorax,  or  abscess  of  the  brain.  Eupture  of  an 
ichorous  empyema  outwardly,  or  into  the  peritoneum,  or  into  other  cavities, 
is  rare. 

Special  mention  must  be  made  of  the  fact  that  the  symptoms  of  pulmonary 
gangrene  are  not  always  so  very  pronounced.  In  persons  who  are  weak  and 
run  down  we  often  see  pulmonary  gangrene  at  the  autopsy,  although  during 
life  there  have  been  no  marked  symptoms,  not  even  offensive  sputum  or  fetor 
from  the  mouth. 

Diagnosis. — The  diagnosis  cannot  be  made  with  certainty  unless  the  char- 
acteristic sputum  is  present.  We  can  decide  whether  the  sputum  comes  from 
a  fetid  bronchitis"  or  from  the  fetid  contents  of  a  bronchiectasis,  or  from 
actual  gangrene,  only  by  finding  under  the  microscope  the  remains  of  lung 
tissue  in  the  expectoration.  Physical  examination  in  gangrene,  at  least  in 
part  of  the  cases,  also  gives  the  signs  of  infiltration  or  of  cavity  formation  in 
the  lungs.  In  addition  to  the  ordinary  methods  of  physical  examination,  X-ray 
examination  is  of  great  importance. 

Prognosis. — The  prognosis  depends  first  upon  the  nature  of  the  underly- 
ing disease,  and  then  upon  the  extent  of  the  affection,  the  strength  of  the 
patient,  and  the  possibility  of  sufficient  care  and  proper  treatment.  If  the 
process  in  the  lung  becomes  sequestrated,  marked  improvement  may  follow, 
even  in  the  severest  conditions;  but  we  must  always  remember  that  a  relapse 
is  possible.  Complete  recovery  from  pulmonary  gangrene  is  certainly  ex- 
tremely rare,  if  it  ever  occurs.  We  have  already  mentioned  the  dangers  which 
may  lead  to  a  fatal  termination. 


DISEASES   FROM   THE   INHALATION   OF   DUST  329 

Treatment. — Prophylaxis  plays  an  important  part  in  those  eases  in  which 
there  is  clanger  of  the  entrance  of  bits  of  food  into  the  air-passages  from 
defective  deglutition.  We  must  think  of  the  possibility  of  this  with  all 
patients  who  show  great  stupor,  and  also  with  patients  who  have  pharyngeal 
paralysis,  in  order  to  watch  them  while  taking  food,  and  eventually  to  try 
artificial  feeding  with  an  oesophageal  tube. 

The  treatment  of  already  existing  pulmonary  gangrene  has,  as  its  chief 
aim,  to  check  the  putrid  processes  of  decomposition  in  the  lungs.  Unfortu- 
nately, the  remedies  at  our  command  are  not  in  all  cases  sufficient  for  this. 
The  different  disinfecting  inhalations  are  the  most  effective.  They  are  used 
in  the  same  way  as  in  fetid  bronchitis  (vide  supra).  Turpentine  deserves  the 
most  confidence,  and  it  may  also  be  given  internally  with  good  results.  Ac- 
cording to  Lepine,  however,  terpin  hydrate  acts  even  better  than  turpentine. 
We  may  also  call  attention  to  inhalations  with  carbolic  acid,  Curschmann's 
carbolic  mask,  inhalations  with  salicylic  and  boric  acids  (4  parts  of  salicylic 
and  20  of  boric  acid  to  1,200  of  distilled  water),  bromin  (bromin  and  bromid 
of  potassium,  2  parts  of  each  to  1,000  of  water),  and  similar  remedies. 

Besides  oil  of  turpentine,  other  internal  remedies  are  recommended:  0.5 
to  1  gr.  (gm.  0.03  to  0.06)  of  acetate  of  lead  every  two  hours,  creosote,  guaia- 
col,  etc.  Their  action  is  uncertain.  Of  late,  myrtol  has  been  greatly  extolled. 
It  is  given  in  capsules  containing  gr.  ijss.  (gm.  0.15),  of  which  two  or  three 
are  to  be  taken  every  two  hours. 

The  general  treatment  of  the  patient  is  very  important — he  should  have 
good  food,  and  live  in  as  good  air  as  possible.  We  must  treat  the  pain  in  the 
chest  and  the  cough  symptomatically,  local  applications  and  morphin  being 
most  useful.  The  fever  seldom  gives  occasion  for  direct  interference.  We 
may  try  to  relieve  the  gastric  and  intestinal  symptoms  by  giving  antiseptics 
internally,  especially  by  small  doses  of  muriatic  *acid,  salicylic  acid,  or  creo- 
sote, as  well  as  by  the  ordinary  remedies,  such  as  bitters  and  opium. 

If  a  secondary  ichorous  pleurisy  develops,  with  or  without  pneumothorax, 
removal  of  the  fluid  by  operation  is  necessary,  if  the  patient  has  sufficient 
strength  to  bear  it.  Direct  incision  and  drainage  of  the  gangrenous  area  in 
the  lung  has  also  recently  been  tried.  It  is  an  operative  procedure  that  is  at 
least  worthy  of  further  trial  and  development.  Lenhartz,  of  Hamburg,  in 
particular,  has  reported  some  encouraging  results  from  operative  intervention. 


CHAPTEK   IX 

DISEASES   FROM   THE   INHALATION    OF   DUST 

(Pneumonoconiosis) 

Although  there  are  a  number  of  important  contrivances  in  the  respira- 
tory apparatus  to  prevent  the  entrance  of  foreign  substances  into  the  lungs, 
still,  if  a  person  remains  in  a  dusty  atmosphere,  so  many  particles  of  dust 
may  be  inhaled  that  they  are  not  without  effect  on  the  lung  tissue.  The 
diseases  arising  from  the  inhalation  of  dust  are  usually  purely  vocational  dis- 
eases, which  occur  especially  in  workmen  whose  occupation  involves  the  con- 


330  DISEASES  OF  THE  RESPIRATORY  ORGANS 

tinual  inhalation  of  some  kind  of  dust.  In  earlier  chapters  of  this  book,  par- 
ticularly while  considering  chronic  bronchitis,  we  have  already  emphasized 
the  harmful  influence  of  the  inhalation  of  dust.  We  have  seen  how  the 
habitual  respiration  of  organic  dust  in  particular  (from  grain,  wool,  wood,  and 
tobacco)  is  very  apt  to  lead  to  severe  forms  of  bronchitis  and  bronchiolitis.  We 
must  now  draw  attention  to  certain  specific  diseases  similarly  caused. 

We  must  first  mention,  however,  a  condition  of  the  lungs  which  can  scarcely 
be  regarded  as  pathological,  although  it  has  its  origin  in  the  constant  inhala- 
tion of  dust,  especially  of  coal  dust — the  ordinary  black  pigmentation  of  the 
lungs.  There  can  now  no  longer  be  any  doubt,  although  there  was  once  a  long 
dispute  about  it,  that  the  black  pigment  in  the  lung  comes,  in  large  part,  at 
least,  from  the  inhalation  of  carbon.  The  particles  of  carbon  pass  into 
the  lungs  themselves,  and  thence  into  the  bronchial  glands  by  means  of  the 
lymphatics.  A  certain  part  of  the  coal  dust  inhaled  is  removed  with  the 
expectoration,  and  it  may  easily  be  found  in  it  microscopically,  and  often  by 
the  naked  eye,  as  we  see  it  in  the  well-known  black  expectoration  which  we 
often  have  in  the  morning,  if  we  have  spent  the  previous  evening  in  a  room 
filled  with  smoke.  In  Germany,  Traube  was  the  first  to  discover  the  particles 
of  carbon  in  the  expectoration  of  a  charcoal  burner.  In  the  man's  lungs,  after 
death,  the  vegetable  origin  of  these  particles  could  be  recognized,  and  Traube 

gave    the    correct    explana- 

.r,  ■  v^o  tion  of  them.     In  workmen 

%r  -J* '[■■■'&  wno   inhale   large   amounts 

\iy£  ■&'    - .  '.-f^y^i'r-  °^    charcoal    dust,    anthra- 

*  £®f  "  St$&  c^e     coa^     dust>     soot,     or 

rJlrtJ*.#.;'~M-[*v    V    3|pr,,^.  graphite,    the    "normal" 

',;£,>  t'jt      'f'\     *  ■  ,*  '%>*£?,       pigmentation    of    the    lung 

>v'**ri  }      t$>k     ''*'         passes    into    a    pathological 

'  'if0^0;(l  O&M        ■"  on         $t'e  condition,    anthracosis   pul- 

'-%'■  "'-  *&!&?'  ^r  monum.     With  this  is  usu- 

Fig.  56.-Expectoration  of  a  man  who  worked  on  graphite.  a1^  ass°ciated  an  extensive 
Numerous  cells  filled  with  particles  of  carbon.  (Er-  chronic  bronchitis.  In  the 
langen  Medical  Clinic.)  expectoration    of    such    pa- 

tients are  found  many  cells 
filled  with  black  particles  of  coal,  even  long  after  they  have  left  the  dusty  at- 
mosphere. The  pigmented  cells  are  leucocytes,  or  perhaps  some  of  them 
epithelial  cells   (see  Fig.  56). 

Zenker  first  discussed  comprehensively  the  fact  of  the  entrance  of  the  dif- 
ferent sorts  of  dust  into  the  lungs  and  the  consequent  results.  Besides  the 
anthracosis  already  mentioned,  the  pulmonary  disease  from  inhaling  the  dust 
of  flint  and  other  stones  is  of  especial  importance,  the  so-called  stonecutter's 
lung — chalicosis  pulmonum — and  also  that  from  inhaling  metallic  dust,  espe- 
cially oxid  of  iron — siderosis  pulmonum.  The  "  stone  lungs  "  have  been 
observed  in  workmen  in  the  stamping  rooms  of  glass  factories,  in  millstone 
cutters,  stone  polishers,  stone  hammerers,  plasterers,  workers  in  porcelain, 
masons,  slate  quarrymen,  potters,  etc.  "  Metal-dust  lungs  "  occur  in  file  cut- 
ters, iron  workers,  mirror  polishers,  and  especially  in  grinders,  who  inhale  a 
mixture  of  stone  and  iron  dust.  The  first  case  of  a  "  red-iron  lung "  was 
observed  by  Zenker,  in  a  girl  who  had  inhaled  a  thick  dust  of  iron  for  ten 


DISEASES   FROM   THE   INHALATION   OF   DUST  331 

or  twelve  hours  a  day.  Her  work  was  to  color  blotting  paper  with  a  powder 
of  red  oxid  of  iron.  During  the  inhalation  of  all  these  and  similar  kinds  of 
dust,  a  portion  of  the  inspired  particles  of  dust  are  taken  up  by  the  leucocytes, 
and  perhaps  also  by  the  epithelial  cells,  finally  reaching  the  lymph-channels 
of  the  lungs.  Some  of  the  particles  of  dust  remain  in  the  interstitial  con- 
nective tissue  of  the  lungs.  Others  find  their  way  to  the  bronchial  and  retro- 
bronchial  lymph-glands. 

If  the  inhalation  of  dust  is  long  continued,  it  causes  not  only  this  abnormal 
pigmentation  of  the  lungs,  but  also  macroscopic  anatomical  lesions.  These 
consist,  partly,  in  a  more  or  less  severe  and  extensive  chronic  bronchitis,  and 
partly  in  an  interstitial  inflammation  which  is  due  to  the  chronic  irritation 
of  the  foreign  matter  (e.g.,  flinty  particles),  and  leads  to  the  formation  of 
connective  tissue.  The  lungs  are  studded  with  nodules,  which  feel  hard  to 
the  touch,  and  grate  on  section  with  a  knife.  All  of  these  nodules  consist  of 
firm  connective  tissue,  in  which  the  particles  of  stone  or  iron  are  encapsuled. 
By  the  union  of  single  nodules  we  may  get  more  extensive  induration  and 
cicatricial  formation.  Chemical  examination  of  such  lungs  gives,  as  might 
be  supposed,  a  large  amount  of  silicic  acid,  iron,  etc. 

In  most  of  the  cases  which  come  to  autopsy  we  find  further  changes  in  the 
lungs,  which  are  not  the  immediate  result  of  the  inhalation  of  dust,  but  consist 
of  sequelae  and  complications.  Chronic  diffuse  bronchitis  in  the  worker  in 
dust,  like  any  other  chronic  bronchitis,  may  give  rise  to  pulmonary  emphysema, 
and  later  to  cardiac  hypertrophy,  etc.  We  very  often  find  in  the  lungs  co- 
existing and  pronounced  tuberculous  changes.  It  need  hardly  be  emphasized 
that  these  changes  are  not  the  direct  result  of  the  inhalation  of  dust,  but  that 
the  changes  in  the  lungs  set  up  by  such  an  inhalation  furnish  merely  a  favor- 
able soil  for  infection  with  tuberculosis.  In  most  cases,  the  "  dust  lungs  " 
acquire  a  marked  clinical  significance  chiefly  from  the  sequelae  mentioned — 
namely,  emphysema  and  tuberculosis.  The  circumscribed  nodules  of  inter- 
stitial pneumonia  have  no  very  marked  symptoms  following  them.  In  all 
cases  in  which  there  is  a  fatal  termination,  with  pulmonary  symptoms,  we 
should  regard  the  immediate  action  of  the  dust  as  much  less  the  cause  of  death 
than  are  the  secondary  diseases. 

The  essential  points  to  be  considered  in  judging  of  the  clinical  symptoms 
of  the  diseases  from  inhaling  dust  are  contained  in  what  has  been  said.  The 
symptoms  are  those  of  chronic  bronchitis,  pulmonary  emphysema,  or  chronic 
phthisis,  and  attention  to  the  injurious  influences  associated  with  the  patient's 
calling  is  the  only  possible  way  of  making  a  diagnosis,  but  in  individual  cases 
it  may  always  be  a  matter  of  doubt  how  far  other  accidental  causes  of  disease 
may  come  into  play. 

The  prognosis  depends,  in  the  first  place,  upon  whether  the  patient  can  be 
removed  from  the  action  of  these  injurious  influences  or  not,  but  we  must  also 
mention  the  fact,  which  has  been  often  observed,  that  many  individuals  get 
somewhat  used  to  the  dust.  After  they  have  once  recovered  from  the  initial 
bronchitis,  such  persons  can  live  in  an  atmosphere  of  dust  for  a  long  time 
without  any  noticeable  injury. 

The  prophylaxis  of  diseases  from  inhaling  dust  forms  an  extended  chapter 
in  the  hygiene  of  occupations,  which  we  cannot  dwell  upon  here.  The  work- 
man must  be  taught  the  danger  to  which  he  is  exposed,  and  the  danger  itself 


332  DISEASES   OF  THE   RESPIRATORY   ORGANS 

must  be  diminished  as  much  as  possible  by  sufficient  ventilation  of  the  work- 
rooms., by  cleanliness,  and,  under  some  circumstances,  by  a  change  in  the 
technicalities  of  the  business. 

We  need  not  give  any  special  directions  regarding  the  treatment  of  diseases 
from  inhaling  dust.  It  is  founded  on  the  same  principles  as  the  treatment  of 
chronic  bronchitis,  emphysema,  and  chronic  pulmonary  tuberculosis. 


CHAPTEE    X 


EMBOLIC    PROCESSES   IN    THE   LUNGS 

{Hemorrhagic  Infarction  of  the  Lungs) 

etiology. — The  sources  from  which  the  material  for  an  embolic  plugging 
of  branches  of  the  pulmonary  artery  comes  lie  either  in  the  right  side  of  the 
heart  or  in  the  veins  of  the  body.  Pathological  anatomy  teaches  us  how  often 
thrombi  are  formed  in  the  veins,  especially  in  the  veins  of  the  lower  extremities 
and  in  the  pelvic  veins,  and  in  the  right  side  of  the  heart,  in  the  recesses 
between  the  trabecule,  in  the  auricles,  on  the  valves  and  the  chordas  tendinge, 
and  at  the  apex  of  the  ventricle.  The  particles  torn  loose  from  a  thrombi  so 
situated  are  carried  on  by  the  blood  current,  reach  the  lungs,  plug  a  larger  or 
a  smaller  branch  of  the  pulmonary  artery,  according  to  the  size  of  the  particles, 
and  thus  cause  further  changes  in  the  lung  tissue.  Since  the  branches  of  the 
pulmonary  artery  are  "  terminal  arteries,"  and  since  thus  the  vascular  territory 
belonging  to  each  branch  cannot  be  supplied,  or  can  be  supplied  only  to  a  small 
amount,  with  blood  by  collateral  circulation  from  other  vessels,  the  closure  of 
a  branch  of  the  artery  shuts  the  territory  supplied  by  it  out  of  the  circulation. 
The  pressure,  in  the  part  of  the  vessel  lying  peripherally  to  the  point  of  plug- 
ging, becomes  almost  nil,  and,  as  a  result,  there  is  a  collateral  or  backward 
current  into  the  region  shut  off,  flowing  from  the  capillaries  in  the  vicinity, 
and  probably  even  from  the  veins  belonging  to  it.  Yet  the  blood  which  flows 
in  is  under  so  slight  a  pressure  that  it  does  not  flow  through,  but  stagnates 
in  the  affected  area.  The  walls  of  the  capillaries  and  veins,  in  which  the  nor- 
mal blood  current  has  ceased,  lose  their  natural  consistence  as  a  result  of  this. 
The  vascular  walls  become  abnormally  pervious.  The  fluid  of  the  blood,  the 
white  blood  corpuscles,  and  also  very  many  red  blood  corpuscles,  penetrate 
through  the  walls  of  the  vessel  into  the  surrounding  tissue,  and  change  it 
into  the  so-called  hemorrhagic  infarction.  All  these  changes  develop  more 
readily  if  the  pulmonary  vessels  have  already  been  subjected  to  chronic  stasis. 
For  this  reason,  pulmonary  infarcts  are  very  apt  to  develop  in  cases  of  cardiac 
disease  (especially  in  mitral  stenosis),  whereas  we  quite  frequently  find,  espe- 
cially in  central  portions  of  the  lung,  embolism  of  single  branches  of  the 
pulmonary  artery  without  the  formation  of  an  infarction.  In  such  cases  there 
must  necessarily  be  a  little  circulation  in  the  vascular  territory  which  has  been 
shut  off,  either  by  anastomoses  between  the  territory  of  the  pulmonary  artery 
and  that  of  the  bronchial  or  mediastinal  artery,  or  by  the  neighboring  capil- 
laries, whose  arteries  of  supply  remain  open.  Death  may  immediately  fol- 
low the  sudden  embolic  obturation  of  a  main  trunk  or  of  several  of  the  larger 


EMBOLIC   PROCESSES   IN   THE   LUNGS  333 

branches  of  the  pulmonary  artery;  thus  further  changes  in  the  pulmonary 
tissues  may  not  have  time  to  develop. 

The  changes  thus  far  described  are  the  result  of  a  purely  mechanical  clos- 
ure of  a  pulmonary  artery.  We  have  noticed  this  especially  when  simple 
fibrinous  plugs  have  given  the  occasion  for  the  embolic  process.  Pulmonary 
infarctions  are  most  frequent  in  chronic  heart  disease,  in  all  forms  of  primary 
and  secondary  dilatation  of  the  heart,  but  especially  in  disease  of  the  mitral 
orifice,  most  often  mitral  stenosis.  Thrombus  formation  is  frequent  in  the 
dilated  right  side  of  the  heart,  and  furnishes  material  for  pulmonary  emboli; 
but  these  emboli  are  seen  in  all  other  possible  conditions  of  disease,  in  which 
thrombosis  in  the  right  side  of  the  heart  or  in  the  veins  may  occur  (varices  of 
the  lower  extremities,  etc.).  Numerous  observations  in  recent  years  have 
taught  me  the  great  importance  and  frequency  of  pulmonary  embolism  as  a 
sequel  to  various  operations  (especially  laparotomies),  and  to  confinements. 
We  need  not  discuss  the  ease  with  which  the  smaller  veins  may  become  throm- 
bosed under  these  circumstances,  and  the  likelihood  of  a  pulmonary  embolism 
from  such  a  source.  Very  many  cases  of  pneumonia  and  of  pleurisy  develop- 
ing after  major  operations  or  during  the  puerperium  are  unquestionably  of 
embolic  origin. 

The  question  as  to  whether  the  embolic  material  is  composed  of  fibrin 
alone,  or  of  fibrin  combined  with  special  infectious  substances,  is  one  of  con- 
siderable importance.  Inasmuch  as  that  portion  of  the  lung  thrown  out 
of  circulation  by  an  infarct  offers  no  opposition  to  invasion  by  bacteria,  a 
simple  infarct  may  also  be  followed  by  inflammatory  changes  in  the  pulmo- 
nary tissue  or  in  the  neighboring  pleura.  Embolic  inflammatory  processes 
occur  more  promptly,  however,  when  the  embolus  itself  is  of  an  infectious 
nature. 

If,  for  example,  emboli  reach  the  lungs  from  an  acute  malignant  endo- 
carditis in  the  right  side  of  the  heart,  or,  as  is  most  frequently  the  case,  from 
a  purulent  (septic)  phlebitis  anywhere  in  the  body,  giving  rise  to  a  puri- 
form,  liquefying  thrombus,  the  specific  factors  in  inflammation— that  is, 
bacteria — get  into  the  lungs.  Thus  arise  embolic  abscesses  and  embolic  gan- 
grenous nodules  in  the  lungs.  We  have  already  spoken  of  the  latter,  and  the 
former  are  among  the  most  constant  lesions  in  every  typical  case  of  pysemia. 

The  fundamental  facts  as  to  the  occurrence  and  significance  of  embolic 
processes  in  general,  and  those  located  in  the  lungs  in  particular,  were  dis- 
covered by  Virchow.  For  a  fuller  understanding  of  the  results  of  embolic 
closure  of  the  vessels  we  must  thank  chiefly  Cohnheim. 

Pathological  Anatomy.- — Hemorrhagic  infarctions  may  involve  one  or  more 
lobules,  or  almost  a  whole  lobe  of  the  lung,  according  to  the  situation  of  the 
embolus.  Most  infarctions  are  situated  at  the  periphery  of  the  lung,  and  have 
approximately  a  conical  shape,  corresponding  to  the  extent  of  the  region  of 
the  vessel.  The  base  of  the  cone  lies  against  the  surface  of  the  pleura.  It 
generally  projects  a  little  above  that  surface,  and  its  dark  color  can  usually 
be  plainly  recognized  through  it.  The  pleura  itself  is  the  seat  of  a  fibrinous 
inflammation  at  the  point  to  which  the  infarction  reaches,  and  sometimes 
for  a  large  space  around  it.  The  conical  shape  of  the  infarction  is  plainly 
recognized  on  section.  The  lung  tissue  is  changed  to  a  solid,  fragile,  uni- 
formly black-red  tissue  devoid  of  air.     The  embolus  can  usually  be  readily 


334  DISEASES  OF  THE  RESPIRATORY  ORGANS 

found  in  the  branch  of  the  pulmonary  artery  leading  to  the  infarction.  Under 
the  microscope  we  see  a  diffuse  infiltration  of  tissue,  with  red  blood  corpus- 
cles in  the  infarcted  portion.  The  alveoli  and  finer  bronchi  are  also  filled 
with  coagulated  blood.  Under  favorable  circumstances,  in  cases  of  longer 
standing,  the  blood  may  be  reabsorbed  in  part ;  so  that  the  lung  again  contains 
air,  but  it  remains  much  pigmented  in  that  place,  and  more  or  less  indurated 
from  the  development  of  interstitial  connective  tissue.  In  other  cases  vari- 
ous inflammatory  changes  result  from  the  infarction  (embolic  pneumonia, 
embolic  pleurisy).  Destruction  and  absorption  of  the  infarcted  tissue  with 
secondary  formation  of  scar  tissue  is,  in  contrast  to  other  organs,  only  rarely 
observed  in  the  lungs. 

Hemorrhage  infarctions  are  almost  always  found  in  the  lower  lobes,  some- 
times in  the  right  middle  lobe,  rarely  in  the  upper  lobes.  The  embolic 
abscesses  are  sometimes  very  numerous,  and  are  disseminated  over  the  whole 
lung.  In  larger  abscesses  the  conical  shape  may  often  be  plainly  recognized. 
When  an  abscess  extends  to  the  pleura,  a  purulent  pleurisy  arises  from  direct 
infection.  Combinations  and  transitional  forms  between  the  ordinary  hemor- 
rhagic infarction  and  embolic  abscesses  are  occasionally  found  in  the  lungs. 

Symptoms. — We  often  find  at  the  autopsy  embolism  of  single  branches  of 
the  pulmonary  artery,  with  or  without  infarction,  which  has  caused  no  symp- 
toms at  all  during  life. 

Embolism  of  the  main  trunk,  or  of  a  large  branch  of  the  pulmonary  artery, 
may  cause  sudden  death,  as  has  not  infrequently  been  observed  in  patients 
with  heart  disease,  or  with  venous  thrombosis  (sudden  death  in  cases  of 
thrombosis  of  the  femoral  vein,  after  operations,  etc.).  If  death  be  not 
immediate,  sudden  severe  dyspnoea  and  a  sense  of  oppression  occur.  The 
patients  become  pallid,  cyanosed,  and  pulseless;  consciousness  is  lost,  and 
death  ensues  in  the  briefest  space  of  time,  often  ushered  in  with  slight  con- 
vulsive twitchings.  The  diagnosis  may  at  least  be  suspected  in  such  a  case 
if  we  know  of  a  possible  source  for  an  embolus.  In  some  instances,  when 
an  embolus  is  situated  in  a  large  branch  of  the  pulmonary  artery,  but  has  not 
completely  filled  it,  we  can  hear  a  systolic  vascular  murmur  over  the  affected 
spot,  as  has  been  observed  by  Litten. 

If  we  are  dealing  with  cases  of  nonfatal  embolism  of  the  smaller  vessels, 
the  first  result  of  the  embolism  is  usually  a  sudden  onset  of  severe  pain  in 
the  side,  combined  with  interference  with  respiration  and  a  sense  of  oppres- 
sion. In  cases  of  centrally  situated  infarctions,  pain  may  be  absent,  since  it 
probably  is  dependent  on  pleural  involvement.  The  characteristic  bloody 
sputum  seen  in  many  cases  usually  appears  at  a  somewhat  later  date.  Either 
the  sputum  consists  almost  entirely  of  dark  blood,  or  the  blood  is  mixed  with 
more  or  less  mucus ;  but  there  is  never  much  air  in  it.  The  bloody  expectora- 
tion often  lasts  for  several  days.  It  is  sometimes  absent  altogether,  despite 
existing  infarction;  or,  when  no  marked  infarction  of  the  tissues  has  devel- 
oped, it  may  be  only  slightly  or  not  at  all  blood-tinged.  In  a  few  cases  of 
pulmonary  infarctions  we  have  noticed  an  exceedingly  large  number  of  cast- 
off  alveolar  epithelial  cells  in  the  sputum. 

We  try  to  learn  more  of  the  size  and  situation  of  the  lesions  by  a  physical 
examination  of  the  lungs.  Of  course  this  often  gives  a  negative,  or  at  least 
a  doubtful,  result.     It  goes  without  saying  that  small  infarctions,  and  also 


BROWN   INDURATION   OF  THE   LUNGS  '    335 

those  which  are  central,  cannot  he  made  out  by  physical  examination.  Large 
peripheral  infarctions  may  give  rise  in  many  cases  to  dullness  on  percussion, 
crepitant  rales,  and  harsh  or  bronchial  respiration,  but  it  is  often  hard  to 
decide  in  an  individual  case  whether  the  physical  signs  which  we  meet  with 
are  not  due  to  other  pathological  changes,  such  as  bronchitis,  pleurisy,  or 
hydrothorax.  We  sometimes  hear  a  pleuritic  friction-sound  in  some  part  of 
the  chest  a  few  days  after  we  suspect  that  an  infarction  has  occurred,  by 
which  the  diagnosis  gains  additional  certainty. 

Fever  may  be  wholly  absent,  though  we  sometimes  see  a  moderate  rise 
of  temperature  at  the  onset.  Fever  often  appears  one  or  two  days  after  the 
onset  of  the  subjective  symptoms;  a  circumstance  that  appears  to  us  to  be 
specially  characteristic  of  embolic  inflammation.  Embolism  occasions  pain 
and  a  sense  of  oppression;  the  subsequent  secondary  inflammation  (vide  supra) 
causes  the  fever. 

The  embolic  abscesses  in  the  lungs  hardly  ever  give  rise  directly  to  clinical 
symptoms.  They  form  a  part  of  the  general  picture  of  pyaemia  and  similar 
general  infectious  processes.  Marked  symptoms  on  the  part  of  the  respiratory 
apparatus  are  seen  only  when  the  abscesses  are  present  in  very  large  number. 
If  an  empyema  develops  from  a  focus  which  extends  to  the  pleura,  it  some- 
times occasions  definite  physical  signs. 

It  follows  from  all  that  has  been  said,  that  in  the  diagnosis  of  embolic 
processes  the  chief  stress  must  always  be  laid  on  the  presence  of  an  serological 
factor.  "We  must  regard  the  bloody  sputum  as  the  main  direct  symptom  in 
hemorrhagic  infarction.  Embolic  abscesses  in  the  lungs  may  often  be  sus- 
pected in  pysemic  diseases,  but  they  can  hardly  ever  be  diagnosticated  with 
certainty. 

The  prognosis  is  entirely  dependent  upon  the  underlying  •  disease.  In 
heart  disease  the  occurrence  of  a  hemorrhagic  infarction  is  usually  on  the 
whole  an  unfavorable  sign,  since  it  points  to  weakness  of  the  right  ventricle, 
occasionally  the  formation  of  a  thrombus  in  it;  yet  it  often  happens  that  the 
symptoms  of  a  pulmonary  infarction  may  pass  away  entirely. 

We  need  not  give  special  directions  for  treatment.  It  is  in  part  purely 
symptomatic,  and  in  part  coincident  with  treatment  of  the  underlying  affec- 
tion. As  regards  prophylaxis,  we  must  bear  in  mind  the  absolute  necessity 
of  as  perfect  rest  as  possible  for  those  patients  in  whom  the  presence  of  venous 
thrombi — e.g.,  in  the  femoral  veins — suggests  the  possibility  of  pulmonary 
embolism. 


CHAPTER    XI 

BROWN   INDURATION    OF    THE    LUNGS 
(Lungs  of  Heart  Disease) 

In  heart  disease,  especially  in  mitral  stenosis,  we  often  find  a  peculiar 
change  in  the  lungs,  whose  origin  must  be  sought  in  the  long-persisting  en- 
gorgement of  the  pulmonary  circulation.  The  lungs  are  hard  and  dense,  and 
show  on  a  fresh  section  an  abnormal  brownish-yellow  color.  In  the  larger 
pulmonary  vessels,  both  arteries  and  veins,  there  is  a  thickening  and  cloudi- 


336 


DISEASES   OF  THE   RESPIRATORY   ORGANS 


ness  of  the  intima  as  a  result  of  the  stasis.  We  see  here  and  there  on  the 
surface  of  the  section,  and  beneath  the  pleura,  little  dark  spots  of  pigment 
and  fresh  hemorrhages.  We  term  this  condition  brown  induration  of  the  lungs. 
Microscopic  examination  shows  that  the  capillaries  are  evidently  dilated 
and  twisted  as  a  result  of  the  persistent  stasis.  They  even  extend  a  good 
way  into  the  alveoli,  whose  lumen  is  thus  actually  diminished.  The  inter- 
stitial connective  tissue  seems  somewhat  thickened,  and  we  find  in  it  many 
brown  pigment  granules,  the  remains  of  the  extravasated  and  decomposed 
red  blood  corpuscles.  The  pigment  granules  are  some  of  them  free,  and  some 
contained  in  cells.  In  the  intima  of  the  larger  vessels  we  often  find  fatty 
degeneration  of  the  endothelium. 

With  regard  to  the  clinical  importance  of  the  pulmonary  changes  due  to 
heart  disease,  we  should  say  that  it  is  very  probable  that  the  dyspnoea  of  such 
patients  is  aggravated  by  the  diminution  of  the  alveolar  spaces  throughout 
the  lungs,  as  a  result  of  their  being  crowded  with  desquamated  pulmonary 
epithelium.  Clinically,  however,  we  cannot  well  distinguish  this  factor  from 
the  other  causes  of  dyspnoea. 

We  have  no  positive  factors  by  which  to  diagnosticate  brown  induration  of 
the  lungs  during  life.  The  anatomical  lesions,  too,  show  a  certain  variation, 
not  always  to  be  explained,  in  that,  under  apparently  the  same  conditions,  the 
brown  induration  is  often  very  marked,  and  often  extremely  slight.  In  cases 
in  which  we  find  this  induration  in  the  cadaver  we  have  repeatedly  heard,  dur- 
ing the  patient's  life,  a  very  sharp,  puerile  respiratory  murmur,  which  seems 

to  be  characteristic  of  many  cases 
of  the  "  heart-disease  lung.*'  In 
the  diagnosis  of  "heart-disease 
lung,"  I  place  the  greatest  weight 
on  the  ofttimes  highly  characteristic 
sputum.  Even  on  macroscopic  ex- 
amination, the  latter  often  presents 
an  appearance  peculiarly  its  own. 
It  is  rather  tenacious,  mucoid  spu- 
tum containing  scarcely  any  pus 
cells,  and  showing  a  large  number 
of  areas  that  have  a  dirty  brown, 
coffee-colored  appearance.  If  the 
brown  spots  be  examined  under  the 
microscope,  their  color  will  be  seen 
to  be  due  to  numerous  large  cells 
which  are  closely  filled  with  smaller 
and  larger,  yellow  to  brown-colored 
pigment  granules  (see  Fig.  57). 
These  large  pigmented  cells  ("  cells 
of  heart  disease")  are  identical  with  the  above-mentioned  pigmented  cells 
found  on  the  interior  of  the  alveoli  upon  anatomical  examination  of  the 
lungs.  They  are  certainly  for  the  most  part  alveolar  epithelium  filled 
with  pigment;  some,  however,  are  probably  leucocytes  that  have  taken  up  the 
pigment  from  degenerated  red  blood  cells.  When  the  sputum  is  treated  with 
hydrochloric  acid  and  potassium  ferrocyanid,  a  distinct  blue  color  appears. 


Fig.  57. — Sputum  of  a  patient  with  mitral  steno- 
sis, containing  the  so-called  "  cells  of  heart  dis- 
ease."      (Personal  observation.) 


TUMORS  OF  THE  LUNGS  337 

This  test  for  iron  may  be  macroscopically  performed  in  the  sputum  glass,  or 
microscopically,  on  the  stage  of  the  microscope.  Besides  the  pigment  cells,  a 
remarkably  large  number  of  "  myelin  drops  "  as  well  as  unaltered  red  blood 
cells  are  usually  to  be  seen. 


CHAPTER    XII 

TUMORS    OF    THE    LUNGS.      CANCER    OF    THE    LUNGS.      ECHINOCOCCUS    OF 
THE    LUNGS.      PULMONARY    SYPHILIS 

1.  NEW  GROWTHS  IN  THE  LUNGS.  CANCER  OF  THE  LUNGS 

Secondary  New  Growths. — Most  of  the  new  growths  which  are  met  with  in 
the  lungs  are  of  a  secondary  nature.  Secondary  cancers  are  sometimes  found 
in  the  lungs,  with  carcinoma  of  other  organs,  whose  origin  may  almost  always 
he  explained  by  supposing  a  growth  of  the  primary  tumor  into  a  vein,  and 
the  consequent  carriage  of  the  germs  of  the  growth  to  the  lungs.  In  other 
cases,  the  tumor  material  reaches  the  lungs  by  way  of  the  lymph-channels. 
In  such  cases  the  spread  of  the  tumor  not  infrequently  occurs  in  the  form  of 
strands  along  the  axes  of  the  lymph-vessels.  These  secondary  nodules  in  the 
lungs  often  cause  no  special  clinical  symptoms,  unless  they  are  very  numerous 
and  extensive,  when  they  give  rise  to  dyspnoea  and  physical  signs.  There  once 
came  to  the  clinic  in  Leipsic  a  case  of  secondary,  and  very  extensive,  miliary 
carcinosis  of  the  lungs,  which  ran  a  brief  and  fatal  course,  simulating  acute 
miliary  tuberculosis  with  predominant  pulmonary  s}rmptoms. 

Other  secondar}'  new  growths  deserving  mention  are  enchondroma  and  sar- 
coma. We  have  seen  an  extensive  development  of  secondary  pulmonary  sar- 
coma, following  primary  sarcoma  of  the  bronchial  lyrnph-glands,  and  also  in 
another  case  following  lympho-sarcoma  of  the  lymph-glands  of  the  neck,  which 
grew  into  the  jugular  vein.  We  have  also  seen  secondary  deposits  of  sarcoma 
repeatedly  in  connection  with  primary  congenital  sarcoma  of  the  kidney  (q.v.). 

Primary  Cancer. — Of  the  primary  new  growths  of  the  lungs,  only  pulmo- 
nary or  bronchial  carcinomata  have  any  great  clinical  significance.  All  other 
new  growths  (enchondroma,  sarcoma,  fibroma,  osteoma,  etc.)  are  rare,  and 
possess  scarcely  any  but  an  anatomical  interest.  Primary  cancer  of  the  lungs 
"usually  originates  in  the  epithelium  of  the  bronchial  wall,  though  sometimes 
it  originates  in  that  of  the  alveoli.  It  is  especially  common  in  elderly  persons, 
over  forty,  and  seems  to  be  found  somewhat  more  frequently  in  the  right  lung 
than  in  the  left,  and  in  the  upper  lobes  than  in  the  lower.  By  its  diffusion 
the  lung  tissue  in  the  parts  affected  by  cancer  is  changed  to  a  yellowish-gray 
and  quite  soft  and  crumbling  mass,  devoid  of  air.  We  can  usually  scrape 
away  from  the  section  the  characteristic  cancer  juice,  in  which  the  microscope 
shows  the  typical  cancerous  elements.  The  pleura  is  very  often  involved.  The 
new  growth  has  either  extended  directly  into  it,  or  single,  and  more  circum- 
scribed, secondary  nodules  have  formed  in  it.  The  lymph-glands  are  almost 
invariably  affected,  especially  the  bronchial  glands,  and  also  the  axillary  and 
cervical  glands.  Secondary  carcinoma  of  other  organs  is  rare,  but  it  is  found 
in  some  cases  in  the  other  lung,  the  liver,  the  brain,  and  elsewhere. 


338  DISEASES   OF  THE   RESPIRATORY  ORGANS 

It  is  almost  always  difficult  to  correctly  interpret  the  clinical <  symptoms  of 
cancer  of  the  lungs  at  the  beginning  of  the  disease.  They  are  referred  to  some 
other,  more  common  chronic  pulmonary  disease,  such  as  chronic  bronchitis, 
phthisis,  or  pleurisy,  but  in  the  further  course  of  the  disease  we  succeed,  at 
least  in  a  number  of  cases,  in  making  a  correct  diagnosis.  In  other  cases,  espe- 
cially in  old  people,  the  growth  may  remain  latent. 

The  general  pulmonary  symptoms  have  little  that  }&  characteristic.  The 
patient  complains  of  gradually  increasing  difficulty  in  respiration,  and  of 
pressure  and  distress  in  the  chest,  which  may  finally  increase  to  the  most  in- 
tense dyspnoea.  Most  patients  suffer  very  much  from  the  labored,  frequent,  and 
spasmodic  cough.  The  expectoration  in  some  cases  has  no  peculiarity,  but  it 
often  assumes,  at  least  for  a  time,  a  characteristic  consistence  which  is  extremely 
important  for  diagnosis.  The  presence  of  blood  in  the  sputum  is  of  the  great- 
est importance.  Repeated  slight  or  even  considerable  hemoptyses  are  often  the 
first  symptom  to  call  attention  to  the  beginning  of  serious  disease.  In  some 
cases  the  expectoration  becomes  permanently  hemorrhagic,  and  then  it  not  in- 
frequently assumes  a  peculiar  "  raspberry- jelly  "  appearance.  Under  the  micro- 
scope we  can  sometimes  make  out  the  characteristic  elements  of  the  tumor  in  it. 

Physical  examination  frequently  gives  no  positive  results  at  the  outset.  In 
the  cases  observed  by  the  author,  a  striking  diminution  of  the  respiratory 
murmur  over  localized  areas,  despite  normal  pulmonary  resonance,  was  often 
the  first  decided  change  in  the  physical  signs.  It  was  due  to  the  increased 
obstruction  of  the  afferent  bronchus  by  the  growing  tumor.  A  stridor  is  also 
occasionally  heard  when  the  bronchial  lumen  is  encroached  upon.  After  the 
tumor  has  extended,  naturally  more  distinct  signs  are  to  be  found  (dullness,, 
bronchial  breathing,  rales,  pleuritic  friction  sounds,  etc.).  Frequently  the 
peculiar  situation  of  the  areas  of  dullness  (in  the  sternal  region,  for  example) 
of  itself  leads  one  to  think  of  a  new  growth.  As  soon  as  the  pleura  becpmes 
involved,  the  sense  of  resistance  upon  percussion  is  very  marked.  Not  infre- 
quently a  diffuse  protrusion  of  the  chest  wall,  in  the  region  of  the  disease, 
appears.  Sometimes  there  is  also  a  slight  cedematous  swelling  of  the  skin. 
The  X-ray  examination  of  the  lungs  is  of  almost  greater  importance  than  per- 
cussion and  auscultation.  It  permits  of  the  distinct  recognition  of  deep- 
seated  tumors,  and  gives  the  best  indication  of  the  extent  of  the  disease.  It 
should,  therefore,  never  be  neglected  in  any  case  of  moment. 

The  occurrence  of  certain  sequelae  is  of  great  diagnostic  significance.  The 
chief  ODe  is  swelling  of  the  lymph-glands  in  the  neck  or  axilla,  and  also  certain 
symptoms  of  compression,  which  either  are  produced  directly  by  the  new 
growth,  or  are  due  to  the  secondary  enlargement  of  the  lymph-glands.  Pres- 
sure on  the  superior  vena  cava,  or  a  large  branch  of  it,  causes  oedema  in  the 
face,  neck,  over  the  wall  of  the  chest,  or  in  one  arm.  The  subcutaneous  veins 
in  the  regions  named  appear  dilated  and  tortuous.  Pressure  on  the  oesophagus 
causes  difficulty  in  deglutition ;  on  the  brachial  plexus,  intense  neuralgic  pains, 
and  paresis  of  one  arm ;  on  the  recurrent  nerve,  paralysis  of  the  vocal  cords  and 
hoarseness;  on  the  trachea  or  a  primary  bronchus,  symptoms  of  tracheal  or 
bronchial  stenosis.  The  pleura  is  often  involved  so  that  the  signs  of  a  pleuritic 
effusion  associate  themselves  with  the  other  symptoms.  In  such  cases  the  exu- 
dation is  not  infrequently  hemorrhagic  (see  new  growths  of  the  pleura). 

Besides  the  symptoms  already  mentioned  we  must  consider  the  constitu- 


ECHINOCOCCUS  OF  THE   LUNGS  339 

tional  symptoms.  As  in  carcinoma  in  general,  so  in  pulmonary  carcinoma,  the 
well-known  cancerous  cachexia  gradually  develops.  The  patient  grow6  dull,  loses 
his  appetite  more  and  more,  disturbances  of  digestion  and  sometimes  moderate 
elevations  of  temperature  develop, until  he  finally  succumbs  to  general  marasmus. 

The  whole  duration  of  the  disease  is  from  six  months  to  two  years.  The 
prognosis  is  fatal.  The  treatment  can  be  only  symptomatic,  and  we  employ  the 
same  remedies  as  in  other  pulmonary  affections.1  X-ray  treatment  or  subcuta- 
neous injections  of  arsenic  may  be  tried  in  cases  of  sarcoma  or  lympho-sarcoma 
of  the  lungs.  Palliative  results,  at  least,  are  sometimes  attained  by  these  means. 

Lympho-sarcomata  of  the  Lungs.— We  must  still  briefly  consider  a  new 
growth  in  the  lungs  which  is  extremely  interesting  from  a  theoretical  point 
of  view.  In  workmen  in  the  cobalt  mines  of  Schneeberg,  in  the  Saxon  Yoigt- 
land,  the  development  of  malignant  lympho-sarcomata  in  the  lungs,  with  the 
occasional  formation  of  metastases  in  the  glands,  the  liver,  the  spleen,  etc.,  is 
of  frequent  occurrence.  The  disease  runs  its  course  under  the  type  of  a  chronic 
pulmonary  affection,  and  almost  always  ends  fatally.  The  endemic  occurrence 
seems  to  point  to  an  infectious  origin  for  the  tumor. 

2.  ECHINOCOCCUS   OF  THE  LUNGS 

Primary  echinococcus  of  the  lungs  is  very  rare.  In  most  cases  the  echino- 
cocci  are  brought  to  the  lungs  secondarily  from  other  organs,  either  by  way  of 
the  blood  current,  or,  as  is  far  oftener  the  case,  by  perforation  of  an  echino- 
coccus of  the  liver  through  the  diaphragm. 

The  symptoms  of  echinococcus  of  the  lungs  are  manifold.  The  parasite 
sometimes  remains  entirely  concealed.  In  other  cases  a  more  or  less  severe, 
and  often  febrile,  affection  of  the  lungs,  is  developed,  with  pain  in  the  chest, 
cough,  and  sometimes  bloody  expectoration,  and  dyspnoea.  Physical  examina- 
tion of  the  lungs  gives  in  some  cases  dullness,  absence  of  respiratory  murmur, 
and  diminished  vocal  fremitus,  while  after  the  expectoration  of  the  echino- 
coccus symptoms  of  a  cavity  may  ensue.  A  correct  interpretation  of  all  these 
symptoms  is  possible  only  when  the  echinococcus  cysts  are  coughed  up,  or  parts 
of  them,  like  the  membranes  of  the  hooklets,  are  found  in  the  expectoration. 
In  some  cases  of  echinococcus,  the  sputum  is  of  a  peculiar  ocher-yellow  color. 

The  termination  of  the  disease  may  be  favorable  if  the  echinococci  are 
expectorated,  or  if  we  succeed  in  removing  them  by  operative  means.1  We  can 
hardly  hope  to  be  able  to  kill  the  parasite  by  inhalations  of  turpentine  or  ben- 
zine. Sometimes  the  echinococcus  cyst  becomes  gangrenous  or  suppurates. 
Eupture  into  the  pleura,  into  the  peritoneum,  into  the  pericardium,  and  ex- 
ternally, has  also  been  observed.  This  last  termination  is  the  most  favorable, 
since  otherwise,  if  the  affection  progresses,  a  fatal  result  may  be  caused  by 
the  sequelae,  or  rarely  by  the  occurrence  of  suffocation.  The  details  of  the 
natural  history  of  the  echinococcus  are  given  under  echinococcus  of  the  liver. 

JThe  recent  introduction  of  the  various  Sauerbruch  and  Brauer  air-pressure  cabinets,  and  the 
Meltzer-Elsberg  apparatus  for  direct  inhalation  of  compressed  air  through  an  intratracheal 
tube,  have  revolutionized  thoracic  surgery.  Brilliant  results  have  already  been  reported  from 
operations  upon  tumors,  abscesses,  and  other  conditions  of  the  pleura,  lungs,  and  mediastinum  and 
upon  diverticula,  stenoses,  and  neoplasms  of  the  oesophagus.  With  increased  experience,  improve- 
ment of  apparatus  and  technic  must  follow,  and  if  later  results  bear  out  the  promise  of  these  early- 
successes,  the  prognosis  of  many  conditions  within  the  thorax  will  become  more  hopeful. 


.340  DISEASES   OF  THE   RESPIRATORY   ORGANS 

3.  PULMONARY  SYPHILIS 

This  would  also  be  the  place  to  speak  of  syphilitic  new  growths  in  the 
lungs,  but,  in  our  opinion,  in  spite  of  the  quite  abundant  literature  of  this  sub- 
ject in  recent  times,  no  definite  clinical  description  of  pulmonary  syphilis  can 
be  given.  Those  physicians  who  are  disposed  to  consider  every  pulmonary 
•disease  in  a  previously  syphilitic  subject  to  be  of  a  syphilitic  nature,  certainly 
regard  many  things  as  pulmonary  syphilis  which  have  nothing  at  all  to  do 
with  syphilis.  At  least,  we  have  found  that  all  those  cases  which  at  first  sug- 
gested a  diagnosis  of  pulmonary  syphilis,  finally,  upon  more  accurate  exami- 
nation and  after  longer  observation,  have  turned  out  to  be  something  else, 
usually  tuberculosis.  There  are  a  few  indubitable  cases  of  chronic  indurative 
contraction  of  the  lungs  following  primary  syphilitic  infiltration.  The  clinical 
picture  here  does  not  differ  in  any  characteristic  manner  from  that  of  ordinary 
chronic  interstitial  pneumonia.  A  probable  diagnosis  may  be  made  from  the 
knowledge  of  the  syphilitic  taint,  the  simultaneous  existence  of  other  syphilitic 
lesions — e.  g.,  of  the  liver — the  physical  signs  of  chronic  pulmonary  disease, 
and  the  failure  to  find  tubercle  bacilli  in  the  sputum  on  repeated  examinations. 
It  is  also  well  established  that  there  may  be  syphilis  of  the  larger  and  medium- 
sized  bronchi,  which  is  recognized  at  the  autopsy  by  extensive  radiating  cica- 
trices in  the  bronchial  mucous  membrane,  which  sometimes  lead  to  stenosis. 
Single  gummatous  nodules  in  the  lungs  are  of  the  greatest  rarity.  We  some- 
times find  in  the  pleura  peculiar  radiating  cicatrices,  which  probably  are  of 
syphilitic  origin.  The  pulmonary  syphilis  of  the  newborn,  which  occurs  in 
the  form  of  single  nodules  or  as  a  diffuse  syphilitic  infiltration,  the  so-called 
pneumonia  alba,  has  only  a  pathological  interest. 

If  the  existence  of  a  syphilitic  disease  of  the  lungs  is  suspected,  of  course 
specific  treatment  should  be  employed.  Iodid  of  potassium  must  be  adminis- 
tered and  perhaps  also  a  course  of  mercurial  inunctions.  The  results  are  not 
apt  to  be  brilliant,  however,  because  it  is,  of  course,  impossible  to  restore  the 
portions  which  have  been  cicatrized. 


SECTION   V 
Diseases  of  the  Pleura 

CHAPTEE    I 

PLEURISY 

(Pleuritis) 

JETIOLOGY 

Pleurisy  is  divided  into  primary  and  secondary.  In  a  strict  sense,  the 
only  cases  of  pleurisy  which  can  be  termed  primary  are  those  in  which  the 
pathogenic  organisms  penetrate  into  a  healthy  body,  and  become  localized  in 
the  pleura  without  any  previous  organic  lesion  elsewhere.     No  doubt  many  a 


PLEURISY  341 

case  of  pleurisy  seems  primary  from  a  clinical  standpoint,  which  is  really  not 
so.  The  disease  antecedent  to  the  pleurisy  ma}'  be  so  slight  as  to  present  no 
symptoms  and  attract  no  attention.  The  pleurisy  appears  as  an  apparently 
independent  disease,  and  is  the  first  thing  which  attracts  attention  to  the  pre- 
viously existing  affection. 

Exclusive  of  traumatic  pleurisy,  resulting  from  such  injuries  as  a  pene- 
trating thoracic  wound,  we  know  positively  of  only  one  form  of  pleurisy — viz., 
the  rheumatic — which  is  primary.  This  is,  from  an  astiological  point  of  view, 
most  closely  allied  with  acute  articular  rheumatism  (Fiedler).  In  poly- 
arthritis (q.  v.)  it  is  not  very  exceptional  to  have  pleurisy  develop  second- 
arily. In  many  cases  the  rheumatic  affection  attacks  the  pleura  at  first, 
without  any  great  involvement  of  the  joints.  Then  often  follow  articular 
trouble,  endocarditis,  and  the  like,  confirming,  or  for  the  first  time  disclosing, 
the  astiology  of  the  attack.  Whether  still  other  pathogenic  influences  may  pro- 
duce primary  pleurisy  is  not  settled.  Some  cases  of  acute  pleurisy,  setting  in 
with  high  fever,  we  have  felt  justified  in  referring  to  diplococcus  infection, 
as  suggested  by  the  association  of  herpes  and  other  symptoms.  In  such  in- 
stances it  is  scarcely  possible  to  exclude  with  certainty  the  presence  of  a  small 
focus  of  pneumonia.  In  genuine  primary  pleurisy  the  pathogenic  germs  must 
first  enter  the  circulation,  and  by  that  means  reach  the  pleura. 

Among  those  varieties  of  pleurisy  which  appear  from  a  clinical  standpoint 
as  primary,  while  their  existence  is  really  referable  to  a  previous  lesion  of  the 
body,  by  far  the  most  frequent  and  important  is  the  tuberculous.  On  this  point 
it  was  only  gradually  and  by  means  of  long  experience  that  physicians  ob- 
tained a  correct  conception  of  the  truth.  We  believe  it  right  to  say  that  the 
great  majority  of  all  cases  of  apparently  primary  pleurisy  are  tuberculous. 
The  infection  of  the  pleura  is  due  to  the  invasion  of  it  by  germs  from  some 
tuberculous  focus,  situated  near  by.  Either  there  are  small  tuberculous  patches 
in  the  lungs  which  extend  to  the  pleura,  or,  probably  yet  more  frequently, 
bronchial  or  retrobronchial  lymph-glands,  being  tuberculous,  break  into  the 
pleural  cavity  and  promptly  excite  pleurisy.  In  many  of  these  cases  the  fur- 
ther course  of  this  disease  clearly  shows  that  the  pleurisy  was  tuberculous  at 
the  start,  and  not  infrequently  the  physician  is  justified,  even  at  the  very  be- 
ginning of  the  illness,  in  expressing  his  suspicion  of  tuberculosis. 

In  many  other  cases  of  pleurisy  its  secondary  character  is  clear  from  the 
start.  Most  of  these  occur  from  the  direct  extension  of  the  inflammatory 
process  from  some  neighboring  organ  to  the  pleura.  When  considering  pul- 
monary diseases,  we  had  occasion  to  point  out  that  the  various  pathological 
changes  in  the  lungs,  when  they  extend  to  the  pleura,  involve  it  in  the  disease. 
Thus  we  see  pleurisy,  associated  with  croupous  pneumonia,  lobular  catarrhal 
pneumonia,  pulmonary  gangrene,  hemorrhagic  infarction,  embolic  abscesses, 
and,  most  important  of  all,  pulmonary  tuberculosis.  Many  of  the  diseases  just 
enumerated  are  frequent  complications  of  the  most  diverse  diseases.  Hence, 
it  is  easy  to  understand  that  pleurisy  is  a  not  infrequent  phenomenon  in  all 
sorts  of  severe  illnesses. 

Because  of  their  practical  importance,  the  rather  frequent  pleurisies  of 

the  puerperium  and  those  following  major  operations  should  be  particularly 

mentioned  in  this  place.     Puerperal  pleurisy  is  sometimes  tuberculous.     We 

know  that  the  post-partum  period  often  favors  the  outbreak  of  a  previously 

22 


342  DISEASES  OF  THE  RESPIRATORY  ORGANS 

latent  tuberculosis.  Very  often  the  pleurisies  are  of  an  embolic  nature,  and 
depend  on  small  emboli  of  the  lungs  (vide  supra,  page  325),  whose  source  is 
to  be  sought  for  in  thrombosed  uterine,  femoral,  and  other  veins.  Finally, 
pleurisy  may  be  one  of  the  manifestations  of  a  general  sepsis.  Pleurisy  fol- 
lowing major  operations  is  almost  always  of  an  embolic  nature  and  results 
from  thrombosis  of  veins  following  operative  trauma. 

Inflammation  from  other  neighboring  organs  besides  the  lungs  may  extend 
to  the  pleura.  Inflammation  of  the  contiguous  serous  membranes  may  spread 
to  the  pleura  by  continuity;  thus  pleurisy  complicates  pericarditis  and  peri- 
tonitis.  Inasmuch  as  the  pleura  and  the  outer  surface  of  the  pericardium  lie 
in  direct  apposition  and,  furthermore,  the  pleural  cavity  and  the  peritoneal 
cavity  are  directly  connected  by  the  lymph-channels  of  the  diaphragm,  we  can 
easily  understand  that  not  only  serous  and  purulent,  but  also  diplococcus,  in- 
flammation of  the  pericardium  and  peritoneum  may  have  pleurisy  for  a  sequel. 

Another  variety  of  secondary  pleurisy  is  due  to  the  conveyance  of  the  in- 
flammatory organisms  not  from  the  immediate  neighborhood,  but  from  other 
parts,  by  way  of  the  circulation.  Here  should  be  mentioned  pleurisy  due  to 
general  sepsis,  to  polyarthritis,  to  nephritis  (q.  v.),  to  genuine  gout  (q.  v.) 
and  the  like.  The  factors  which  give  rise  to  the  inflammation  are  either  or- 
ganic or,  in  the  case  of  gout  and  nephritis,  chemical  in  their  nature.  The 
inflammation  they  excite  in  the  pleura  is  most  varied  in  its  kind  and  degree. 

Of  late  years  bacteriological  investigations  have  been  made  by  E.  Levy, 
Prince  Ludwig  Ferdinand,  and  others,  to  obtain  a  more  accurate  knowledge 
as  to  the  special  variety  of  germs  in  the  various  forms  of  pleurisy,  due  to  in- 
fection with  organized  material.  It  must  not  be  forgotten,  however,  that  these 
bacteriological  investigations  have  been,  for  the  most  part,  directed  not  to  the 
diseased  tissue,  but  to  the  inflammatory  pleuritic  exudation.  This,  however, 
in  many  cases  contains  no  bacteria  whatever.  In  particular,  the  exudation  in 
most  cases  of  tuberculous  pleurisy,  whether  serous  or  purulent,  is  absolutely 
sterile,  and  in  the  secondary  pleuritic  exudations,  in  acute  polyarthritis  and 
nephritis,  the  search  for  bacteria  has  failed  again  and  again.  In  other  cases 
of  pleurisy,  however,  staphylococci  have  been  found  in  the  exudate,  and  in 
empyema  streptococci  also.  MetajDneumonic  pleurisy,  whether  serous  or  puru- 
lent, is  often,  though  not  always,  characterized  by  the  presence  of  genuine 
pneumococci.  In  general,  the  question  with  regard  to  the  special  cause  of 
the  disease  will  have  to  be  whether  the  pleurisy  is  caused  by  the  original  pri- 
mary agent  of  the  disease  (e.  g.,  tubercle  bacilli  in  tuberculosis,  diplococci  in 
pneumonia,  etc.)  or  whether  it  is  to  be  considered  as  a  secondary  complication 
(streptococci  in  typhoid  fever,  for  example). 

Special  predisposing  causes  (above  all,  colds,  and  occasionally  trauma) 
must  be  taken  into  account  in  some  of  the  cases  in  all  the  different  varieties 
of  pleurisy.  Positive  judgment  on  these  factors  is  often  a  very  difficult 
matter. 

PATHOLOGICAL   ANATOMY 

The  inflamed  pleura  is  markedly  injected,  it  has  lost  its  normal  luster, 
and  instead  has  a  dull  surface.  This  dullness  is  due  to  the  coagulated  fibrinous 
exudation  upon  the  pleura,  the  exudation,  in  mild  cases,  forming  only  a  thin 
layer.    In  more  advanced  cases,  however,  the  surface  of  the  pleura  is  covered 


PLEURISY  343 

with  thick,  rough,  and  shaggy  masses  of  fibrin.    As  long  as  the  fluid  in  the 
pleura  is  little  or  not  at  all  increased,  we  speak  of  a  simple  fibrinous  or  dry 

pleurisy  (pleuriiis  fibrinosa  vel  sicca). 

In  other  cases,  however,  besides  the  layer  of  fibrin  there  is  an  abundant 
exudation  of  fluid  from  the  capillaries  of  the  pleura,  forming  a  pleuritic 
effusion.  This  is  ordinarily  of  a  simple  serous  character — serous  and  sero- 
fibrinous effusions.  The  fluid  collects  between  the  surfaces  of  the  pleura,  or,  if 
there  is  at  the  same  time  an  abundant  coating  of  fibrin,  between  the  gaps  and 
in  the  meshes  of  the  fibrinous  exudation.  In  such  cases  there  are  often  many 
flakes  of  fibrin  floating  in  the  fluid. 

Upon  microscopic  examination  there  are  invariably  found  a  few  leucocytes 
even  in  serous  exudations  (detailed  description  of  the  special  varieties  of  leu- 
cocytes in  the  effusion  is  given  in  the  section  on  the  diagnosis  of  pleurisy),  and 
also  sometimes  a  very  few  blood  corpuscles  and  endothelial  cells  (often  swollen 
or  fatty-degenerated),  and  plates  of  cholesterin. 

If  the  number  of  pus  corpuscles  in  the  exudation  becomes  much  increased, 
we  have  a  seropurulent  or  a  purulent  exudation.  This  is  always  due  to  the 
presence  of  a  specific  organized  poison  which  excites  the  suppuration.  The 
pleurisies  which  come  from  embolic  abscesses,  from  gangrenous  foci  in  the 
lungs,  and  from  carious  ribs,  and  those  which  arise  from  the  rupture  of  tuber- 
culous cavities  into  the  pleura,  are  almost  always  of  a  suppurative  character. 
We  call  the  purulent  pleuritic  effusion  empyema.  If  putrefactive  agencies 
enter  the  pleural  cavity  at  the  same  time  with  the  pus  poison,  as  in  the  pleu- 
risies which  develop  in  pulmonary  gangrene,  the  purulent  exudation  assumes 
an  ichorous,  putrid  character — ichorous  effusion. 

Under  certain  circumstances  the  effusion  assumes  a  hemorrhagic  character 
— hemorrhagic  effusion — especially  if  hemorrhages  occur  from  the  old  or  newly 
formed  capillaries  dilated  by  the  inflammation.  They  arise  partly  by  diape- 
desis  and  partly  from  rupture  of  the  walls  of  the  vessels.  The  exact  cause  of 
the  hemorrhages  is  usually  unknown.  We  know  by  experience  that  hemor- 
rhagic effusions  are  most  frequent  in  tuberculous  pleurisy,  a  fact  which  is  of 
diagnostic  importance.  The  exudation  may  also  be  hemorrhagic  in  connection 
with  new  growths  of  the  pleura,  after  severe  croupous  pneumonia,  in  septic 
disease  (e.  g.,  puerperal  fever),  and  finally  when  there  is  a  general  hemorrhagic 
diathesis,  as  seen  in  scurvy,  purpura  hemorrhagica,  and  leuksemia.  In  all  these 
last-mentioned  cases  it  should,  of  course,  be  considered  that  we  are  not  always 
dealing  with  a  true  inflammatory  exudation,  but  merely  with  a  hemorrhage 
into  the  pleural  cavity. 

The  amount  of  fluid  collected  in  one  pleural  cavity  is,  in  the  majority 
of  cases,  somewhere  between  a  pint  and  a  quart  (500  to  1,000  c.c),  but  it  may 
reach  three  or  four  quarts.  Every  large  effusion  must  influence  the  position  of 
the  yielding  walls  of  the  pleural  cavity,  the  chest  wall,  the  lungs,  the  medias- 
tinum, and  the  diaphragm,  through  the  consequent  increase  of  pressure  in  the 
affected  pleural  cavity;  and  the  resultant  symptoms  of  pressure  on  the  neigh- 
boring organs  are  of  the  greatest  clinical  significance.  Attention  is  first  called 
to  the  lungs  themselves.  Since  the  normal  lung  is  expanded  in  the  thorax 
beyond  its  elastic  equilibrium,  it  will  retract  as  soon  as  a  part  of  the  pleural 
cavity  is  occupied  with  fluid.  Until  it  has  reached  its  position  of  elastic  equi- 
librium there  can  be  no  question  of  a  positive  pressure  on  the  lung.    The  lung 


344  DISEASES   OF  THE   RESPIRATORY  ORGANS 

floats  on  the  effusion,  in  a  certain  way,  if  there  be  no  adhesions,  but,  as  the 
amount  of  the  fluid  further  increases,  compression  of  the  lung  follows.  With  a 
very  large  effusion  the  lung  is  pushed  wholly  up  and  back  against  the  vertebral 
column,  and  is  changed  to  an  almost  bloodless,  airless,  flat  mass.  It  is,  how- 
ever, possible  that  the  atelectasis  of  the  lung  is  not  caused  exclusively  by  com- 
pression from  without,  but  that,  after  the  normal  respiratory  movements  have 
ceased,  a  part  of  the  air  in  the  lung  may  be  absorbed  by  the  vessels,  or  even  by 
the  effusion. 

We  also  see  the  results  of  the  pressure  exerted  by  the  pleuritic  effusion  on 
the  mediastinum  and  diaphragm,  as  well  as  on  the  lungs.  Displacements  of 
the  heart  arise  from  the  lateral  pressure  on  the  mediastinum,  which  must  take 
place  if  the  pressure  in  the  diseased  pleural  cavity  is  equal  to  that  of  the 
atmosphere,  for  a  greater  and  positive  pressure  is  unnecessary,  since  a  negative 
pressure  prevails  on  the  healthy  side.  The  downward  pressure  of  the  dia- 
phragm, which  usually  affects  both  halves  of  it,  although  in  unequal  degree, 
makes  itself  manifest  on  the  right  by  the  low  position  of  the  liver,  and  on  the 
left  by  the  downward  displacement  of  the  stomach  and  large  intestine  (vide 
infra) .  It  must  be  particularly  noticed,  however,  that  adhesions  may  prevent 
all  the  pressure  displacements  which  we  have  mentioned,  both  of  the  lungs 
and  of  the  neighboring  organs. 

As  regards  the  further  changes  and  terminations  of  the  pleuritic  processes, 
they  depend  upon  the  amount  and  character  of  the  effusion.  Favorable  cases 
may  result  in  complete  recovery  and  absorption  of  the  effusion.  The  fluid  con- 
tents are  taken  up  directly  by  the  lymphatics  of  the  pleura,  and  the  solid  con- 
stituents, the  fibrin  and  the  white  blood  corpuscles,  are  decomposed,  dissolved, 
and  absorbed. 

In  most  of  the  severe  cases,  however,  an  extensive  new  growth  of  connective 
tissue  and  blood  vessels  takes  place.  The  fluid  exudate  is  often  absorbed  in 
very  large  part,  but  the  pleura  itself  becomes  thickened  and  converted  into  a 
dense  inflammatory  exudate.  Extensive  softer  or  firmer  adhesions  between 
the  visceral  and  parietal  pleura  are  a  very  common  sequel  (adhesive  pleurisy). 
Between  the  adhesions  there  may  still  be  isolated  areas  in  which  remains  of 
the  fluid  exudate  may  be  encapsulated  ("encysted  pleuritic  exudate").  In 
cases  of  pleural  inflammation  of  long  duration,  and,  especially,  in  frequently 
recurring  cases  (particularly  those  following  chronic  pulmonary  tuberculosis), 
the  dry  pleuritic  exudate  may  finally  acquire  a  thickness  of  from  0.4  to  0.8 
inch  (1  to  2  cm.).  Deposits  of  calcium  salts  and  new  growths  of  bone  tissue 
are  sometimes  to  be  found  in  old  pleuritic  exudates.  Such  diseased  condi- 
tions, when  associated  with  pronounced  retraction,  are  sometimes  termed 
"  pleuritis  deformans." 

Whenever  a  case  of  extensive  pleurisy,  with  an  abundant  fibrinous  or  fluid 
exudation,  gets  well,  there  is  a  marked  cicatricial  contraction  of  the  pleura, 
in  which  the  whole  thoracic  wall  is  involved.  It  requires  months  for  the  lungs 
and  the  thorax  to  regain  their  normal  expansion,  if  they  can  ever  do  so. 

That  recovery  from  large  pleuritic  exudation  is  so  often  incomplete,  is 
explained  for  the  most  part  by  the  nature  of  the  original  disease.  We  often 
find  that  temporary  improvement  is  followed  by  a  fresh  relapse  of  pleurisy, 
or  by  the  appearance  of  extensive  and  usually  tuberculous  disease  of  the  lungs 
or  other  organs. 


-    PLEURISY  345 

In  the -ease  of  purulent  exudations,  also,  final  absorption  of  the  fluid  is 
possible.  This  is  especially  likely  when  the  empyema  ie  metapneumonic  and 
benign,  but  this  demands  much  time,  and  thick,  cheesy  masses  of  pus  are  often 
left  in  the  pleural  sac.  In  most  cases  of  empyema,  if  there  is  not  timely  oper- 
ative interference,  the  pus  seeks  an  outlet  for  itself.  It  may  break  through 
the  visceral  pleura  into  a  bronchus,  and  be  emptied  externally,  thus  giving 
rise  to  a  pyopneumothorax;  but  in  many  cases  the  pleura  seems  to  be  de- 
stroyed only  superficially,  and  the  pus  is  pressed  into  the  alveoli  as  into 
a  sponge,  especially  by  the  movements  of  coughing,  and  thence  reaches 
the  bronchi,  without  letting  the  air  enter  the  pleural  cavity  (Traube).  In 
other  cases  the  empyema  breaks  externally  through  the  chest  wall — em- 
pyema necessitatis.  The  point  of  rupture  is  usually  found  in  the  vicinity 
of  the  sternum,  where  the  chest  wall  is  thinnest.  In  very  rare  cases  the  em- 
pyema breaks  through  the  deeper  parts  of  the  trunk,  or  into  the  abdominal 
cavity. 

Course  of  the  Disease.— We  will  speak  in  what  follows  especially  of  the 
course  and  symptoms  of  ordinary,  apparently  primary  (vide  supra),  fibrinous 
or  serofibrinous  pleurisy,  the  so-called  simple  pleuritic  effusion.  What  is  said 
of  it  obtains  in  large  measure  in  the  other  form  of  pleurisy  also.  The  physical 
signs,  of  course,  are  almost  wholly  independent  of  the  character  of  the  effusion. 
As  far  as  the  different  forms  of  pleurisy  differ  clinically,  we  will  mention  their 
peculiarities  below. 

Only  rarely  is  the  onset  of  pleurisy  quite  acute  and  sudden,  beginning  with 
a  rigor.  In  such  cases  we  must  guard  against  confusing  it  with  croupous 
pneumonia.  Cases  of  pleurisy  of  embolic  origin  (vide  supra)  usually  have 
a  sudden  onset.  As  a  rule,  however,  pleurisy  begins  slowly  and  gradually. 
The  symptoms,  which  the  patient  himself  feels,  are  in  many  cases  to  be  re- 
ferred directly  to  the  disease  of  the  pleura.  One  of  the  most  constant  is  the 
pleuritic  pain,  the  stitch  in  the  side.  A  more  or  less  severe  pain  comes  on  in 
the  side  at  every  deep  breath,  and  hence  upon  any  physical  exertion ;  also  upon 
movements  of  the  body,  in  stooping,  coughing,  or  gaping.  Shortness  of  breath 
soon  appears,  and  constantly  increases.  There  is  often  a  frequent,  dry  cough. 
Sometimes  there  are  scarcely  any  cough  and  expectoration.  Such  expectora- 
tion as  there  may  be  is  usually  simply  mucous.  Besides  that,  severe  general 
symptoms  almost  always  develop;  the  patient  feels  dull,  looks  pale,  and  has 
no  appetite.  Patients  who  can  endure  a  good  deal  often  keep  at  work  for  a 
long  time,  until,  after  feeling  miserable  for  three  or  four  weeks,  they  are 
forced  to  stay  at  home  and  summon  a  physician.  It  is  very  important  to  know 
that  in  not  a  few  cases  the  general  symptoms  are  much  more  prominent,  at 
the  beginning  of  pleurisy,  than  the  local  ones.  The  patient  comes  to  the 
physician  complaining  only  of  weakness,  loss  of  appetite,  or  headache,  and  the 
physical  examination  is  the  first  thing  that  shows  the  presence  of  perhaps  a 
large  pleuritic  effusion. 

In  most  of  the  severe  cases  the  further  course  is  slow  like  the  beginning, 
but  sometimes  the  severest  symptoms,  most  intense  dyspnoea,  marked  cyanosis, 
etc.,  may  come  on  in  a  short  time,  owing  to  a  sudden  increase  of  the  effusion. 
On  the  other  hand,  in  mild  cases  the  symptoms  may  disappear  again  in  a  few 
weeks,  but  the  objective  signs  in  such  cases  are  generally  to  be  made  out  for 
a  longer  time.    The  disease  ordinarily  lasts  for  at  least  five  or  six  weeks,  and 


346  DISEASES   OF  THE   RESPIRATORY   ORGANS 

often  much  longer.     Gradual  recovery  follows,  or  some  new  disease,  usually 
tuberculous   (vide  supra). 

SYMPTOMS 

Single  Symptoms. — Pleuritic  Pain. — The  pleuritic  pain,  the  stitch  in  the 
side,  is  one  of  the  most  frequent  subjective  symptoms.  We  have  previously 
mentioned  that  in  primary  diseases  of  the  lungs,  too,  as  in  croupous  pneu- 
monia, the  stitch  in  the  side  is  due  to  the  accompanying  pleurisy.  It  is  re- 
markable that  the  intensity  of  the  pain  in  no  way  corresponds  to  the  apparent 
intensity  of  the  disease.  There  is  often  the  severest  pain  in  the  side  when  the 
physical  examination  shows  almost  nothing.  On  the  other  hand,  we  often  hear 
a  decided  pleuritic  rub  without  the  patient's  complaining  of  any  special  pain. 
Pressure  on  the  chest  wall  on  the  affected  side  is  often  very  painful.  With 
severe  pain  we  may  consider  the  possibility  of  an  invasion  of  the  intercostal 
nerves  by  the  inflammation.  We  believe  we  have  observed  a  few  cases,  like 
those  described  by  some  authors,  of  "  crossed  pleuritic  pain  " — that  is,  cases  in 
which  the  pain  is  localized  on  the  side  not  affected. 

Cough  and  Expectoration. — The  cough  is  probably  excited  directly  by  the 
disease  of  the  pleura.  We  often  find  that  the  pain  in  the  side  and  also  the 
cough  are  brought  on  by  a  deep  inspiration.  Expectoration  is  entirely  absent 
in  uncomplicated  pleurisy,  or  it  is  scanty,  and  consists  simply  of  mucus.  Much 
expectoration  always  means  a  pulmonary  complication.  A  large  amount  of 
purulent  sputum  is  evacuated  if  a  purulent  effusion  breaks  into  the  lungs 
(vide  supra). 

Dyspnoea. — The  respiration  is  usually  shallow,  and  consequently  frequent, 
because  of  the  pleuritic  pain.  In  every  large  effusion  which  prevents  respira- 
tion in  one  lung  the  dyspnoea  becomes  more  severe,  and  may,  with  a  very 
extensive  effusion,  reach  the  highest  degree  of  orthopncea.  The  stronger  the 
patient  was  before  the  disease,  and  the  more  rapidly  the  effusion  develops,  the 
more  severe,  as  a  rule,  is  the  dyspnoea. 

Fever. — Most  severe  pleurisies  are  associated  with  fever,  but  its  height  is 
not  very  great,  so  that  it  quite  rarely  reaches  104°  F.  (40°  C).  The  fever  has 
no  typical  course.  In  cases  with  an  acute  beginning  it  is  sometimes  quite 
continuous,  or  slightly  remitting  at  first.  If  improvement  takes  place,  the 
fever  goes  down  in  about  two  or  three  weeks  by  lysis,  so  that  this  part  of  the 
temperature  curve  may  be  precisely  like  the  period  of  defervescence  in  typhoid. 

In  the  more  protracted  cases  the  fever  gradually  becomes  more  remitting, 
varying  between  100°  and  101°  F.  (38  to  38.5°  C),  and  it  assumes  more  and 
more  the  form  of  hectic  fever.  The  longer  the  evening  rise  of  temperature 
lasts,  the  more  we  are  justified  in  suspecting  tuberculosis.  In  empyema  we  see 
a  higher,  irregular  fever,  sometimes  associated  with  severe  chills. 

The  pulse  is  constantly  rapid,  up  to  100  and  over.  In  all  severe  cases  the 
strength  and  tension  of  the  pulse  are  much  diminished.  Irregularity  of  the 
pulse  is  not  infrequent.  All  these  changes  are  probably  due  in  great  part  to 
the  pressure  of  the  effusion  on  the  heart  and  large  vessels.  Lichtheim  has  dis- 
covered experimentally  that  it  is  not  the  compression  of  the  vessels  in  the  com- 
pressed lung  which  lowers  the  arterial  tension. 

General  Symptoms. — Pleurisy  is  almost  always  associated  with  a  pro- 
nounced general  malaise,  muscular  weakness,  and  dullness.     The  patient  is 


-PLEURISY  347 

pale,  and  often  markedly  cyanotic  in  cases  with  much  disturbance  of  respira- 
tion.   There  is  great  emaciation  if  the  disease  is  of  long  duration. 

The  appetite  declines  from  the  outset.  There  is  often  occasional  vomiting, 
especially  in  the  first  period  of  the  disease.  The  bowels  are  usually  constipated. 
Many  patients  complain  of  headache. 

The  condition  of  the  urinary  secretion  is  very  important.  In  every  pleuritic 
effusion  the  amount  of  urine  is  decidedly  diminished  so  long  as  the  effusion 
increases  or  remains  at  the  same  height.  The  daily  amount  is  sometimes  only 
8  to  13  ounces  (200  to  400  c.c).  The  urine  is  also  concentrated,  its  specific 
gravity  being  about  1.020  to  1.028.  Sediments  of  urates  often  form.  This 
diminution  of  the  excretion  of  water  by  the  kidneys  is  generally  referred  to 
the  diminished  arterial  pressure. 

But  other  unknown  conditions  (the  retention  of  sodium  chlorid,  possibly) 
also  play  a  role.  Even  in  cases  of  only  moderate  exudation  it  is  remarkable 
how  long  the  urinary  excretion  is  diminished  before  it  finally  becomes  normal. 
Therefore,  an  increase  of  the  amount  of  urine  is  always  a  favorable  symp- 
tom, often  the  first  sign  of  beginning  absorption  of  the  effusion.  If  a  large 
effusion  is  rapidly  absorbed,  the  amount  of  urine  may  increase  to  80  or  100 
ounces  (2,500  to  3,000  c.c.)  daily.  The  urine,  then,  of  course,  is  abnormally 
clear  and  of  low  specific  gravity.  This  pronounced  diuresis  often  persists  for 
so  long  a  time  during  the  period  of  absorption  of  pleural  exudates  that  here, 
also,  other  factors  than  the  mere  elimination  of  the  absorbed  fluid  must  be 
taken  into  account. 

Physical  Signs. — 1.  Fibrinous  Pleurisy  —  Pleuritis  Sicca. — Simple 
fibrinous  pleurisy  sometimes  gives  rise  to  no  physical  signs  at  all.  If  it  de- 
velops as  a  result  of  some  pulmonary  affection,  the  physical  signs  present  are 
often  dependent  upon  the  latter  alone. 

In  many  cases,  however,  dry  pleuris}*-  may  cause  marked  objective  signs. 
On  inspection,  we  are  struck  by  the  impaired  mobility  of  the  affected  side  on 
respiration,  which  is  due  to  the  pain  caused  by  breathing.  Because  of  this 
same  tenderness  the  patient  at  first  often  lies  on  the  sound  side.  Percussion 
gives  no  qualitative  change  of  resonance  as  yet.  With  the  beginning  of  exu- 
dation slight  dullness  appears,  at  first  almost  always  in  the  posterior  portion 
of  the  lungs.  Sometimes  the  resonance  becomes  tympanitic  as  a  result  of 
retraction  of  the  lung.  We  can  almost  constantly  make  out,  especially  in  the 
back,  that  the  lower  edge  of  the  lung  moves  less  than  usual  on  respiration. 
Auscultation  gives  a  respiratory  murmur  that  is  either  qualitatively  unchanged 
or  indefinite,  but  it  is  always  diminished.  The  peculiar  pathognomonic  sign 
of  dry  pleurisy,  however,  is  the  pleuritic  friction  rub,  that  characteristic  rub- 
bing, grating,  creaking  sound  which  arises  from  the  sliding  of  the  rough 
pleural  surfaces  over  each  other,  and  is  detected  especially  in  the  lateral  por- 
tions of  the  thorax.  We  can  hear  it  both  on  inspiration  and  on  expiration. 
It  is  often  jerky,  one  rub  following  another  after  a  considerable  interval.  If 
we  are  sure  we  hear  a  pleuritic  rub,  it  is  direct  evidence  of  the  existence  of 
a  dry  pleurisy,  but  its  absence  will  not  let  us  exclude  pleurisy.  The  friction 
sound  must  be  absent  if  there  are  pleuritic  adhesions.  We  can  often  feel  a 
marked  rub  lay  laying  the  hand  on  the  chest.  Sometimes  the  patient  feels  it 
himself,  but  in  other  cases  he  has  no  sensation  of  it.  We  may  confound  a  slight 
rub  with  fine  crepitant  rales.     Repeated  examinations  before  and  after  the 


348  DISEASES  OF  THE   RESPIRATORY   ORGANS 

patient  has  coughed  usually  confirm  the  diagnosis,  since  the  rales  are  often 
changed  by  coughing. 

To  be  distinguished  from  the  mild  form  of  dry  pleurisy  just  described  is 
that  variety  in  which  there  is  an  extensive  and  abundant  fibrinous  exudation, 
with  scarcely  any  liquid.  We  have  repeatedly  seen  cases  following  pneumonia, 
polyarthritis,  or  even  apparently  primary  cases,  which  displayed  marked  dull- 
ness and  sense  of  resistance  on  percussion  over  the  whole  of  one  side  of  the 
chest,  with  diminished  or  absent  respiration,  and  yet  upon  exploratory  punc- 
ture only  a  few  drops  of  serous  exudation  could  be  obtained.  Evidently  we 
had  to  do  with  the  formation  of  large  amounts  of  coagulated  fibrin.  Attacks 
of  this  sort  usually  run  a  severe  and  tedious  course,  but  they  may,  nevertheless, 
get  well  at  last. 

2.  Pleuritic  Effusion. — Small .  amounts  of  fluid  in  a  pleural  cavity  es- 
cape discovery.  Physical  signs  first  appear  when  the  amount  of  effusion  reaches 
8  to  10  ounces  (200  to  300  c.c). 

Inspection  shows  first  the  more  or  less  marked  impairment  of  motion  on 
the  affected  side  on  respiration.  If  the  amount  of  the  effusion  is  large,  there 
is  an  evident  distention  of  the  affected  side  in  the  lower  posterior  and  lateral 
portions  of  the  thorax.  The  intercostal  spaces  are  flattened  or  even  a  little 
convex.  The  nipples  and  shoulder  blades  are  farther  removed  from  the  me- 
dian line  on  the  affected  side  than  on  the  healthy  side.  The  hypochondrium 
on  the  affected  side  is  more  prominent.  In  an  extraordinarily  large  effusion 
on  the  left  side  we  have  seen  and  felt,  in  the  left  hypochondrium,  the  lower 
surface  of  the  diaphragm,  which  was  actually  arched  downward.  By  direct 
measurement  in  severe  cases  we  can  make  out  that  the  affected  side  is  expanded 
several  centimeters. 

With  every  large  effusion  there  is  marked  dyspnoea  and  accelerated  respira- 
tion. The  slight  excursions  of  the  affected  side  on  respiration  are  usually  very 
striking,  while  the  sound  side  moves  so  much  the  more.  In  this  stage  of  pleu- 
risy the  patient  often  lies  upon  the  affected  side,  in  order  to  breathe  with  the 
healthy  lung  with  as  little  restraint  as  possible.  With  large  effusions  complete 
orthopncea  may  develop. 

The  signs  due  to  displacement  of  the  neighboring  organs,  which  are  notice- 
able on  inspection,  will  be  mentioned  below  in  the  appropriate  connection. 

Everywhere  that  a  layer  of  fluid  comes  between  the  lung  and  the  chest  wall 
there  is  a  loss  of  clearness  in  the  percussion  note.  If  the  thickness  of  the  layer 
of  effusion  is  5  or  6  cm.,  the  resonance  seems  completely  dull  or  flat.  The 
pleuritic  dullness  is  almost  always  made  out  first  in  the  lower  posterior  por- 
tions of  the  thorax,  more  rarely  in  the  lower  lateral  portions.  With  a  slight 
effusion  the  height  of  the  dullness  is  only  a  few  centimeters,  but,  with  much 
effusion,  it  rises  higher  in  the  back  and  the  lateral  portions  of  the  thorax ;  and 
on  the  right,  resonance  gradually  grows  dull  anteriorly  and  inferiorly,  above 
the  liver.  With  very  large  effusions  the  dullness  may  begin  in  front  at  the 
second  or  third  rib,  or  in  rare  cases  even  the  whole  half  of  the  chest,  front  and 
back,  may  give  a  totally  flat  percussion  note.  Pleuritic  dullness  is  always  at- 
tended with  a  marked  feeling  of  resistance  on  percussion. 

With  medium-sized  effusions,  when  the  dullness  does  not  extend  over  the 
whole  back,  the  upper  boundary  of  the  dullness  usually  forms  an  oblique  line, 
highest  at  the  vertebral  column  and  thence  running  obliquely  downward  to  the 


PLEURISY  349 

side  of  the  thorax.  This  is  especially  observed  in  cases  that  have  taken  to 
their  beds  early  in  the  disease;  under  such  circumstances  the  exudate  must 
naturally  collect  in  the  posterior  portions  of  the  pleural  cavity.  The  upper 
border  of  the  dullness  has  a  more  horizontal  line  in  patients  who,  despite  be- 
ginning pleuritic  effusion,  are  up  and  about  a  good  deal.  Again,  the  highest 
level  of  the  upper  border  of  dullness  is  not  infrequently  found  in  the  pos- 
terior axillary  line ;  from  this  point  the  line  of  dullness  drops  somewhat,  both 
anteriorly  as  well  as  toward  the  vertebral  column.  This  depends,  in  part,  on 
the  lateral  posture  so  often  assumed  by  the  patient  (vide  supra),  and,  in  part, 
on  the  compression  of  the  lung  against  the  vertebral  column.  Hence  a  more 
tympanitic  percussion  zone  may  develop  posteriorly  and  below  alongside  the 
vertebral  column.  Occasionally,  when  there  is  very  large  effusion  into  the  left 
pleura,  a  small  area  of  dullness  may  also  be  found  on  the  normal  side,  pos- 
teriorly and  below,  near  the  vertebral  column  (Rauchfuss,  Grocco).  It  is 
probably  principally  dependent  upon  the  displacement  of  the  mediastinum. 
An  alteration  in  the  position  of  the  patient  (lying  down  or  sitting  up)  gen- 
erally causes  very  little  or  no  change  in  the  upper  border  of  the  dullness,  be- 
cause of  the  permanent  or  temporary  union  of  the  pleural  surfaces.  On  the 
right  it  is  not  possible  to  distinguish  by  percussion  the  lower  limit  of  the  exu- 
dation from  the  liver.  On  the  left  we  can  often  distinguish  its  lower  limit 
from  the  tympanitic  resonance  of  the  stomach,  and  are  thus  aided  in  diagnosis 
(vide  infra,  displacement  of  organs). 

The  percussion  note  above  a  pleuritic  effusion  deserves  attention.  The  be- 
ginning of  pleuritic  dullness  is  almost  always  relative,  gradually  passing  to  an 
absolute  flatness.  The  pulmonary  resonance  above  the  beginning  of  dullness  is 
usually  tympanitic,  from  retraction  of  the  lung  tissue.  We  find  the  tympa- 
nitic resonance  beautifully  distinct  in  large  effusions  in  the  first  and  second 
intercostal  spaces  in  front.  It  is  loud  and  deep,  and  remains  unchanged  with 
the  mouth  open — Skoda's  resonance.  With  very  large  effusions,  which  cause 
an  actual  compression  of  the  lung,  we  sometimes  find,  in  the  second  intercostal 
space,  a  dull  tympanitic  resonance,  which  becomes  higher  on  opening  the 
mouth.  This  resonance  arises  from  the  vibrations  of  air  in  a  large  bronchus 
surrounded  by  compressed  lung — "  Williams's  tracheal  tone."  With  large 
effusions  we  sometimes  hear  over  the  retracted  lung,  in  the  upper  anterior 
intercostal  spaces,  a  distinct  buckram  sound — the  "  cracked-pot  sound." 

Displacement  of  the  neighboring  organs,  which  is  made  out  chiefly  by  per- 
cussion, forms  one  of  the  most  important  physical  signs  in  pleurisy  with 
effusion. 

In  right-sided  effusions  the  liver,  especially  the  right  lobe,  is  displaced 
downward.  We  find  the  lower  border  of  the  liver  dullness  extending  several 
centimeters  below  the  ribs.  In  very  large  effusions  the  liver  may  be  pushed 
down  to  the  level  of  the  umbilicus.  The  pushing  of  the  mediastinum  to  the 
left  in  large  effusions  may  be  recognized  upon  percussing  from  the  right  toward 
the  left,  by  dullness  over  the  upper  part  of  the  sternum,  reaching  to  or  beyond 
the  left  border  of  the  sternum.  The  displacement  of  the  heart  to  the  left  in 
the  majority  of  well-marked  cases  is  associated  with  a  displacement  of  the 
apex  of  the  heart  upward.  This  is  easily  explained  by  considering  the  position 
of  the  heart  and  the  direction  of  the  pressure,  which  first  acts  from  below.  We 
recognize  the  displacement  of  the  heart  chiefly  by  the  position  of  the  apex 


350  DISEASES   OF  THE   RESPIRATORY   ORGANS 

beat,  which  is  seen  and  felt  at  or  outside  the  left  mammillary  line  in  the  fifth 
space,  or  often  higher,  as  we  have  said — in  the  fourth.  Percussion  gives .  a 
corresponding  displacement  of  the  left  boundary  of  the  cardiac  dullness  to 
the  left. 

In  left-sided  effusions  the  displacement  of  the  heart  to  the  right,  which  can 
usually  be  made  out  even  in  moderate  effusions,  is  especially  noticeable.  Eeso- 
nance  over  the  lower  part  of  the  sternum  is  diminished,  the  heart's  dullness 
extends  to  the  right  border  of  the  sternum  or  several  centimeters  beyond  it. 
In  the  most  marked  cases  the  heart  is  pushed  to  the  right  mammillary  line. 
The  displacement  of  the  mediastinum  is  also  to  be  made  out  over  the  upper  part 
of  the  sternum,  the  dullness  reaching  to  the  right  border  of  the  sternum  or 
beyond.  The  low  position  of  the  diaphragm  is  made  out  by  a  depression  of  the 
left,  and  in  marked  cases  of  the  right,  lobe  of  the  liver.  It  is  an  especially 
important  sign,  however,  that  dullness  occurs  in  the  zone,  about  a  hand- 
breadth  wide,  of  normal  tympanitic  resonance  above  the  left  border  of  the  ribs 
— the  "  semilunar  space  "  of  Traube.  The  normal  tympanitic  resonance  here 
comes  from  the  stomach  or  large  intestine.  As  the  diaphragm  is  pressed  down- 
ward the  pleuritic  effusion  presses  on  these  organs.  The  semilunar  space  is 
therefore  diminished,  and  finally,  with  large  effusions,  there  is  absolute  dull- 
ness down  to  the  edge  of  the  ribs. 

Changes  in  dullness  in  pleuritic  effusions  may  occur  with  a  change  of  the 
patient's  position,  but  they  may  often  be  absent  on  account  of  adhesions.  As  a 
rule,  the  normal  change  in  the  position  of  the  lower  border  of  the  lung  corre- 
sponding with  respiration  is  abolished. 

Auscultation  always  gives  a  diminished  respiratory  murmur  over  the  pleu- 
ritic effusion.  With  a  beginning  effusion  it  may  sound  approximately  vesicu- 
lar, but  later  it  becomes  indefinite,  harsh,  and  finally  bronchial,  if  the  larger 
bronchi  remain  open  for  the  respiratory  current  of  air.  The  bronchial  respi- 
ration sounds  distant  and  low,  and  has  the  character  of  the  sharp  German  ch, 
but  in  rare  cases  it  also  assumes  a  distinct  amphoric  tone,  so  that  it  sounds 
almost  like  a  cavernous  respiration.  The  respiratory  murmur  may  finally  dis- 
appear entirely  over  very  large  effusions.  Above  the  upper  boundary  of  the 
effusion  the  respiration  almost  always  sounds  harsh.  Among  the  adventitious 
sounds  we  must  mention  the  pleuritic  friction  sound,  which  of  course  can  be 
heard  only  at  the  upper  boundary  of  the  effusion,  where  the  two  pleural  sur- 
faces meet.  Moist  rales  and  rhonchi  signify  a  coexisting  disease  in  the  lungs. 
With  slight  effusions  we  often  hear,  on  deep  breathing,  pure  crepitant  rales 
on  inspiration,  as  the  walls  of  the  alveoli  and  bronchioles  in  the  atelectatic 
lung,  which  were  stuck  together,  are  torn  apart. 

On  auscultation  of  the  voice  we  sometimes  hear  bronchophony,  and  some- 
times that  bleating,  nasal  sound  known  as  segophony.  Baccelli  advanced  the 
theory  that  auscultation  of  the  whispered  voice  might  be  of  service  in  diagnos- 
ticating the  character  of  the  effusion.  With  a  serous  effusion  we  can  under- 
stand a  whisper  distinctly  through  the  thorax,  but  not  with  a  purulent  effu- 
sion, since  theoretically  the  cell  elements  destroy  the  waves  of  resonance.  This 
theory  holds  true  in  many  cases,  but  by  no  means  in  all. 

On  auscultation  of  the  heart  we  notice,  as  a  result  of  its  displacement,  an 
abnormal  etxension  of  the  region  over  which  the  heart  sounds  are  audible. 
If  the  inflammation  spreads  from  the  pleura  to  the  outer  surface  of  the  peri- 


PLEURISY  35] 

cardium,  we  can  sometimes  hear  an  extrapericardial  friction  rub,  accompany- 
ing both  the  respiration  and  the  action  of  the  heart. 

The  vocal  fremitus  is  always  diminished  over  the  pleuritic  effusion,  and  in 
marked  cases  is  entirely  absent. 

3.  Absorption  of  the  Effusion — Pleuritic  Contraction. — The  be- 
ginning absorption  of  the  effusion  is  usually  first  made  evident  by  the  per- 
cussion note  in  the  upper  part  of  the  dullness  becoming  clearer  and  some- 
times tympanitic.  The  respiratory  murmur  is  also  plainer.  Where  it 
bronchial  it  becomes  indefinite  and  gradually  vesicular  again.  The  vocal 
fremitus  is  again  to  be  felt.  All  these  improvements  take  place  gradually 
but  slowly.  It  is  usually  a  very  long  time  before  the  percussion  note  resumes 
its  normal  clearness. 

The  changes  in  the  form  of  the  thorax  are  especially  striking.  Only  in 
pleurisies  with  slight  effusion  does  the  somewhat  expanded  thorax  resume 
its  old  form  without  further  change.  After  every  severe  pleurisy  with  large 
effusion  there  is,  during  its  absorption,  a  marked  contraction  of  the  affected 
half  of  the  chest.  In  cases  of  moderate  intensity  the  contraction  principally 
affects  only  the  lower  lateral  portions  of  the  thorax,  in  severe  cases  the  upper 
and  anterior  portions  as  well.  We  find  the  most  marked  contractions  in  chil- 
dren and  young  persons  with  a  yielding  thorax.  The  circumference  of  the 
affected  side  is  much  less  than  that  of  the  sound  side.  The  ribs  are  pressed 
together  and  the  intercostal  spaces  become  very  narrow.  The  fossa?  are  deep- 
ened and  the  nipples  and  shoulder  blades  are  drawn  nearer  the  vertebral 
column,  which  takes  on  an  abnormal  lateral  curvature,  in  which  its  convex- 
ity is  directed  usually  toward  the  affected  side,  hut  sometimes  to  the  sound 
side.  Dullness  and  diminution  of  the  respiratory  murmur  and  vocal  fremitus 
continue  with  the  contraction  of  the  pleura,  but  they  no  longer  depend  upon 
the  presence  of  a  fluid  effusion,  but  are  due  to  the  pleuritic  thickening. 

The  process  of  marked  contraction  always  lasts  for  months,  or  even  longer. 
In  favorable  cases  the  contraction  of  the  thorax  may  be  readjusted  very  much 
later,  often  after  years.  The  thickening  is  absorbed,  and  the  lungs  and  thorax 
gradually  expand,  but  in  other  cases  there  are  extensive  adhesions  between  the 
pleural  surfaces,  especially  over  the  lower  lobe,  which  result  in  a  permanent 
disturbance  of  respiration.  In  almost  all  cases  of  pleurisy  with  contractions 
there  arises  a  vicarious  emphysema  in  the  lung  on  the  sound  side. 

COMPLICATIONS 

Peculiar  complications  of  pleurisy  are  rare.  Where  such  occur  they  are 
due  either  to  the  primary  disease  which  has  led  to  the  pleurisy,  or  to  the 
simultaneous  action  of  the  same  cause  of  disease,  such  as  tuberculosis.  Hence 
it  happens  that  we  speak  of  the  frequent  "  complication  "  of  pleurisy  with 
chronic  bronchitis  or  with  tuberculosis  of  the  lungs  or  other  organs.  It  is 
important  to  bear  in  mind  that,  by  a  direct  advance  of  the  inflammation, 
the  pleurisy  may  also  invade  the  pericardium,  and  rarely  the  peritoneum, 
through  the  diaphragm;  but  we  see  this  extension  of  the  process  almost 
solely  in  tuberculous  and  purulent  pleurisies.  We  must  mention,  finally,  that 
we  have  seen  several  cases  with  a  large  serous  effusion,  in  which  an  acute  hem- 
orrhagic nephritis  occurred.     For  the  paralysis  of  the  arm  on  the  correspond- 


352  DISEASES  OF  THE   RESPIRATORY  ORGANS 

ing  side  observed  in  some  cases  of  empyema,  compare  what  is  said  in  regard 
to  reflex  paralyses  in  Volume  II. 

VARIOUS  FORMS  OF  PLEURISY 

1.  Primary  Rheumatic  Pleurisy. — As  we  have  already  pointed  out,  when 
considering  the  aetiology  of  pleurisy,  clinical  observations  have  lately  led  to 
the  belief  that  some  of  the  cases  of  acute  primary  pleurisy  are  due  to  the 
same  cause  as  acute  articular  rheumatism  (which  see).  Although  there  are 
as  yet  no  sufficient  number  of  decisive  bacteriological  investigations,  we  are, 
nevertheless,  strongly  inclined,  from  our  present  experience,  to  acknowledge 
the  correctness  of  this  view,  even  if  we  do  not  estimate  the  frequency  of  rheu- 
matic pleurisy  nearly  so  high,  as,  e.  g.,  does  Fiedler,  on  the  ground  of  his 
observations  in  Dresden. 

Rheumatic  pleurisy  usually  develops  rather  suddenly  in  persons  previ- 
ously healthy.  Sometimes  it  is  preceded  by  mild  rheumatic  pains  in  the  mus- 
cles or  some  of  the  joints.  The  local  discomforts,  such  as  pain  in  the  side, 
are  often  very  severe,  the  fever  is  moderately  high,  though  rarely  over  104° 
F.  (40°  C.)  ;  and  as  the  case  progresses  such  rheumatic  symptoms  as  swelling 
of  the  joints  and  endocarditis  may  also  associate  themselves  with  the  pleurisy 
and  confirm  the  diagnosis.  In  general,  however,  the  course  of  the  disease  is 
favorable.  The  fever  lasts,  as  a  rule,  only  a  week  or  two,  and  even  when  there 
is  a  large  exudation  it  finally  undergoes  complete  absorption  with  recovery. 

2.  Tuberculous  Pleurisy. — In  an  ^etiological  sense  we  must  declare  by  far 
the  larger  part  of  the  ordinary  "  pleuritic  effusions,"  which  clinically  seem 
primary,  to  be  tuberculous.  The  further  course  of  the  cases,  if  we  can  watch 
them  long  enough,  almost  always  permits  us  finally  to  recognize  the  tuber- 
culous nature  of  the  disease;  yet  we  cannot  say  that  some  other  tuberculous, 
disease,  particularly  phthisis,  is  always  the  immediate  sequel  of  the  pleurisy. 

In  a  comparatively  small  number  of  cases  do  the  symptoms  of  acute  tuber- 
culosis, or  more  frequently  of  chronic  phthisis,  appear  as  an  immediate  result 
of  the  pleurisy,  which  at  that  time  is  usually  still  present  or  in  the  contracting 
stage.  The  objective  changes  of  phthisis  are  evident  either  in  the  apex  or 
in  the  lower  lobe  of  the  affected  side.  The  fever  continues,  the  pulmonary 
affection  advances,  the  other  lung  is  also  attacked,  and  the  disease  takes  a 
fatal  course  under  the  type  of  an  ordinary  phthisis,  now  more  acute  and  now 
more  chronic. 

In  other  cases  acute  tuberculous  affections  arise  sooner  or  later  as  a  result 
of  the  pleurisy — tuberculous  meningitis  or  general  miliary  tuberculosis.  In 
other  cases  still  the  disease  develops  under  the  form  of  tuberculosis  of  the 
serous  membranes,  to  which  we  will  return  again  in  the  description  of  tuber- 
culous pericarditis  and  tuberculous  peritonitis.  We  often  have  to  do  with  a 
double  pleurisy  with  no  evident  complication  in  the  lungs.  In  varying  succes- 
sion are  added  the  symptoms  of  chronic  tuberculous  peritonitis,  with  pain, 
swelling,  and  effusion  of  fluid  into  the  abdomen,  or  the  symptoms  of  tubercu- 
lous pericarditis.  Death  finally  ensues  with  persistent  hectic  fever  and  increas- 
ing general  emaciation  and  weakness.  The  whole  affection  usually  runs  a 
chronic  course,  lasts  for  months,  and  often  shows  marked  remissions  and  tem- 
porary improvements. 


PLEURISY  353 

In  very  many  instances,  on   the  other  hand,  the  pleuritic  effusion   has 

throughout  an  apparently  favorable  course.  After  some  weeks  the  {<■■■>■!■ 
ceases,  the  effusion  is  absorbed,  the  patient  gets  up,  and  is  finally  discharged 
as  nearly  well.  Of  course,  some  dullness  and  retarded  motion  often  remain 
in  the  affected  side,  but  even  these  may  gradually  disappear.  These  cases, 
too,  very  often  turn  out  in  the  end  to  he  tuberculous.  After  a  longer  or  shorter 
period  of  apparent  health,  sometimes  after  the  lapse  of  years,  a  "new"  dis- 
ease appears — that  is,  either  a  return  of  the  pleurisy,  a  pleurisy  on  the  other 
side,  or  some  other  acute  or  chronic  tuherculous  affection.  In  such  cases,  too, 
we  must  look  upon  the  former  pleurisy,  in  an  ^etiological  sense,  as  tuberculous. 
It  is  not  impossible,  however,  for  even  a  tuberculous  pleurisy  to  recover,  and 
for  the  recovery  to  be  permanent,  if  no  other  organ  is  at  the  same  time  affected 
by  tuberculosis,  especially  if  the  lungs  remain  intact. 

Finally,  we  must  mention  the  cases  in  which  a  pleuritic  effusion  develops 
secondarily  to  an  already  pronounced  phthisis.  Here,  too,  we  almost  always 
have  to  do  with  a  tuberculous  pleurisy. 

The  anatomical  changes  in  tuberculous  pleurisy  consist  in  the  ordinary 
;signs  of  inflammation,  and  also  the  presence  of  the  specific  nodules  of  tubercle. 
The  number  of  tubercles  differs  very  much  in  different  cases.  The  pleura  is  in 
some  cases  completely  studded  with  miliary  nodules,  and  in  others  we  find  the 
tubercles,  at  least  with  the  naked  eye,  only  in  single  spots.  The  effusion  is 
usually  of  a  serofibrinous  character.  Sometimes  it  is  hemorrhagic,  as  the 
majority  of  cases  of  apparently  primary  "  hemorrhagic  pleurisy  "  are  gener- 
ally of  a  tuberculous  nature.  Empyema  also  (vide  infra)  occurs  not  infre- 
quently in  association  with  tuberculosis ;  and  finally,  in  a  few  cases  the  exuda- 
tion has  been  of  a  peculiar  milky  character,  and  has  contained  numerous  oil 
globules,  probably  originating  from  fatty-degenerated  and  disintegrated  leuco- 
cytes and  endothelium. 

3.  Purulent  Pleurisy — Empyema. — A  purulent  exudation  is  developed  in 
the  pleura  when  the  inflammation  of  that  organ  is  due  to  a  specific  cause 
which  excites  suppuration.  So  far  as  is  yet  known,  the  Streptococcus  pyogenes 
seems  to  be  the  most  frequent  factor  in  producing  empyema.  It  is  found  in 
the  pus  of  empyema,  due  to  such  causes  as  external  injury,  caries  of  the  ribs, 
pulmonary  tuberculosis,  pneumonia,  and  pysemia.  Less  often  empyema  is  ex- 
cited by  staphylococci.  This  is  almost  always  a  rather  favorable  form  of  the 
disease.  Likewise  comparatively  benign  is  metapneumonic  empyema,  which 
in  most  instances  is  caused  by  the  pneumococcus.  The  empyema  of  tubercu- 
losis is,  as  has  been  already  pointed  out,  in  most  cases  devoid  of  bacteria  (A. 
Erankel  and  others),  and  here  we  may  have  to  do  with  the  formation  of 
chemical  poisons  capable  of  exciting  suppuration. 

Empyema  usually  causes  severe  symptoms.  The  fever  is  higher  than  in  the 
other  forms  of  pleurisy,  but  is  irregularly  intermittent,  and  is  often  associated 
with  chills.  There  are  severe  general  symptoms  besides  the  fever,  such  as  great 
languor,  headache,  a  dry  tongue,  and  a  rapid  pulse.  We  sometimes  notice  a 
slight  oedema  of  the  chest  wall  on  the  affected  side.  Otherwise  the  local  symp- 
toms and  disturbances  are,  of  course,  the  same  as  in  the  other  forms  of  pleu- 
risy. If  the  pus  is  not  evacuated  artificially,  the  empyema  may  finally  break 
externally  or  into  the  lungs  (vide  supra).  In  the  latter  case  a  very  large  ex- 
pectoration of  pus  suddenly  occurs,  and  is  usually  followed  by  pneumothorax. 


354  DISEASES  OF  THE  RESPIRATORY  ORGANS 

DIAGNOSIS 

Our  chief  attention  in  regard  to  diagnosis  is  directed  to  the  distinction 
between  pleurisy  and  acute  or  chronic  pneumonia,  which  is  not  very  easy  in 
all  cases.  We  will  briefly  contrast  the  distinctive  features  as  made  out  on 
physical  examination. 

Inspection. — A  marked  distention  of  the  affected  side  points  to  effusion ;  it 
does  not  occur  in  pneumonia. 

Percussion. — The  dullness  in  pleurisy  is  complete,  and  the  feeling  of  resist- 
ance on  percussion  is  very  marked;  in  pneumonia,  however,  the  dullness  is 
rarely  so  marked,  and  there  is  often  a  tympanitic  sound.  The  discovery  by 
percussion  of  signs  of  displacement  of  the  neighboring  organs  is  of  especial 
weight,  as  these  signs  are  always  absent  in  uncomplicated  pneumonia,  while 
with  few  exceptions  they  can  be  easily  demonstrated  in  every  case  of  pleurisy 
when  the  exudation  is  at  all  considerable. 

Auscultation. — Diminished  or  suppressed  respiratory  murmur  points  to 
pleurisy,  loud  bronchial  breathing  and  rales  to  pneumonia;  but  we  must  not 
forget  that  in  pneumonia  auscultation  may  give  the  same  signs  as  in  pleurisy, 
if  a  bronchus  is  plugged. 

Vocal  Fremitus. — Marked  vocal  fremitus  over  dullness  is  direct  evidence 
of  pneumonia,  diminished  or  absent  vocal  fremitus  of  pleurisy;  but  the  vocal 
fremitus  may  also  be  diminished  in  pneumonia  if  a  bronchus  is  plugged. 

Besides  the  physical  signs,  other  phenomena  to  be  observed  are  the  mode 
of  commencement,  the  course  of  the  disease,  the  fever,  the  expectoration,  and 
the  appearance  of  herpes.  The  most  reliable  means  of  deciding  in  all  doubt- 
ful cases  is  exploratory  puncture,  although  even  then  we  may,  of  course,  be  left 
in  doubt  whether  an  infiltration  of  the  corresponding  portion  of  the  lung  may 
not  exist  in  addition  to  pleurisy.  If  the  exudation  is  largely  fibrinous,  or  if 
there  is  an  abundant  new  growth  of  inflammatory  connective  tissue,  the  results 
of  aspiration  may  be  negative.  Hence,  in  doubtful  cases  we  should  always 
make  repeated  trials. 

If  we  have  diagnosticated  a  pleuritic  effusion,  the  next  question  is  always 
as  to  the  character  of  the  effusion,  because  the  prognosis  and  treatment  are  to 
a  large  degree  dependent  upon  this.  Although  certain  well-known  setiological 
circumstances,  and  the  severity  of  the  fever  and  the  general  symptoms,  often 
permit  us  to  suspect  the  nature  of  the  effusion,  whether  serous  or  purulent, 
the  only  certain  information  comes  from  an  exploratory  puncture  with  a 
hypodermic  syringe.  If  the  syringe  is  carefully  disinfected,  and  the  opera- 
tion is  cautiously  conducted,  this  procedure  is  entirely  devoid  of  danger,  and 
we  must  urgently  advise  its  employment  in  all  doubtful  cases  in  order  to 
settle  the  diagnosis.  It  is  indeed  of  practical  importance  to  know  that  there 
is  a  likelihood  in  empyema  of  obtaining  no  fluid  by  means  of  exploratory 
puncture  (vide  supra),  even  when,  upon  incision,  pus  is  found.  We  have  had 
this  experience  repeatedly.  In  doubtful  and  severe  cases  in  which  there  is  sus- 
picion of  empyema,  it  is  therefore  decidedly  advisable,  when  life  is  threatened, 
to  make  an  incision  of  the  pleura.  Besides  a  macroscopic  inspection,  a  careful 
microscopic  examination  of  the  fluid  withdrawn  is  sometimes  of  importance. 
Besides  the  ordinary  constituents — red  and  white  blood  corpuscles,  endothelial 


-  PLEURISY  365 

cells,  and  eholesterin  crystals — we  may  sometimes  find  something  of  special 
diagnostic  significance,  such  as  bacteria  in  septic  pleurisy,  carcinoma  cells  in 
cancerous  pleurisy,  etc. 

We  cannot  always  judge  from  the  beginning  whether  a  pleurisy  is  tuber- 
culous or  not;  but  we  should  never  forget,  as  has  already  been  affirmed,  that  in 
every  case  of  pleurisy,  even  if  it  is  apparently  primary,  there  is  a  strong  sus- 
picion of  tuberculosis.  We  must  observe  in  particular  the  general  habit  and 
the  nutrition  of  the  patient,  and  inquire  into  the  hereditary  predisposition  and 
any  previous  illness.  In  the  further  course  of  the  disease  persistent  hectic  fever, 
slowly  increasing  emaciation  and  pallor,  fresh  relapses,  and  the  onset  of  pul- 
monary symptoms,  point  to  the  tuberculous  character  of  the  pleurisy.  Every 
case  of  double  pleurisy,  and  of  pleurisy  associated  with  pericardial  symptoms, 
leads  us  most  decidedly  to  suspect  tuberculosis.  Since  tuberculous  nodules  of 
the  serosa  almost  never  ulcerate,  tubercle  bacilli  cannot  usually  be  found  in 
those  cases  of  tuberculous  pleurisy  in  which  microscopical  examination  of  the 
centrifuged  sediment  is  made.  On  the  other  hand,  the  tuberculous  nature  of 
the  disease  can  often  be  demonstrated  by  the  injection  of  about  10  c.c.  of  the 
fluid  into  the  peritoneal  cavity  of  a  guinea  pig;  within  four  to  six  weeks  tu- 
berculous peritonitis  develops.  The  examination  of  the  sputum,  too,  is  impor- 
tant, even  in  cases  of  apparently  simple  pleurisy.  We  have  often  been  able  to 
demonstrate  tubercle  bacilli  in  the  scanty  expectoration  of  such  patients,  even 
when  there  were  scarcely  any  pulmonary  symptoms.  Careful  microscopical 
examination  of  the  cellular  elements  of  the  centrifugalized  sediment  of  the 
aspirated  pleural  fluid  (the  "  cyto-diagnosis  "  of  Widal  and  others)  is  of  consid- 
erable importance  in  determining  the  nature  of  the  disease.  We  are  nearly 
always  dealing  with  a  tuberculous  pleurisy  if  mononuclear  leucocytes  compose 
the  main  part  of  the  leucocytes  present  in  the  fluid.  In  cases  of  pleurisy  from 
other  causes,  the  cellular  elements  of  the  fluid  are  in  largest  part  made  up  by 
the  usual  polynuclear  leucocytes.  As  we  have  indicated,  a  hemorrhagic  effu- 
sion is  strongly  in  favor  of  tuberculosis,  but  also  occurs  in  new  growths  of  the 
pleura  (vide  infra). 

The  differentiation  between  inflammatory  pleuritic  exudates  and  pleuritic 
transudates  (hydrothorax,  vide  infra)  usually  is  evident  from  the  general 
clinical  picture  of  the  disease,  but  it  may  occasionally  be  difficult.  The  per- 
centage of  albumen  in  the  fluid  should  be  estimated,  it  being  much  higher  in 
exudates  (usually  not  less  than  4.5  per  cent)  than  in  transudates.  Corre- 
spondingly, the  specific  gravity  of  exudates  is  higher  (more  than  1.015)  than 
that  of  transudates.  A  considerable  admixture  of  leucocytes  in  the  fluid  in- 
variably speaks  for  its  inflammatory  origin.  Endothelial  cells  alone  are  also 
present  in  considerable  quantities  in  the  transudation  fluids  as  well  as  in 
exudates.  Eivalta  has  devised  an  interesting  test  for  the  differentiation  be- 
tween exudates  and  transudates:  A  very  weak  solution  of  acetic  acid  (2  drops 
of  glacial  acetic  acid  to  3.3  ounces  [100  c.c]  of  water)  is  placed  in  a  cylin- 
drical vessel.  A  few  drops  of  the  aspirated  fluid  are  dropped  into  this  solution. 
In  the  case  of  an  exudation,  a  readily  visible,  light  cloud  resembling  "  cigarette 
smoke  "  will  appear  in  the  path  of  the  descending  drops.  This  cloud  is  due 
to  the  precipitation  of  an  albuminous  body,  and  is  entirely  absent  when  a 
transudation  fluid  is  tested. 


356  DISEASES   OF  THE   RESPIRATORY   ORGANS 

PROGNOSIS 

The  prognosis,  as  regards  the  immediate  danger  of  the  disease,  depends 
entirely  upon  the  severity  of  the  symptoms,  and  especially  upon  the  dyspnoea. 
The  prognosis,  as  regards  the  further  course  of  the  disease,  depends  chiefly 
upon  the  nature  of  the  pleurisy.  Many  secondary  and  also  many  apparently 
primary  pleurisies,  although  extensive,  recover  completely  and  permanently 
after  weeks  or  months.  Undoubtedly,  an  apparently  complete  cure  not  infre- 
quently occurs  also  in  cases  of  tuberculous  pleurisy.  A  certain  amount  of 
a23prehension  for  the  future  will,  however,  always  be  entertained,  inasmuch  as 
pulmonary  tuberculosis  only  too  frequently  develops  at  some  later  date.  The 
prognosis  of  emj>yema  depends  partly  upon  the  underlying  disease,  but  espe- 
cially upon  judicious  and  timely  operative  interference.  In  benign  cases  of 
empyema  recovery  is  usually  complete  in  a  few  weeks  after  operation,  but 
sometimes  months  are  required.  The  possibilities  of  a  spontaneous  rupture 
of  empyema,  internally  or  externally,  have  been  mentioned  above.  With 
incomplete  healing,  which  leaves  a  pleural  fistula,  we  must  fear  the  appearance 
of  general  amyloid  disease  in  various  organs. 

In  rare  instances  with  large  effusions  sudden  death  occurs,  an  event  which 
cannot  always  be  satisfactorily  explained.  Probably  there  are  different  factors 
in  different  cases,  such  as  pulmonary  embolism,  cerebral  embolism,  sudden 
cerebral  aneemia,  weakness  of  the  heart,  or  the  onset  of  pulmonary  oedema. 

TREATMENT 

In  the  beginning  of  the  disease  the  treatment  is  purely  symptomatic.  We 
Try  to  alleviate  the  patient's  symptoms,  the  pain  and  dyspnoea,  by  cold  or  warm 
applications  (the  latter  are  usually  more  grateful),  sometimes,  too,  by  dry 
cups,  also  by  embrocations  with  chloroform  liniment  and  sinapisms,  with 
severe  symptoms,  by  morphin  internally  or  subcutaneously.  Unfortunately, 
we  have  but  few  remedies  to  check  the  inflammatory  process  in  the  pleura. 
If  an  ice  bag  is  well  borne,  it  may  be  of  service.  The  efficacy  of  the  much- 
used  painting  with  iodin  is  doubtful,  but  it  may  always  be  tried  if  there  is  a 
severe  pleuritic  pain.  Perhaps  more  efficient  is  the  application  of  iodized 
vasogen.  In  recent  years  the  author  has  extensively  employed  soap  inunc- 
tions with  apparently  very  good  results.  Sometimes  tincture  of  green  soap 
is  used,  and  sometimes  a  salve  made  of  green  soap,  20  parts,  and  10  parts  each 
of  lanolin  and  vaselin.  The  inunctions  are  given  once  daily,  care  being  taken 
to  avoid  any  inflammatory  eczema.  If  the  skin  is  very  sensitive,  the  inunc- 
tion should  be  washed  off  with  lukewarm  water  in  an  hour. 

If  a  large  serous  effusion  has  formed,  it  is  the  universal  custom  to  prescribe 
diuretics.  The  idea  is  to  cause,  or  at  any  rate  promote,  the  absorption  of  the 
exudation  by  increasing  the  excretion  of  urine.  It  is,  however,  very  difficult  to 
obtain  any  real  proof  of  the  usefulness  of  diuretics  in  pleurisy  with  effusion. 
They  often  are  of  no  use  whatever,  but,  again,  the  absorption  of  the  fluid  may 
follow  the  administration  of  a  diuretic,  so  that  it  does  not  seem  impossible  that 
the  latter  has  a  therapeutic  influence.  With  regard  to  a  choice  of  the  diuretics 
fo  be  employed  we  would  name,  first,  salicylate  of  sodium,  75  to  120  gr.  (gm. 
-5  to  8)  a  day,  because  a  specific  influence  has  been  ascribed  to  this  drug  in 


PLE1  risi  357 

pleurisy.  This  applies  particularly  to  cases  of  supposed  rheumatic  origin  (vide 
supra).  Many  good  observers  asserl  that  primary  pleuritic  exudations  often 
run  a  remarkably  rapid  and  favorable  course  when  treated  with  salicylate  of 
sodium.  Moreover,  the  drug  lias  a  direct  diuretic  effect.  Besides  this,  the  ace- 
tates of  potassium  and  of  -odium  are  frequently  prescribed,  as  well  as  squills, 
and,  of  late,  diuretin  (sodio-salicylate  of  theobromin),  given  in  doses  of  15 
to  30  gr.  (gm.  1  to  2)  two  or  three  times  a  day.  We  have  sometimes  found 
this  remedy  apparently  very  efficient.  If  there  are  signs  of  cardiac  weak] 
and  diminished  arterial  tension,  digitalis  must  be  prescribed,  alone  or  with  a 
diuretic.  Other  internal  remedies  are  at  present  seldom  employed  in  pleu 
with  effusion.  The  influence  of  iodid  of  potassium  as  an  "  absorbent  " 
extremely  doubtful.  Drastie  purgatives  and  such  diaphoretic  remedies  as 
hot  packs  and  piloearpin  usually  affect  the  general  condition  unfavorably,  and 
are  of  little  use.  Probably  there  are  to-day  few  advocates  of  the  so- 
called  Schroth  method  of  treatment,  according  to  which  the  amount  of  fluid 
ingested  is  reduced  to  a  minimum,  so  as  to  promote  the  absorption  of  the 
exudation. 

In  many  cases  the  evacuation  of  the  effusion  by  puncture  (introduced  by 
Trousseau)  is  of  the  greatest  importance.  Many  cases  of  pleurisy  with  effusion 
run  a  favorable  course  without  it,  and  we  consider  it  at  least  superfluous  to 
puncture  every  effusion  without  sufficient  grounds,  but  puncture  is  often  one 
of  the  most  serviceable  therapeutic  influences  at  our  command,  and  may  occa- 
sionally be  a  life-saving  procedure.  The  first  and  most  important  indication 
for  puncture  is  present  when  the  effusion  becomes  so  large  as  to  be  directly 
dangerous  to  life.  As  soon  as  the  patient's  dyspnoea  reaches  a  dangerous 
degree,  and  the  cyanosis  becomes  marked  and  the  pulse  weaker,  a  puncture 
must  be  made  as  a  direct  vital  indication.  "When  the  exudation  is  of  consid- 
erable size  there  may  be  a  very  sudden  aggravation  of  the  symptoms,  so  that 
in  such  cases  one  should  not  wait  too  long.  It  is  much  better  to  puncture  too 
early  than  too  late !  Trousseau  urged  that  tapping  should  invariably  be  per- 
formed when  the  dullness  caused  by  the  exudation  involves  not  only  the  back, 
but  also  the  whole  or  nearly  all  of  the  anterior  wall  of  the  thorax,  a  rule  which 
the  author  almost  always  follows.  The  benefit  of  such  a  puncture  is  often  pro- 
nounced. The  second  indication  is  a  too  protracted  absorption  of  the  effusion. 
Puncture  is  indicated  if  the  effusion  does  not  disappear  after  an  apparent 
remission  of  the  inflammatory  symptoms,  especially  after  the  fever  has  gone. 
We  often  see  the  further  absorption  stimulated  by  such  a  puncture.  It  has 
been  said  that,  if  possible,  tapping  should  be  delayed  until  the  fever  has  ceased, 
but  to  us  this  does  not  seem  at  all  necessary.  When  the  exudation  was  large, 
or  the  absorption  was  delayed,  we  have  repeatedly  aspirated  even  when  the 
patient  was  still  feverish,  and  have  not  infrequently  found  that  the  fever 
diminished  remarkably  upon  the  removal  of  the  exudation  (see  the  tempera- 
ture chart,  Fig.  58). 

As  regards  the  performance  of  the  puncture,  we  cannot  here  go  into  all  the 
numerous  methods  and  forms  of  apparatus  proposed.  The  distinctions  are 
immaterial.  The  simpler  the  method,  the  easier  it  is  to  perform,  and  hence 
the  better  it  is. 

Every  puncture  must  be  preceded  by  an  exploratory  puncture  in  order  to 
settle  the  diagnosis  as  to  the  presence  and  character  of  the  exudation.     A 
23 


358 


DISEASES   OF   THE   RESPIRATORY   ORGANS 


medium-sized  trocar  with  a  lateral  opening,  to  which  a  rubber  catheter  can  be 
fastened,  serves  to  evacuate  the  fluid.  Billroth's  and  Frantzel's  trocars  are" 
useful.  Aspiration  can  be  performed  still  more  conveniently  with  a  hollow 
needle,  and,  best  of  all,  according  to  our  experience,  with  that  proposed  by 
Fiedler,  which  is  now  exclusively  employed  in  the  author's  wards,  because  the 
point  of  this  needle  is  guarded  so  that  it  cannot  scratch  the  tissues,  and  also, 
if  it  becomes  plugged  with  clots  of  fibrin    these  can  be  pushed  out.1     The 


40 


39. 


38.' 


37. c 


Fig 


58. — Temperature  curve  in  pleurisy  with  effusion  before  and  after  tapping. 
(Erlangen  Medical  Clinic.) 


instruments  and  the  cbest  wall  at  the  point  of  puncture  must  be  carefully 
disinfected.  We  usually  choose  a  point  for  puncture  somewhere  about  the 
sixth  intercostal  space,  in  the  middle  or  posterior  axillary  line.  The  patient 
sits  up  in  bed,  but  is  held  and  supported  by  another  person,  when  it  is  possible. 
Before  and  during  the  puncture  he  takes  a  little  strong  wine,  strophantus, 
or  similar  stimulant.  The  pain  of  the  operation  may  be  mitigated  by  previ- 
ously injecting  morphin,  or,  still  better,  by  causing  local  anaesthesia  at  the 
site  of  puncture  with  ethyl  chlorid.  In  the  overwhelming  majority  of  cases, 
and  especially  if  the  exudation  is  abundant,  we  can  remove  a  large  part  of  the 
fluid  by  simple  puncture  with  siphonage.  With  few  exceptions,  the  pleuritic 
exudation  is  under  a  positive  pressure  of  10  to  25  mm.  of  mercury.  The 
evacuating  tube  of  the  trocar  must  be  previously  filled  with  sterile  water  and 
conducted  under  a  layer  of  the  same  into  the  vessel  prepared  to  receive  the 
effusion.  The  evacuation  of  the  effusion  should  always  be  slow  and  gradual. 
Many  physicians  advise  stopping  when  1,500  c.c.  have  been  removed,  but  if 
the  fluid  is  allowed  to  escape  slowly  and  everything  is  going  well,  this  quantity 
may  often  be  exceeded  with  impunity  in  the  case  of  large  exudations.  While, 
as  we  have  said,  in  most  instances  the  exudation  may  be  satisfactorily  re- 
moved by  simple  puncture  arjd  siphonage,  it  will  sometimes  prove  necessary 
to  employ  aspiration.  Hence  some  physicians  invariably  do  so,  and  to  this 
there  is  no  objection,  even  if  it  is  unnecessary.  The  forms  of  apparatus  most 
used  for  this  are  those  invented  by  Dieulafoy  and  Potain.  In  puncture  with 
aspiration  we  proceed  more  slowly  and  cautiously. 


1  [Fiedler's  instrument  consists  essentially  of  a  sharp  hollow  needle,  with  an  outer  jacket,  which 
can  be  moved  so  as  to  cover  the  sharp  point  after  the  chest  wall  has  been  penetrated.  If  the 
lumen  is  stopped  up,  a  pointed  steel  wire  thrust  directly  through  the  attached  rubber  tubing  dis- 
places the  obstruction.  Probably  the  least  pain  in  tapping  is  felt  after  previous  infiltration  of  the 
local  tissues  with  0.5-per-cent  solution  of  cocain.] 


-pleurisy  35g 

[The  necessity  for  two  punctures — one  exploratory,  the  other  distinctly 
operative — dues  not  seem  clear.  The  two  can  be  perfectly  combined,  a  fair- 
sized  trocar  or  needle  being  as  easy  of  introduction  and  producing  really  no 
more  pain  than  a  very  fine  one,  and  being  more  sure  to  give  results  on  which 
reliance  can  be  placed.  An  ordinary  Davidson's  syringe  makes  a  very  satisfac- 
tory pump  and  can  always  be  obtained.] 

Unpleasant  incidents  which  may  cause  a  cessation  of  the  process  are  rare. 
If  the  patient  complains  of  dizziness  or  faintness  we  musi  cease,  or,  al  any  rate, 
pause.  Usually  everything  goes  well  until  the  needle  begins  to  rub  againsl  the 
pleura:  then  there  is  pain  and  generally  a  violent  cough.  It  is  well,  then,  to 
remove  the  needle  at  once.  The  cough  can  usually  be  promptly  quieted  by 
rest  and  a  little  morphin,  but  sometimes  after  aspiration  there  will  develop 
a  sort  of  pulmonary  oedema,  with  the  expectoration  of  a  large  amount  of  frothy 
serous  sputum  (expectoration  albumineuse) .  This  is  perhaps  due  to  the  in- 
creased permeability  of  the  vascular  walls  in  a  lung  that  has  been  compressed 
for  a  long  time. 

When  the  process  is  over,  we  close  the  little  opening  with  a  bit  of  sticking- 
plaster  or  with  iodoform  collodion.  A  regular  surgical  dressing  is  scarcely  ever 
necessary. 

If  the  exploratory  puncture  has  shown  a  purulent  effusion,  we  can  first 
evacuate  the  pus  by  puncture  if  the  vital  indication  exists;  but  a  permanent 
cure  from  tapping  is  exceptional.  The  pus  almost  always  reappears.  Empy- 
ema is  like  an  abscess,  which  cannot  be  cured  until  a  permanent,  free  exit  for 
the  pus  has  been  provided.  We  must,  therefore,  not  only  remove  the  pus,  but 
institute  drainage  of  the  pleural  cavity.  The  best  method,  and  the  one  which 
is  almost  exclusively  practiced  in  the  surgical  wards  in  Erlangen,  is  b}^  incision 
of  the  pleural  cavity,  preceded  by  resection  of  a  portion  of  a  rib  for  the  pur- 
pose of  completely  emptying  out  the  pus,  and  obtaining  a  better  final  result. 
This  comparatively  simple  method  gives  results  so  good  and  so  entirely  satis- 
factory that  the  employment  of  other  methods  is  entirely  unnecessary.  We 
nevertheless  concede  that  the  so-called  Bulau's  siphon  drainage  gives  very 
good  results,  especially  in  early  and  benign  cases.  It  consists  in  the  intro- 
duction of  a  rubber  tube  into  the  pus  cavity  through  a  large  trocar  cannula, 
and  the  provision  then  for  continuous  drainage  through  the  establishment  of 
siphonage.  The  method  has  the  advantage  of  entirely  avoiding  a  pneumo- 
thorax and  of  not  requiring  narcosis.  In  many  cases,  however,  the  pro- 
cedure is  found  insufficient,  so  that  thoracotomy  must  be  performed  later. 
The  reader  is  referred  to  surgical  text-books  for  the  details  of  the  above- 
mentioned  methods,  and  of  some  others  of  a  like  nature,  as  well  as  their 
practical  application. 

In  treating  the  chronic,  contracted  pleurisies  with  thickening,  but  without 
fluid  effusion,  methodical  respiratory  efforts,  "  lung  gymnastics,"  are  of  use. 
Besides  these,  we  should  strengthen  the  general  conditions  as  much  as  possible. 
We  should  advise  the  patient  to  breathe  deeply,  and  prescribe  cold  sponging  of 
the  chest  daily.  Inspiration  of  compressed  air  by  means  of .  a  pneumatic 
apparatus  is  often  accompanied  by  good  results.  Well-to-do  patients,  who  have 
had  a  severe  pleurisy,  should  be  sent  to  a  suitable  climatic  health  resort. 


360  DISEASES   OF  THE  RESPIRATORY  ORGANS 

CHAPTEE    II 

PERIPLEURITIS 

Under  the  name  of  "  peripleuritis  "  Wunderlicli  was  the  first  to  describe  a 
rare  form  of  disease,  consisting  of  an  inflammation  of  the  connective  tissue 
between  the  costal  pleura  and  the  ribs,  and  terminating  in  the  formation  of 
an  abscess.  Such  cases  have  since  been  repeatedly  observed,  and  all  were  char- 
acterized by  the  absence  of  any  discoverable  serological  factors.  There  is  nei- 
ther a  previous  injury  nor  a  primary  disease  of  the  ribs  or  the  pleura.  Never- 
theless, the  cause  must  be  sought  in  an  invasion  of  micrococci,  which  excite 
the  suppuration.  A  knowledge  of  the  particulars,  however,  can  only  be  gained 
from  future  investigations.  It  is  as  yet  undetermined  whether  peripleuritis 
can  be  regarded  as  an  independent  disease  or  not. 

The  disease  occurs  chiefly  in  men.  It  usually  begins  suddenly  with  a  chill, 
and  runs  its  course  with  quite  a  high  fever.  In  pronounced  cases  the  local 
symptoms  have  the  greatest  similarity  to  those  of  an  empyema,  but  the  greater 
protrusion  of  the  chest  wall  is  striking.  The  ribs  are  crowded  apart  by  the 
abscess,  and  there  is  often  spontaneous  rupture  externally,  scarcely  ever  into 
the  pleura.  Percussion  gives  no  symptoms  of  displacement  of  the  neighboring 
organs,  a  distinguishing  point  from  empyema.  It  is  of  diagnostic  significance 
that  we  can  often  discover  normal  lung  tissue  containing  air  below  the  abscess. 
The  mobility  of  the  lower  border  of  the  lung  is  also  usually  retained,  contrary 
to  what  is  the  case  in  empyema.  Another  important  sign  was  first  brought 
to  notice  by  Bartels :  the  wall  of  the  abscess  relaxes  on  inspiration  and  becomes 
tense  on  expiration.  We  may  also  mention  that  acute  nephritis  has  often  been 
observed  among  the  complications. 

Prom  these  points  we  may  be  able  to  make  the  diagnosis  during  life,  at 
least  in  many  cases.  The  prognosis  is  quite  unfavorable,  but  recovery  does 
occur.    The  treatment *ean  be  only  operative. 


CHAPTEE    III 

PNEUMOTHORAX 

(Pyopneumothorax .  Hydropneumothorax.) 

iEtiology. — Pneumothorax — that  is,  a  collection  of  air  or  gas  in  the 
pleural  cavity — arises,  in  an  overwhelming  majority  of  cases,  from  the  penetra- 
tion of  air  into  the  pleural  cavity  through  an  opening  in  the  pleura.  The 
opening  may  be  in  the  external  chest  wall  from  a  penetrating  wound  of  the 
chest  or  an  empyema  operation,  or  it  may  be  in  the  pulmonary  pleura.  Pneu- 
mothorax is  by  far  most  frequently  associated  with  phthisis,  when  a  cavity 
lying  beneath  the  pulmonary  pleura  perforates  into  the  pleural  cavity.  This 
is  more  apt  to  happen  in  comparatively  acute  phthisis  than  in  very  chronic 
forms,  because  the  extensive  adhesions  and  contractions  in  the  latter  hinder 


PLATE    III 


Radiogram  of  a  Right-sided  Pneumothorax  without  Much  Pleuritic  Exudate. 
a,  pneumothorax;  b,  compressed  right  lung;  c,  left  lung  infiltrated  with  tuberculosis; 
d,  the  heart  crowded  over  to  the  left. 

Note  the  lighter  area  corresponding  to  the  large  air  space.  In  the  left  portion  of  this 
is  the  shadow  of  the  lung,  which  is  entirely  compressed  against  the  vertebral  column. 
The  heart  and  mediastinum  are  pushed  over  to  the  left  side  and  the  diaphragm  strongly 
crowded  downward.  The  left  lung,  particularly  in  its  upper  lobe,  is  studded  with  numer- 
ous tuberculous  infiltrations. 


PNEUMOTHORAX  361 

its  development.  It  usually  appears  in  quite  far-advanced  cases,  but  it  may 
sometimes  arise  with  but  slighl  changes  in  the  lung. 

Pulmonary  gangrene  or  abscess,  as  well  as  phthisis,  may  cause  pneumo- 
thorax by  perforation  into  tbe  pleural  cavity.  It  may  also  arise  from  the  rup- 
ture of  an  empyema  into  the  Lung.  In  some  cases  a  perforation  of  the  < >  -<»pL- 
agus  or  stomach  into  the  pleura,  as  in  gastric  ulcer,  has  been  observed,  with 
the  formation  of  pneumothorax. 

The  development  of  t bis  condition  from  severe  injuries,  as  from  laceration 
of  the  previously  healthy  lung,  without  injury  to  the  chest  wall,  is  rare.  Forced 
respiratory  movements,  associated  with  physical  exertion,  seem  especially 
capable  of  exciting  such  a  process.  We  have  ourselves  seen  pneumothorax 
develop  suddenly  in  a  previously  healthy  woman  while  hanging  out  her  wash- 
ing, and  another  time  in  a  young  man  during  very  labored  rowing.  Both  cases 
recovered  rapidly  and  completely. 

All  the  last-named  causes,  however,  are  far  less  important  than  pulmonary 
tuberculosis.  We  should  mention  that  in  phthisis,  too,  there  is  sometimes  a 
definite  exciting  cause — severe  coughing,  vomiting,  or  muscular  exertion — 
which  may  favor  the  development  of  the  pneumothorax. 

Many  authors  maintain  that,  by  decomposition  of  a  putrid  pleuritic  effu- 
sion, gas  may  be  produced,  and  thus  we  may  have  pneumothorax ;  but  such  an 
event  is  extremely  rare,  if  it  ever  happens. 

Pathological  Anatomy. — On  opening  the  pleural  cavity  a  part  of  the  air 
usually  rushes  out,  sometimes  with  an  audible  noise.  We  then  look  into  a 
large  cavity  filled  with  air,  and  find,  in  total  pneumothorax,  the  lung  com- 
pletely retracted  and  lying  compressed  against  the  vertebral  column.  If,  how- 
ever, the  air  fills  only  a  part  of  the  pleural  cavity,  as  a  result  of  extensive 
adhesions  of  the  pleura?,  we  speak  of  a  circumscribed  or  sacculated  pneumo- 
thorax. The  amount  of  air  contained  in  the  pleural  cavity  may  reach  2,000 
c.c.  The  pressure  which  it  is  under  is  almost  always  positive — on  an  average 
5  or  10  c.c.  of  water. 

In  the  cases  of  pneumothorax  arising  from  perforation  of  the  pulmonary 
pleura  we  can  usually  make  out  the  point  of  perforation  in  the  lungs.  This  is 
more  frequently  situated  in  the  upper  lobe  than  in  the  lower.  Sometimes  it  is 
already  grown  over  or  is  covered  by  a  layer  of  fibrin,  and  can  no  longer  be 
found.  The  opening  is  usually  quite  small,  but  it  may  reach  the  size  of  a 
ten-cent  piece.  Left-sided  pneumothorax  seems  to  be  somewhat  more  frequent 
than  right-sided. 

The  pleura  itself  is  only  rarely  normal.  Usually  agents  of  inflammation 
have  entered  it  with  the  air,  and  hence  it  is  found  in  a  state  of  inflammation. 
A  part  of  the  cavity  is  then  filled  with  effusion.  This  is  usually  wholly  puru- 
lent— pyopneumothorax— or  seropurulent,  but  it  may  even  be  serous  or  sero- 
fibrinous— seropneumothorax,  or  hydropneumothorax. 

The  neighboring  organs,  especially  the  heart  and  liver,  are  found  pushed 
out  of  their  normal  position,  as  in  large  pleuritic  effusions. 

Symptoms  and  Course. — The  onset  of  pneumothorax  (we  speak  in  what 
follows  especially  of  pneumothorax  in  connection  with  pulmonary  tuberculo- 
sis) is  quite  often  made  known  by  a  sudden  pain,  usually  associated  with  an 
increase  of  the  dyspnoea  and  of  the  general  symptoms.  There  is  sometimes 
collapse.     The  temperature  sinks  below  normal,  the  pulse  rises  to  140  and 


362  DISEASES   OF   THE   RESPIRATORY   ORGANS 

over.  The  patient  looks  pale  and  cyanotic.  He  usually  sits  upright  or  is  in 
a  half-sitting  position  in  bed,  either  more  on  the  affected  side,  in  order  to 
use  the  normal  lung  as  much  as  possible  for  breathing,  or  more  on  the  sound 
side  on  account  of  the  tenderness.  If  the  pneumothorax  has  come  on  as  a 
result  of  the  rupture  of  an  empyema  into  the  lungs,  there  is  at  the  same  time 
a  very  abundant  expectoration  of  pus. 

Although  in  many  cases  the  symptoms  mentioned  lead  to  a  suspicion  of 
pneumothorax,  yet  a  positive  diagnosis  can  be  made  only  after  a  physical  exam- 
ination. 

Inspection  gives  a  very  marked  distention  of  the  affected  side.  The  inter- 
costal spaces  are  flattened,  or  even  convex.  In  some  cases,  as  we  have  our- 
selves noticed,  there  is  a  marked  elastic  "  air-cushion  feeling "  on  palpating 
the  intercostal  spaces.  On  respiration,  the  affected  side  is  almost  entirely 
motionless,  while  the  excursions  of  the  other  side  are  the  more  marked.  The 
displacement  of  the  heart  is  often  evident  from  the  visible  displacement  of  the 
apex  beat. 

Percussion  gives  over  the  pneumothorax  a  remarkably  loud,  full  note, 
abnormally  deep,  but  usually  not  tympanitic,  on  account  of  the  tension  of  the 
walls.  It  is  especially  important  to  note  that  this  resonance  extends  beyond 
the  normal  limits  of  the  lung  on  the  right  down  to  the  seventh  or  eighth  rib, 
and  on  the  left  to  the  fifth  or  sixth  rib,  and  sometimes  even  to  the  edge  of 
the  thorax.  The  lower  limit  of  this  abnormally  loud  percussion  resonance 
shows  no  change  of  position  with  respiration. 

The  displacement  of  the  neighboring  organs  can  also  be  made  out  by  per- 
cussion. With  right-sided  pneumothorax  we  find  the  lower  border  of  the  liver 
dullness  abnormally  low,  and  the  left  border  of  the  cardiac  dullness  pushed 
over  to  the  anterior  axillary  line.  In  left-sided  pneumothorax  the  cardiac 
dullness  is  usually  entirely  absent  from  its  normal  place,  and  is  found  instead 
to  the  right  of  the  sternum.  The  left  lobe  of  the  liver  is  pressed  downward, 
and  in  the  "  semilunar  space  "  we  find,  instead  of  the  normal  tympanitic  reso- 
nance, the  same  deep,  loud,  and  usually  nontympanitic  note  as  in  the  upper 
parts  of  the  thorax. 

Upon  auscultation  we  are  struck  by  the  entire  absence  of  respiratory  mur- 
mur. This  is  in  special  contrast  to  the  clear  resonance  on  percussion.  In 
other  cases,  however,  we  hear  a  number  of  metallic  sounds,  at  least  in  many 
places  and  at  many  times,  which  are  very  characteristic  of  pneumothorax. 
First  among  these  is  amphoric,  metallic  respiration.  This  arises  in  open 
pneumothorax  (vide  infra)  from  the  direct  passage  of  the  air  in  and  out,  but 
in  all  other  cases  it  is  the  ordinary  respiratory  murmur,  which  has  acquired 
a  metallic  timbre  from  resonance  in  the  pneumothorax.  In  an  analogous 
way  arise  the  metallic-sounding  rales  ["metallic  tinkling"],  and  the  metallic 
resonance  of  the  cough  and  voice.  Heubner  has  devised  a  particularly  beauti- 
ful and  practically  important  method  for  demonstrating  the  metallic  sound  in 
pneumothorax.  If  we  strike  lightly  on  a  pleximeter  with  a  little  rod,  usually 
the  handle  of  a  percussion  hammer,  while  we  auscult  near  it — "  rod  percus- 
sion " — we  very  often  hear  quite  a  distinct  high  metallic  sound. 

The  vocal  fremitus  over  a  pneumothorax  is  usually  diminished,  but  it  may 
be  felt  in  spite  of  quite  a  large  collection  of  air. 

A  number  of  special  physical  signs  are  found  if  a  purulent  or  serous  effu- 


PNEUMOTHORAX  363 

sion  be  added  to  the  pneumothorax.  In  the  first  place,  the  resonance  Is  thereby 
rendered  dull,  to  a  greater  or  Less  extent,  id  the  lower  parts  of  the  chest, 
boundaries  of  the  fluid  by  percussion  show  a  very  evident  change  with  the 
patient's  change  of  position,  because  the  fluid  in  pneumothorax  can  n 
easily  in  all  directions.  Inasmuch  as  the  shape  of  the  remaining  air  space 
must  change  correspondingly,  there  is  nol  infrequently  a  change  in  the  pitch 
of  any  metallic  sounds  which  may  be  produced,  whether  by  percussion  or  res- 
piration, varying  with  the  posture  of  the  patient  (Biermer's  change  of  note). 
In  many  cases,  if  the  ear  is  applied  to  the  chest  wall  there  is  beard,  on  every 
motion  of  the  fluid,  produced,  e.g.,  by  gently  shaking  the  patient,  a  metallic 
gurgling  sound,  so-called  Hippocratic  succussion. 

Forms  of  Pneumothorax. — According  to  the  condition  of  the  perforation 
during  life,  we  distinguish  three  kinds  of  pneumothorax  (  Weil ).  We  speal 
an  "open  pneumothorax,"  if  the  point  of  perforation  remain.-  open,  so  that 
the  air  on  respiration  constantly  passes  in  and  out  of  the  pleural  cavity.  If  the 
perforation  is  completely  closed,  we  have  a  "closed  pneumothorax." 
third  and  most  frequent  form  is  the  "  valvular  pneumothorax,"  in  which  air 
enters  the  pleural  cavity  at  each  inspiration,  but  on  expiration  there  is  a 
valvelike  closure  of  the  perforation,  and  thus  the  air  cannot  escape  again;  but 
as  soon  as  the  pressure  in  the  pleural  cavity  increases  so  that  no  more  air  can 
enter  it  on  inspiration,  the  valvular  pneumothorax  becomes  closed.  In  open 
pneumothorax  the  pressure  in  the  pleural  cavity  must  he  the  same  as  the 
atmospheric  pressure.  A  positive  pressure  in  the  pleural  cavity  can  exist  only 
in  a  closed  or  a  valvular  pneumothorax. 

A  clinical  diagnosis  of  the  form  of  pneumothorax  is  not  always  possible, 
and  has  usually  no  great  practical  importance.  The  very  loud,  metallic, 
amphoric  respiratory  murmur,  which  may  he  heard  in  open  pneumothorax, 
must  be  mentioned,  and  Wintrich's  change  of  pitch  (see  page  295)  can  some- 
times be  heard  in  this  form.  It  is  worthy  of  mention  that  symptoms  of  dis- 
placement of  the  neighboring  organs  must  also  arise  in  open  pneumothorax. 
The  predominant  atmospheric  pressure  here  is  positive  in  contrast  to  the  nega- 
tive pressure  in  the  other  pleural  cavit}^,  and  to  the  normal  negative  pressure 
which  previously  acted  on  the  upper  surface  of  the  diaphragm.  The  compres- 
sion of  neighboring  organs  is,  however,  never  as  marked  in  open  pneumothorax 
as  in  the  closed  variety.  In  the  latter,  the  internal  pressure  becomes  decidedly 
higher  with  the  addition  of  a  pleuritic  effusion.  For  this  reason,  a  marked 
protrusion  of  the  affected  side,  and  great  displacement  of  the  heart  and  liver, 
speak  most  strongly  against  an  open  pneumothorax.  The  percussion  note  is 
not  rarely  tympanitic  in  open  pneumothorax  because  of  the  slighter  tension 
of  the  chest  wall;  in  closed  pneumothorax,  on  the  other  hand,  the  percussion 
note  is  almost  invariably  nontympanitic.  Some  authors  have  tried  to  find  a 
point  of  distinction  for  the  different  forms  of  pneumothorax  in  the  composi- 
tion of  the  gas  in  the  pleural  cavity,  but  the  results  of  chemical  analysis  are 
still  contradictory.  According  to  Ewald,  we  find  in  open  pneumothorax  not 
over  five  per  cent  of  carbonic  acid  and  about  twelve  to  eighteen  per  cent  of 
oxygen;  in  closed  pneumothorax,  however,  fifteen  to  twenty  per  cent  of  car- 
bonic acid  and  ten  per  cent  at  most  of  oxygen.  If  in  an  open  pyopneumo- 
thorax or  hydropneumothorax  the  point  of  perforation  lies  below  the  level 
of  the  fluid,  there  sometimes  arise  on  every  inspiration  metallic  sounds,  since 


364  DISEASES   OF  THE   RESPIRATORY   ORGANS 

the  bubbles  of  air  drawn  in  rise  and  come  up  through  the  fluid — "  the  water- 
pipe  sound,"  "  metallic  tinkling."  A  peculiar  sipping  and  short  snapping 
sound  on  inspiration,  heard  by  us  in  a  few  instances,  seemed  to  point  directly 
to  the  existence  of  a  valvular  pneumothorax.  In  valvular  pneumothorax,  the 
intrathoracic  pressure  often  attains  the  highest  degree,  and  therefore  results 
in  very  marked  manifestations  of  displacement. 

Course  of  the  Disease. — In  many  cases  the  occurrence  of  pneumothorax 
causes  such  a  high  degree  of  respiratory  disturbance  that  death  ensues  in  a 
few  hours  or  days.  In  other  cases  the  patient  improves,  and  may  feel  quite 
well  for  a  long  time  in  spite  of  the  condition.  We  have  ourselves  frequently 
observed  patients  who  passed  the  entire  day  out  of  bed  with  scarcely  any 
inconvenience.  I  know  of  several  cases  in  which  the  condition  finally  became 
completely  stationary,  and  in  which  the  patients  went  about  with  their  pneu- 
mothorax for  months  or  even  years  ( !  )  without  any  symptoms.  Usually, 
however,  the  disease  which  gives  rise  to  the  pneumothorax,  most  often  pulmo- 
nary tuberculosis,  leads  in  a  shorter  or  longer  time  to  death.  Sometimes, 
again,  the  patient  recovers.  This  almost  always  occurs  in  those  rare  cases 
above  mentioned,  when  a  healthy  lung  has  been  torn,  but  sometimes,  also,  in 
cases  of  pulmonary  tuberculosis.  The  healing  usually  takes  place  in  this  way, 
that  the  air  is  first  replaced  by  a  fluid  effusion,  and  then  the  latter  is  gradually 
.absorbed,  but  the  air  may  also  be  directly  absorbed  in  whole  or  in  part.  It 
depends  upon  the  origin  of  the  lesion,  then,  and  upon  the  intensity  of  the 
underlying  disease,  whether  the  recovery  is  permanent  or  not. 

Diagnosis. — The  diagnosis  of  pneumothorax  is  usually  easy  with  careful 
■examination.  The  most  striking  feature  is  usually  the  absence  of  the  respira- 
tory murmur,  despite  the  tympanitic  percussion  note.  When  the  attention  is 
attracted  by  this  sign,  search  is  then  to  be  made  for  the  other  sign.  An  X-ray 
examination  may  prove  of  great  value  in  doubtful  cases.  It  is  sometimes 
very  difficult  to  make  a  differential  diagnosis  between  very  large  cavities  and 
a  saccular  pneumothorax.  We  may  mention  as  the  chief  points  in  distinction : 
a  cavity  is  apt  to  be  situated  in  the  apex,  pneumothorax  in  the  lower  part  of 
the  thorax ;  over  a  cavity  the  chest  wall  is  often  sunken  in,  over  pneumothorax 
it  is  prominent ;  the  vocal  fremitus  is  usually  marked  over  a  cavity,  weak  over 
pneumothorax.  Signs  of  the  displacement  of  organs  point  to  pneumothorax, 
as  does  distinct  succussion,  while  a  metallic  respiratory  sound  and  metallic 
resonance  on  rod  percussion  may  also  be  heard  over  large  cavities  with  smooth 
walls.  Besides  the  above  signs,  we  should  also  carefully  regard  the  general 
course  of  the  disease.  On  careful  questioning  we  shall  almost  always  find  that 
the  severe  symptoms  depending  upon  the  development  of  a  pneumothorax  set 
in  with  more  or  less  suddenness. 

Treatment. — Whenever  pneumothorax  has  developed  we  must  seek  to  ob- 
tain perfect  quiet  for  the  patient  as  well  as  diminution  of  his  sufferings,  by 
means  of  morphin  given  subcutaneously  or  internally.  The  result  of  the 
administration  of  this  drug,  in  a  sufficient  though  careful  dosage,  is  often  very 
satisfactory.  We  must  also  stimulate  cardiac  activity,  if  it  is  impaired,  by 
means  of  strophanthus,  camphor,  and  the  like.  In  cases  presenting  marked 
pressure  symptoms  and  severe  dyspnoea,  we  may  attempt  to  remove  some  of  the 
air  in  the  pleural  cavity  by  aspiration  with  a  hollow  needle,  and,  by  this  means, 
to  relieve  the  dyspnoea.     As  a  rule,  however,  we  wait  to  see  to  what  extent 


HYDROTHORAX.     HEMATOTIIORAX  365 

the  condition  will  improve  spontaneously.  If  there  is  an  abundanl  exudation 
it  is  always  useful  to  puncture  and  remove  the  fluid,  repeating  the  operation 
if  necessary.  If  the  exudation  is  purulent,  the  treatment  is  precisely  the  same 
as  for  empyema.  In  hopeless  cases  of  Ear-advanced  tuberculosis,  we  should 
limit  our  efforts  to  purely  symptomatic  treatment,  or  to  the  simple  evacuation 
of  the  pus  by  puncture. 


CHAPTER    IV 

HYDROTHORAX.  HEMATOTHORAX 

1.  Hydrothorax. — We  term  the  occurrence  of  a  serous  transudation  into  the 
pleural  cavity,  independent  of  an  inflammation  of  the  pleura,  hydrothorax,  or 
thoracic  dropsy.  The  cause  of  hydrothorax  is  in  rare  cases  a  local  hindrance  to 
the  outflow  of  venous  blood  or  lymph  from  the  thorax,  as  in  compression  of  the 
veins  or  of  the  thoracic  duct  by  tumors ;  but  in  the  great  majority  of  cases  the 
hydrothorax  is  part  of  a  general  dropsy,  occurring  especially  in  cardiac  or  renal 
disease.  Hydrothorax  is  often  first  developed  after  marked  oedema  of  the  sub- 
cutaneous cellular  tissue  and  ascites,  but  it  may  sometimes  be  one  of  the  first 
symptoms  of  dropsy,  particularly  in  renal  cases.  It  is  usually  bilateral,  but  it 
is  often  unilateral,  or  at  least  much  greater  on  one  side  than  on  the  other. 
The  pleura  itself  is  normal  or  else  cedematous.  We  often  find  it  traversed 
with  a  network  of  dilated  lymphatics.  The  serous  fluid  in  hydrothorax  is  dis- 
tinguished from  an  inflammatory  serous  effusion  (compare  above  with  page 
355)  by  the  smaller  amount  of  albumen  in  it,  and  a  correspondingly  low 
specific  gravity  (usually  below  1.018),  by  the  scanty  number  of  cell  elements 
(aside  from  the  frequent  admixture  of  exfoliated  endothelial  cells),  and  by 
the  absence  of  or  the  slight  tendency  to  spontaneous  coagulation. 

The  clinical  importance  of  hydrothorax  lies  in  the  hindrance  to  respiration 
which  it  causes.  As  a  result  of  this  the  hydrothorax  may  be  regarded  in  many 
cases,  especially  in  renal  disease,  as  the  chief  cause  of  death.  Its  demonstra- 
tion comes  from  the  physical  examination,  which,  in  general,  gives  dullness, 
diminished  vocal  resonance,  and  dislocation  of  neighboring  organs,  the  same 
as  in  pleuritic  effusion.  We  desire  to  emphasize  also  the  bronchial  respiration 
from  compression  in  hydrothorax,  which  is  often  very  loud,  although  at  the 
same  time  usually  high  and  sharp,  and  which  may  even  give  rise  to  a  confu- 
sion with  pneumonic  infiltration  in  the  lungs.  This  very  loud  respiratory 
murmur,  contrasting  with  that  of  pleuritic  effusion,  is  explained  by  the  nor- 
mal condition  of  the  lungs  and  the  absence  of  all  adhesions.  For  the  same 
reason,  too,  the  change  in  the  boimdary  of  the  dullness,  as  a  result  of  the 
patient's  change  of  position,  is  usually  more  marked  in  hydrothorax  than  in 
pleuritic  effusion.  In  the  case  of  a  right-sided  hydrothorax,  the  shifting  of  the 
fluid  is  generally  most  readily  determined  in  front.  In  the  sitting  posture, 
there  is,  anteriorly,  an  area  of  dullness  above  the  upper  border  of  liver  dull- 
ness, which  disappears  in  the  recumbent  posture ;  but  the  change  in  the  extent 
of  percussion  dullness,  with  change  of  position,  can  often  be  made  out  plainly 
enough  in  the  back.    We  often  hear  a  few  fine  crepitant  rales  over  the  hydro- 


366  DISEASES   OF  THE   RESPIRATORY  ORGANS 

thorax,  which  arise  in  the  retracted  and  partly  atelectatic  lung.  The  main 
factor,  however,  in  distinguishing  hydrothorax  from  a  pleuritic  exudation  is, 
in  every  case,  the  consideration  of  the  primary  disease.  It  should  also  be 
noticed  that  hydrothorax  is  usually  bilateral,  while  pleuritic  exudation  is 
usually  unilateral.  Yet,  on  the  other  hand,  we  occasionally  find  a  much 
larger  collection  of  fluid  in  one  pleural  cavity  than  in  the  other  in  hydro- 
thorax. 

Treatment  is  directed,  first  of  all,  to  the  primary  disease.  If  we  succeed  in 
strengthening  and  regulating  the  action  of  the  heart,  or  in  restoring  the  secre- 
tion of  urine,  the  hydrothorax  often  disappears  with  the  other  dropsical  symp- 
toms. If  the  dyspnoea  caused  by  it  reaches  a  dangerous  degree,  we  often  see 
great  relief  from  aspirating  the  fluid.  The  nature  of  the  underlying  condi- 
tion, of  course,  renders  the  benefit  in  many  cases  only  transitory. 

2.  Hematothorax. — Effusions  of  blood  into  the  pleural  cavity  (hemato- 
thorax)  arise  most  frequently  from  traumatic  lacerations  of  blood  vessels, 
rarely  from  the  bursting  of  an  aneurism  of  the  aorta  into  the  pleural  cavity, 
from  erosion  of  an  intercostal  artery  in  caries  of  the  ribs,  from  the  rupture  of 
a  cavity  into  the  pleura  in  phthisis,  if  it  simultaneously  opens  a  blood  vessel, 
etc.  In  many  such  cases  a  typical  exudative  pleurisy  follows  the  effusion  of 
blood.  The  physical  signs  are  the  same  as  in  other  pleural  effusions.  Severe 
dyspnoea  may  demand  the  removal  of  the  blood  by  puncture,  or  even  by  an 
incision. 


CHAPTEK    V 
NEW    GROWTHS    OF    THE    PLEURA 

The  majority  of  new  growths  occurring  in  the  pleura  are  of  a  secondary 
nature.  We  sometimes  find  single  metastatic  nodules  of  cancer  in  the  pleura 
after  primary  carcinoma  of  other  organs,  especially  of  the  mammary  gland 
and  the  lungs,  but  most  carcinomata  of  the  pleura  arise  from  primary  car- 
cinomata  of  the  lungs  and  are  due  to  a  direct  invasion  of  the  pleura  by  the 
new  growth. 

Of  the  primary  new  growths  of  the  pleura,  the  rare  round-celled  sarcoma 
must  be  mentioned,  and  in  addition,  above  all,  there  is  the  endothelial  car- 
cinoma, first  described  by  E.  Wagner.  This  develops,  de  novo,  in  a  diffuse 
manner,  from  a  proliferation  of  the  endothelial  cells  of  the  lymphatics  and 
the  connective  tissue.  Metastases  occur  in  the  lungs,  in  the  lymph-glands,  in 
the  liver,  in  the  muscles,  etc. 

Single  secondary  nodules  of  cancer  in  the  pleura  cause  no  special  clinical 
symptoms,  but  the  cases  of  diffuse  cancer  of  the  pleura  as  a  result  of  primary 
cancer  of  the  lungs  are  important,  inasmuch  as  the  symptoms  of  disease  of  the 
pleura  often  quite  predominate  over  the  pulmonary  disease.  The  dullness  is 
intense,  the  respiratory  murmur  and  the  vocal  fremitus  diminished.  In  one 
such  case  we  saw  a  proliferation  of  the  cancer  upon  the  ribs  in  front  so  that 
there  was  externally  a  very  marked  circumscribed  swelling.  The  character 
of  the  sputum  is  the  only  thing  that  can  give  us  definite  information  as  to 


MEDIASTINAL  TUMORS  367 

the  origin  of  the  new  growth  in  the  Lungs  (see  the  chapter  on  cancer  of  the 

lungs ) . 

Primary  endothelial  carcinoma  of  the  pleura  runs  a  course  similar  to 
chronic  pleurisy.  As  we  sometimes  find  a  coexisting  fluid  effusion  in  the 
pleural  cavity,  displacement  of  the  neighboring  organs  may  occur.  The  affec- 
tion goes  on  for  a  long  time  without  fever,  or  with  slight  and  irregular  eleva- 
tions of  temperature.  There  are  some  forms  of  malignant,  rapidly  growing 
tumors  that  lead  to  death  in  a  few  months.  Most  cancels  of  the  pleura  are 
associated  with  severe  pain. 

The  diagnosis  of  new  growths  in  the  pleura  can  usually  he  made,  if  at  all, 
only  in  the  more  advanced  stages  of  the  disease.  At  first  almost  all  the  cases 
are  regarded  as  simple  or  tuberculous  chronic  pleurisy.  There  are,  however, 
certain  striking  features  of  pleural  new  growths,  viz.,  the  unusual  extent  of 
the  percussion  dullness  (much  more  marked  anteriorly  than  posteriorly,  for 
example),  the  absence  of  the  general  earmarks  of  tuberculosis,  the  appear- 
ance of  slight  oedema  of  the  chest  wall,  of  one  arm,  and  the  like.  The 
examination  of  the  fluid  obtained  by  an  exploratory  puncture  furnishes  impor- 
tant evidence.  It  is  usually  hemorrhagic.  The  red  blood  cells  occasionally 
show  degenerative  changes,  giving  the  effusion  a  brown  color.  The  micro- 
scopical examination  reveals  a  striking  number  of  endothelial  cells  that  show 
variations  in  size  and  shape.  They  have  often  undergone  fatty  degeneration, 
so  that  the  occurrence  of  numerous  cells  containing  fat  granules  or  even  of 
free  fat  globules,  should  always  lead  one  to  think  of  a  new  growth.  In  rare 
cases  more  coherent  fragments  of  tumor  tissue  may  be  microscopically  demon- 
strated in  the  aspirated  fluid. 

The  prognosis  is  absolutely  unfavorable,  and  the  treatment  purely  sympto- 
matic. At  most,  we  may  try  X-ray  treatment,  or  the  subcutaneous  injection 
of  atoxyl  or  cacodyl. 


CHAPTER    VI 
MEDIASTINAL   TUMORS 

In  the  anterior  mediastinum,  in  quite  rare  cases,  extensive  new  growths 
•occur,  which  are  of  importance  on  account  of  their  severe  clinical  symptoms. 
The  point  of  origin  for  the  tumor  is  either  the  mediastinal  lymph-glands,  or 
the  connective  tissue,  or  sometimes  the  remains  of  the  thymus  gland.  In  their 
anatomical  character  the  tumors  are  almost  always  sarcomata,  usually  lympho- 
sarcoma, rarely  alveolar  sarcoma.  They  usually  occur  in  youth  or  middle  age, 
and  are  somewhat  more  frequent  in  men  than  in  women.  The  special  serolog- 
ical factors  are  unknown.  In  some  cases  an  injury  is  stated  to  be  the  cause 
of  their  development.  Sometimes  the  mediastinal  tumors  are  only  a  part  of  a 
general  pseuclo-leukaemia  or  a  lymphatic  leuksemia. 

The  first  clinical  symptoms  are  usually  of  a  very  indefinite  nature.  The 
patient  complains  of  general  languor,  headache,  pain  in  the  chest,  and  slight 
difficulty  in  breathing,  and  only  gradually  do  severe  subjective  and  objective 
symptoms  develop  in  the  chest. 


368  DISEASES   OF  THE   RESPIRATORY   ORGANS 

The  symptoms  are  in  part  due  directly  to  the  tumor,  but  in  larger  part 
they  are  symptoms  of  compression  from  the  gradually  increasing  pressure  of 
the  tumor  on  a  number  of  neighboring  organs. 

The  pain  in  the  chest,  which  is  located  chiefly  in  the  sternal  region,  and  is 
associated  with  a  marked  feeling  of  oppression,  may  be  very  severe.  It  some- 
times shoots  into  the  lateral  portions  of  the  chest  and  into  the  arms,  showing 
pressure  on  the  brachial  plexus. 

The  dyspnoea  may  finally  increase  to  an  extreme  degree.  A  patient  with 
lympho-sarcoma  under  our  observation  could,  in  the  last  days  of  her  life, 
breathe  only  while  standing.  The  dyspnoea  is  clue  to  a  compression  of  the 
heart  and  lungs,  and  sometimes  to  actual  stenosis  of  the  trachea  or  a  primary 
bronchus.  Paralysis  of  the  dilators  of  the  glottis  may  also  occur  from  a  pres- 
sure paralysis  of  the  recurrent  nerves.  Paralysis  of  one  vocal  cord  has  been 
repeatedly  observed.  In  the  case  mentioned  above  a  marked  goiter  developed, 
as  a  result  of  vascular  stasis,  which  further  increased  the  dyspnoea  by  pressure 
on  the  trachea.  A  hydrothorax  from  local  venous  stasis  may  also  aid  in 
increasing  the  dyspnoea. 

Pressure  on  the  oesophagus,  and  disturbances  of  deglutition  due  to  it,  are 
rare.  Pressure  on  the  vagus  nerve  and  the  sympathetic  sometimes  causes 
anomalies  in  the  rate  of  the  pulse — either  marked  acceleration  or  slowing  of 
the  pulse.  If  the  sympathetic  is  involved  there  is  inequality  of  the  pupils. 
In  some  cases,  by  pressing  on  the  tumor,  an  artificial  dilatation  of  the  pupil 
can  be  excited  at  will.  By  pressure  on  the  vessels,  especially  on  the  superior 
vena  cava,  the  subclavian  vein,  etc.,  oedema  and  cyanosis  may  arise  in  the  cor- 
responding parts  of  the  body. 

Objective  examination  of  the  chest  gives  a  marked  diffuse  prominence  of 
the  sternal  region  in  a  part  of  the  advanced  cases;  in  other  cases  this  swelling 
is  absent.  The  discovery  of  an  abnormal  dullness  in  the  anterior  part  of  the 
chest  is  of  diagnostic  importance;  this  usually  joins  the  cardiac  dullness  on 
the  left,  and  on  the  right  it  extends  a  varying  distance  beyond  the  right  border 
of  the  sternum.  The  heart  is  often  pushed  somewhat  to  the  left.  We  heard 
over  the  pulmonary  artery  in  our  case  a  marked  systolic  murmur,  caused  by 
compression  of  the  vessel.  A  dissimilarity  of  the  pulse  on  the  two  sides  is  not 
infrequent. 

The  diagnosis  of  a  mediastinal  tumor  is  usually  possible  in  cases  with 
well-marked  symptoms,  but  in  other  cases  it  is  difficult  and  uncertain.  In 
many  cases  X-ray  examination  gives  decisive  results.  The  differentiation  be- 
tween mediastinal  tumors  and  aneurisms  of  the  aorta  (q.  v.)  sometimes  pre- 
sents great  difficulty.  Tumors  may  also  be  confounded  with  abscesses  in  the 
anterior  mediastinum. 

The  prognosis  is  in  all  cases  absolutely  unfavorable.  The  disease  termi- 
nates fatally,  sometimes  after  a  duration  of  six  months  or  a  year. 

The  treatment  can  be  merely  symptomatic.  Internally  we  may  try  iodid 
of  potassium  or  arsenic.  In  addition  to  these,  X-ray  treatment  is  to  be  prin- 
cipally considered  (compare  with  the  chapter  on  Leukaemia  and  Pseudo-leu- 
kaemia) .  In  the  last  stages  of  the  disease  we  must  try  to  alleviate  the  patient's, 
great  distress  by  narcotics. 


ACTINOMYCOSIS  OF  THE  THORACIC  CAVITY 


369 


CHAPTER    VII 


ACTINOMYCOSIS   OF    THE    THORACIC   CAVITY 

Bollinger  and  others  have  described  a  peculiar  tumor  affecting  the  jaw- 
bones of  cattle,  and  occasioned  by  the  presence  of  a  special  form  of  fui,. 
known  as  the  actinomyces  or  ray  fungus.  More  recently  a  class  of  diseases 
has  been  studied  in  human  beings,  occasioned  by  the  same  fungus  (Ponfick, 
Israel,  and  others).  These  diseases  may,  as  in  cattle,  affect  the  jaws,  the  floor 
of  the  mouth,  and  the  neck;  hut  in  these  cases  they  are  mainly  of  surgical 
interest.  The  actinomycotic  diseases  of 
the  internal  organs,  however,  possess  a 
great  clinical  importance;  and,  inas- 
much as  the  kings  and  pleura  are  the 
most  frequently  affected  organs,  it  will 
be  well  to  present  briefly  here  the  most 
important  facts  which  have  as  yet  been 
learned  with  regard  to  actinomycosis. 

The  botanical  position  of  the  ac- 
tinomyces  is  not  yet  definitely  settled. 
According  to  recent  investigations, 
there  is  quite  a  close  relationship  be- 
tween actinomyces  and  the  tubercle  ba- 
cillus. In  its  growth  the  fungus  forms 
small  or  moderate-sized  gray  or  sul- 
phur-yellow nodules  which  may  be  dis- 
tinguished with  the  naked  eye  in  the 
pus  of  the  diseased  tissue  (see  below), 
and  which  upon  microscopic  examina- 
tion resolve  themselves  into  a  tangle  of 
mycelium.  It  is  an  especial  character- 
istic that  many  of  these  mycelia  bear 

on  their  ends  a  club-shaped  swelling.  These  are  placed  for  the  most  part  like 
radii  on  the  periphery  of  a  nodule,  and  so  surround  the  entire  mass  like  a 
circlet  of  rays  (see  Fig.  59). 

In  nature  actinomyces  seems  to  appear  especially  upon  plants,  for  example 
upon  the  beard  of  spikes  of  wheat.  Thus  is  explained  the  frequency  of  infec- 
tion in  the  plant-eating  cattle,  and  a  similar  direct  infection  seems  occasionally 
to  be  possible  in  man.  It  is  worthy  of  note  that  the  fungus  seems  to  locate 
itself  often  in  carious  teeth.  Thus  apparently  arises  the  above-mentioned  dis- 
ease in  the  buccal  cavity ;  while,  on  the  other  hand,  the  fungus  may  be  carried 
from  its  nidus  in  the  mouth  by  inspiration  into  the  respiratory  tract,  or  by 
swallowing  into  the  primce  vice.  Of  course  it  may  also  be  directly  swallowed 
or  inhaled.  Primary  intestinal  actinomycosis  generally  begins  in  the  caecum 
or  in  the  appendix. 

Wherever  the  fungus  fastens  itself  in  the  body  it  occasions  first  a  new 
growth  of  granulation  tissue,  which  has  a  tendency  to  break  down  into  a 
whitish  or  brownish  pasty  mass.    The  brown  color  is  occasioned  by  the  hemor- 


Fig.  59. — Masses  of  actinomyces. 
(From  Johne.) 


370  DISEASES   OF  THE   RESPIRATORY  ORGANS 

rhage  which  frequently  occurs.  Very  often  actinomycosis  goes  on  to  suppura- 
tiorj ;  in  this,  of  course,  secondary  infection  by  pus  germs  (pus  cocci)  may  also 
play  a  role.  Of  special  importance  is  the  tendency  of  the  disease  to  extend 
from  the  lungs  to  the  pleura  and  from  the  pleura  to  the  peripleuritic  con- 
nective tissue,  and  still  further  to  the  wall  of  the  thorax.  Thus  arise  not  only 
extensive  abscesses  and  wide-branching  fistulous  tracts,  but  also  a  very  charac- 
teristic, extremely  tough  cicatricial  infiltration  of  the  affected  part.  Not 
infrequently  there  is  at  last  a  perforation  reaching  the  outer  surface  of  the 
body. 

The  entire  process,  as  a  rule,  is  slow  and  insidious,  but  constantly  pro- 
gressive. The  symptoms  consist  at  first  in  slight  thoracic  discomfort,  pain, 
cough,  and  expectoration.  Physical  examination  will  often  detect  changes  in 
the  lungs,  but  the  correct  interpretation  of  the  signs  found  is,  of  course,  at  first 
difficult,  if  not  impossible.  Some  cases  are  at  first  regarded  as  pulmonary 
tuberculosis  or  tuberculous  pleurisy,  until  the  appearance  of  the  peculiar 
infiltration  of  the  skin  over  the  area  of  dullness  awakens  a  suspicion  of 
actinonrvcosis.  The  diagnosis  may  be  made  certain  by  exploratory  puncture. 
Actinomycosis  granules  have  also  been  frequently  demonstrated  in  the  spu- 
tum. The  more  the  disease  spreads  the  greater  is  the  distress.  Usually 
there  is  hectic  fever,  which  may  assume  a  pysemic  character  if  there  is  exten- 
sive suppuration.  The  patient  gradually  loses  flesh,  and  in  repeated  instances 
amyloid  degeneration  of  the  liver,  spleen,  and  kidneys  has  been  observed.  If 
a  focus  breaks  into  a  pulmonary  vein,  the  disease  may  be  developed  by  metas- 
tasis in  other  internal  viscera.  Moreover,  there  may  be  a  direct  extension  of 
the  disease  to  the  pericardium,  or  through  the  diaphragm  into  the  peritoneal 
cavity. 

The  treatment  can  be  only  symptomatic,  unless  the  diseased  spot  can  be 
reached  by  operation,  and  then  the  treatment  becomes  surgical.  Permanent 
cure  has  so  far  been  attained  in  but  rare  instances.  The  continued  use  of 
iodid  of  potassium  or  of  sodium  has  occasionallv  been  of  decided  benefit. 


III.    DISEASES   OF  THE   CIRCULATORY  ORGANS 


SECTION  I 
Diseases  of  the  Heart 

CHAPTER    I 

ACUTE    ENDOCARDITIS 

(Endocarditis  verrucosa.     Endocarditis  ulcerosa) 

^Etiology. — Organized  excitants  of  inflammation  of  different  sorts,  which 
circulate  in  the  blood,  may  settle  on  the  endocardium,  especially  on  the  valves 
of  the  heart,  and  there  give  rise  to  an  acute  endocarditis.  Endocarditis,  there- 
fore, in  its  serological  relations,  is  not  to  be  regarded  as  a  single  disease. 
Pathogenic  microorganisms  have  been  injected  into  the  blood  (the  Strepto- 
coccus pyogenes,  Staphylococcus  aureus,  and  others),  and  in  this  way  an  arti- 
ficial endocarditis  has  been  set  up  in  animals.  The  experiments  are  more  apt 
to  succeed  if  the  valves  or  the  inner  coat  of  the  vessels  have  been  subjected  to 
some  slight  injury  before  the  injection,  thus  promoting  the  settling  of  the 
germs  upon  them  (Orth  and  Wyssokowitsch,  Ribbert).  Most  cases  of  endo- 
carditis in  man,  both  the  vegetative  and  ulcerative  forms,  appear  to  be  caused 
by  the  Staphylococcus  pyogenes  aureus.  Streptococci  are  much  less  frequent 
than  staphylococci,  and  it  is  only  in  rare  cases  that  endocarditis  is  occasioned 
by  the  pneumococcus,  gonococcus,  and  perhaps  the  diphtheria  bacillus. 

In  accord  with  these  statements  is  the  fact  that  in  human  beings  acute 
articular  rheumatism,  which  is  probably  to  be  regarded  as  a  staphylococcus 
infection,  is  that  one  of  the  infectious  diseases  which  is  especially  apt  to  have 
acute  endocarditis  as  a  frequent  and  important  complication.  The  staphylo- 
coccus infection  need  not  appear,  however,  in  the  first  place,  as  a  typical  acute 
polyarthritis.  An  acute  endocarditis  may  appear  as  a  sequel  of  many  cases  of 
apparently  primary  pleurisy,  tonsillitis,  or  other  disease.  Indeed,  it  is  some- 
times impossible  to  determine  the  gate  of  entry  of  the  infection,  and  the  whole 
disease  takes  the  shape  of  an  apparently  primary  endocarditis.  In  such  cases 
the  nature  of  the  disease  is  made  evident  by  the  later  appearance  of  multiple 
articular  swellings.  We  also  regard  as  allied  to  polyarthritis  certain  forms  of 
infection  called  the  "  acute  hemorrhagic  diseases  "  (e.  g.,  purpura  rheumatica), 
and  also  chorea  (which  see).  It  is  therefore  not  surprising  that  acute  endo- 
carditis is  not  infrequently  observed  in  association  with  these  affections. 

There  are  other  acute  infectious  diseases  with  which  acute  endocarditis  may 
be  associated.  Probably  in  these  it  is  usually  the  result  of  a  secondary  mixed 
24  371 


372  DISEASES   OF   THE   CIRCULATORY   ORGANS 

infection,  generally  with  the  staphylococcus.  This  explains  the  appearance  of 
acute  endocarditis  in  scarlet  fever,  smallpox,  diphtheria,  measles,  and  typhoid. 
Not  infrequently  mild  cases  of  acute  endocarditis,  without  clinical  significance, 
are  found  in  association  with  primary  tuberculosis  and  ulcerating  carcinoma. 
Again,  acute  and  chronic  nephritis  may  sometimes  occasion  a  development  of 
endocarditis.  An  especially  important  role  in  producing  endocarditis  is  dis- 
played by  grave  septic  and  pysemic  conditions  (vide  supra) .  In  these  cases  the 
acute  endocarditis  appears  as  one  symptom,  but  it  is  often  so  prominent  that 
the  whole  attack  is  called  endocarditis  (vide  infra).  In  such  severe  diseases 
we  have  often  to  do  with  a  streptococcus  disease,  although  it  may  be  a  staphy- 
lococcus infection  of  especial  virulence.  Finally,  gonorrheal  endocarditis  must 
be  mentioned.  Endocarditis  as  a  sequel  of  gonorrhea  is  fortunately  very  rare. 
It  is  often  an  actual  gonococcus  infection,  but  in  other  instances  due  to  a 
mixed  infection. 

Finally,  we  have  still  to  mention  the  important  fact  that  acute  endocarditis 
quite  frequently  develops  on  the  soil  of  an  already  existing  chronic  endocarditis 
- — the  so-called  acute  recurrent  endocarditis.  In  women,  pregnancy  and  the 
puerperal  state  sometimes  seem  to  give  the  occasion  for  a  recrudescence  of  the 
endocarditis. 

Pathological  Anatomy. — We  usually  distinguish  an  endocarditis  verrucosa? 
with  the  formation  of  large  or  small  papillary  nodules  on  the  endocardium, 
and  an  endocarditis  ulcerosa  (endocarditis  diphtheritica),  with  ulcerations  as 
a  result  of  the  destruction  and  wasting  away  of  the  superficially  necrosed  tis- 
sue. The  malignant,  invariably  fatal  form  of  severe  septic  endocarditis  is 
chiefly  ulcerative  endocarditis.  Endocarditis  verrucosa  is  the  milder  form,, 
which  is  seen  especially  in  acute  polyarthritis  and  allied  diseases,  but  we  cannot 
draw  either  a  sharp  anatomical  or  a  sharp  clinical  distinction  between  the  two, 
since  malignant  cases  of  endocarditis  verrucosa  are  also  observed. 

The  endocardial  growths  are  usually  situated  on  the  valves,  especially  on 
their  edges  of  closure.  More  rarely  we  find  them  on  the  chorda?  tendinse  and 
on  the  endocardium  of  the  ventricle  and  auricle.  In  the  mildest  cases  they 
are  scarcely  as  large  as  the  head  of  a  pin,  but  in  severe  cases  they  may  increase 
to  quite  large  warty  and  glandular  masses.  Microscopically,  the  base  of  the 
nodule  consists  of  a  newly  formed  vascular  tissue,  infiltrated  with  small  cells, 
which  on  its  surface  changes  to  a  granular,  coagulated  mass.  This  last  is 
formed  partly  of  coagulated  albumen,  dead  cells,  and  fibrin  deposited  from 
the  blood,  and  partly  of  micrococci  (vide  supra).  The  micrococci  are  found 
without  exception  in  all  cases  of  ulcerative  endocarditis — having  been  first 
discovered  by  Eberth.  The  endocardial  ulcers  arise  from  the  destruction  of 
the  superficially  necrosed  nodules.  If  the  thin  valve  in  any  place  yields  to  the 
blood  pressure,  we  have  the  so-called  acute  valvular  aneurism.  Complete  per- 
foration of  a  valve,  and  tearing  off  of  fragments  of  a  valve  and  of  the  chorda? 
tendinse,  are  also  seen. 

The  great  majority  of  cases  of  acute  endocarditis  are  confined  to  the  valves 
of  the  left  side  of  the  heart — the  mitral  and  aortic  valves.  Endocarditis  on 
the  tricuspid  valve  is  seldom  seen  except  as  a  secondary  affection  in  old  cases 
of  heart  disease.  In  a  case  of  acute  ulcerative  endocarditis  in  a  grown  man 
seen  by  us,  the  process  was  confined  exclusively  to  the  tricuspid  valve,  and 
there  were  very  many  embolic  abscesses  in  the  lungs.    This  may  be  considered 


ACUTE   ENDOCARDITIS  373 

a  great  rarity.  In  contrast  to  the  ordinary  localization  of  endocarditis  we  find 
fetal  endocarditie  most  frequently  in  the  right  side  of  the  heart. 

Many  other  organs  may  I"'  affected  by  the  endocarditis,  through  embolism. 
In  the  henign  endocarditis  verrucosa,  the  masses  of  fibrin  deposited  on  the 
irregularities  of  the  valve  furnish  the  embolic  material.  They  cause  large  or 
small  infarctions  in  the  kidneys  and  spleen,  embolic  softening  of  the  brain, 
etc.  In  the  malignant,  ulcerative  forms,  however,  large  aumbers  of  bacteria 
get  into  the  circulation  at  the  same  time  with  the  necrotic  masses  of  tissue 
which  have  been  torn  off.  Here,  then,  we  have  to  do  not  merely  with  simple 
mechanical  obstruction  but  with  infectious  emboli.  The  emboli  in  ulcerative 
endocarditis,  therefore,  either  give  rise  to  embolic  abscesses  in  the  cardiac 
muscles,  the  kidneys,  the  spleen,  the  lungs,  the  retina,  etc.,  or  they  result  in 
hemorrhages,  especially  into  the  skin,  but  also  into  the  kidneys,  the  brain,  the 
retina,  and  the  serous  membranes.  It  is  not  yet  known  why  in  some  cases 
abscesses  are  more  frequent  and  in  others  hemorrhages.  The  two,  however, 
may  be  combined.  In  general,  we  may  suppose  that  the  development  of  ab- 
scesses is  everywhere  connected  with  the  presence  of  bacteria,  mostly  staphylo- 
cocci, while  hemorrhages  may  also  arise  from  toxic  influences;  but  again 
changes  in  the  vascular  walls  caused  by  bacteria  might  give  rise  to  hemor- 
rhages. Embolic  abscesses  belong  almost  exclusively  to  the  severe  form  of 
septic  endocarditis.  Hemorrhages  are  seen  in  this  form,  and  also — without 
coexisting  abscesses — in  certain  severe  forms  of  endocarditis  occurring  in  the 
course  of  acute  rheumatism  and  allied  diseases. 

Clinical  History. — Since  acute  endocarditis  is  not  aetiologically  a  distinct 
disease,  and  since  its  clinical  course  is  very  different  in  different  cases,  it  seems 
advisable  to  us  to  describe,  in  what  follows,  the  most  important  varieties  sepa- 
rately; but  it  must  be  expressly  noted  that  the  separate  classes  can  by  no 
means  be  sharply  defined,  and.  that  there  are  many  intermediate  forms. 

1.  Slight  endocarditis  verrucosa  is  quite  frequently  found  in  the  cadaver, 
without  the  slightest  signs  of  any  affection  of  the  heart  during  life.  The  little 
papillary  excrescences  on  the  valves  of  the  heart  in  phthisis,  and  carcinoma, 
whose  aetiology  lias  been  explained  above,  are  to  be  classed  under  this  head. 

2.  The  typical  form  of  henign  acute  endocarditis  is  most  frequent,  clinic- 
ally, in  the  course  of  acute  articular  rheumatism.  It  is  much  rarer  in  other 
infectious  diseases  (vide  supra).  In  a  few  cases  it  is  also  seen  as  an  appar- 
ently primary  disease.  Here  there  is  a  constitutional  rheumatic  infection 
which  has  taken  place  in  some  way,  and  which  settles  directly  on  the  valves  of 
the  heart  instead  of  in  the  joints  (so-called  primary  rheumatic  endocarditis). 
Careful  questioning  will  sometimes  reveal,  or  at  least  render  probable,  the 
place  of  infection  (a  mild  case  of  tonsillitis  or  some  slight  external  injury). 
Very  often  there  will  be  later  the  symptoms  of  articular  rheumatism.  It  is 
seldom  that  endocarditis  as  such  is  associated  with  special  local  disturbances, 
such  as  pain  in  the  region  of  the  heart,  palpitation,  and  dyspnoea.  Ordinarily 
the  heart  disease  is  discovered  only  by  physical  examination.  The  impulse  of 
the  heart  in  many  cases  is  abnormally  strong  and  diffuse ;  the  pulse  is  acceler- 
ated, but  strong,  often  somewhat  jerky  (pulsus  celer),  and  usually  regular,  but 
sometimes  a  little  irregular.  Percussion  at  first  shows  no  deviation  from  the 
limits  of  normal  dullness.  On  auscultation,  we  hear  at  the  apex,  more  rarely 
at  the  base,  a  loud  blowing,  systolic  souffle.     Diastolic  murmurs  are  rare  in 


374  DISEASES   OF  THE   CIRCULATORY   ORGANS 

acute  endocarditis.  The  pulmonic  second  sound  is  often  accentuated.  The 
physical  signs  referable  to  the  heart  are  only  slightly  marked  in  many  cases 
of  acute  endocarditis.  This  is  understood  if  we  remember  that  the  occurrence 
of  a  heart  murmur  depends  wholly  on  the  localization  of  the  endocarditis,  on 
the  development  of  some  valvular  insufficiency,  etc. 

Besides  the  direct  symptoms  pointing  to  the  cardiac  affection,  the  onset  of 
an  acute  endocarditis  is  often,  but  not  always,  associated  with  fever,  or,  if  fever 
be  already  present,  with  an  increase  of  it,  and  with  a  slight  aggravation  of  the 
general  disturbance.  Embolic  processes  may  occur  in  the  brain,  the  spleen, 
the  kidneys,  and  the  extremities,  but  they  are  comparatively  rare.  Sometimes 
a  pericarditis  develops  as  a  result  of  the  endocarditis  (vide  infra). 

It  is  hard  to  make  any  accurate  statements  as  to  the  duration  of  this  form 
of  endocarditis.  The  physical  signs  may  last  for  days,  or  for  several  weeks. 
Complete  recovery  is  possible,  but  in  the  majority  of  cases  this  variety  passes 
into  chronic  valvular  disease  of  the  heart. 

3.  Malignant  Form  of  Acute  Endocarditis — Septic  Endocarditis. — In  these 
cases  the  endocarditis  is  only  one  aspect  of  a  general  septic  infection  (vide 
preceding  chapter  on  septic  affections).  The  severe  general  infection  is  there- 
fore usually  quite  prominent.  The  objective  signs  in  the  heart  are  the  same 
as  in  the  preceding  form,  but  more  intense  and  extensive.  The  subjective 
cardiac  symptoms,  such  as  palpitation  and  distress,  may  be  quite  pronounced, 
but  they  may  also  be  almost  wholly  absent  in  this  form.  The  general  condi- 
tion, however,  is  usually  bad.  There  is  sometimes  high  fever  with  an  irregular 
or  intermitting  course,  but  in  many  cases  the  fever  is  remarkably  low  in  spite 
of  quite  severe  constitutional  symptoms. 

The  constitutional  infection  is  very  often  manifested  by  the  appearance  of 
septic  exanthemata  or  hemorrhages  in  the  skin,  sometimes  in  the  mucous 
membranes  (the  conjunctiva  and  the  soft  palate)  and  in  the  retina.  Second- 
ary articular  swellings  often  develop;  they  are  of  a  serious  character  in  the 
milder  cases  and  purulent  in  the  graver  forms.  Eenal  hemorrhages  and  acute 
hemorrhagic  nephritis  are  quite  frequent.  Large  emboli  may  also  occur  in 
the  different  organs  in  this  as  in  every  other  form  of  endocarditis.  Whether 
simple  infarctions  or  metastatic  abscesses  form,  depends  on  the  kind  of  emboli. 

The  course  and  termination  of  the  disease  depend,  above  all,  upon  the 
virulence  of  the  bacteria.  There  are  comparatively  mild  cases  of  septic  endo- 
carditis which  end  after  several  weeks  in  a  complete,  or  more  often  a  relative, 
cure  (with  subsequent  cardiac  lesion),  as  well  as  malignant  forms  (so-called 
malignant  ulcerative  endocarditis),  with  a  rapidly  fatal  course,  or  with  a  more 
protracted  one  that  finally  also  ends  unfavorably. 

4.  The  recurrent  form  of  acute  endocarditis  consists  of  an  acute  increase  of 
the  endocardial  process,  brought  on  by  some  exciting  cause,  in  a  patient  already 
suffering  from  chronic  endocarditis.  The  acute  disease  may  show  all  the  gra- 
dations from  the  mildest  to  the  severest.  The  mild  cases  often  run  their  course 
without  any  special  symptoms.  To  tins  form  we  may  frequently  refer  the  more 
or  less  temporary  elevations  of  temperature  which  we  often  see  in  patients 
with  chronic  valvular  disease  of  the  heart.  In  rarer  cases  the  recurrent  endo- 
carditis comes  on  quite  suddenly  in  the  form  of  a  severe  acute  attack.  This 
sometimes  seems  to  be  clinically  a  primary,  independent  disease,  especially  if 
the  previous  chronic  heart  disease  has  up  to  that  time  caused  no  special  symp- 


ACUTE    ENDOCARDITIS  375 

toms.  The  patient  has  general  malaise,  headache,  chills,  and  fever.  The  last 
may  be  quite  high — 104°  F.  (40°  C.)  and  over — or  moderate,  varying  between 
100°  and  102°  F.  (38°  to  39°  C),  or  it  may  be  entirely  absent.  In  many  ca 
it  is  intermittent,  when  the  return  of  fever  is  often  associated  with  a  chill. 
The  cardiac  symptoms  may  be  quite  pronounced,  Imi  in  this  form,  too,  I 
may  he  obscure  and  indefinite.  Jn  the  further  course  of  the  disease  we  meet 
with  cutaneous  hemorrhages,  retinal  hemorrhages,  articular  swellings,  large 
renal  hemorrhages,  or  typical  hemorrhagic  nephritis — in  short,  just  the  Bame 
general  type  of  disease  as  in  the  other  malignanl  forms  of  acute  endocarditis. 
The  course  is  rarely  rapid,  and  often  lasts  for  weeks.  Severe  cases  almost 
always  end  fatally. 

Diagnosis. — The  diagnosis  of  an  endocarditis,  coming  on  secondarily  in 
the  course  of  articular  rheumatism  and  other  diseases,  can  be  made  only  by  a 
physical  examination  of  the  heart.  We  must  therefore  give  constant  attention 
to  the  condition  of  the  heart  in  diseases  which  we  know  may  give  rise  to 
endocarditis. 

The  diagnosis  of  the  malignant  form  of  endocarditis  often  causes  great  dif- 
ficulty, especially  if  the  patient  is  not  seen  until  the  later  stages.  It  is  confused 
with  typhoid,  meningitis,  or  acute  miliary  tuberculosis.  Examination  of  the 
heart  may  furnish  positive  evidence,  but  sometimes,  as  we  have  said,  there  are' 
no  physical  signs  of  cardiac  disturbance,  or  the  signs  present  are  indefinite. 
Many  a  case  of  long-continued  intermittent  fever  without  demonstrable  ana- 
tomical cause  is  finally  discovered  to  be  an  acute  endocarditis.  A  special 
diagnostic  importance  attaches  to  the  secondary  swelling  of  the  joints,  and  also 
to  the  hemorrhages  into  the  skin  and  retina,  for  these  are  much  more  infre- 
quent in  the  diseases  with  which  this  form  of  endocarditis  may  he  confounded. 
The  acute  hemorrhagic  nephritis,  too,  in  connection  with  the  other  symptoms, 
is,  at  least  to  a  certain  degree,  characteristic  of  malignant  endocarditis.  A 
careful  search  for  some  setiological  factor  is  very  important  for  diagnosis  in 
all  cases.  For  other  points  the  reader  is  referred  to  the  consideration  of  septic 
diseases  (see  page  133),  where  the  importance  of  a  bacteriological  blood  exami- 
nation is  also  emphasized. 

Prognosis. — In  the  description  of  the  course  of  the  disease  we  have  already 
mentioned  the  prognosis  of  the  different  forms.  The  severe  cases  of  acute 
endocarditis  usually,  and  the  cases  of  severe  septic  endocarditis  always,  end 
fatally.  Here,  however,  the  cause  of  death  is  to  be  sought  rather  in  the  accom- 
panying systemic  infection  than  in  the  endocarditis  itself.  In  mild  cases 
recovery  is  possible/  but  the  process  of  repair  is  often  so  incomplete  that 
chronic  valvular  disease  of  the  heart  develops  from  the  acute  endocarditis. 

Treatment. — The  chief  requisite  in  the  treatment  of  every  endocarditis  is  as 
complete  rest  as  possible  for  the  patient.  'If  ice  is  well  borne,  the  continuous 
application  of  an  ice  bag  to  the  cardiac  region  is  of  service.  If  there  are  signs 
of  cardiac  weakness,  such  as  a  small,  rapid,  and  irregular  pulse,  we  must  em- 
ploy cardiac  stimulants,  strophanthus,  camphor,  and,  above  all,  digitalis.  It 
must  be  confessed  that  the  effect  of  these  is  not  very  great.  If  there  are  marked 
subjective  symptoms  (such  as  dyspnoea),  narcotics,  particularly  morphin,  are 
indispensable.  Effort  is  made  to  combat  the  systemic  infection  by  salicylate  of 
sodium  and  similar  remedies,  including  aspirin,  phenacetin,  and  salipyrin. 
Quinin  is  usually  entirely  without  effect,  even  when  the  fever  is  of  an  inter- 


376  DISEASES   OF   THE  CIRCULATORY   ORGANS 

mittent  character.  Arsenic,  however  (by  mouth  or  subcutaneously  in  the  form 
of  atoxyl  or  the  cacodylate),  seems  to  be  useful,  particularly  in  the  more  pro- 
tracted cases. 

[For  remarks  upon  the  alkaline  treatment  of  rheumatism,  see  Vol.  II. 
Attempts  to  cure  septic  endocarditis  by  specific  sera  or  by  injecting  sterilized 
bacteria  (preferably  autogenous)  have  met  with  but  limited  success.] 


CHAPTEE    II 

VALVULAR    DISEASE    OF    THE    HEART 

{Chronic  Endocarditis) 

AETIOLOGY 

A  large  number  of  cases  of  chronic  valvular  disease  of  the  heart  proceed 
from  acute  endocarditis.  Hence  the  frequent  statement  in  the  history  of 
chronic  valvular  disease  that  the  patient  has  had  articular  rheumatism,  once  or 
many  times.  In  a  collection  of  163  cases  of  undoubted  valvular  heart  disease, 
we  were  able  to  ascribe  86  to  a  previous  attack  of  acute  articular  rheumatism. 
Following  the  acute  valvular  endocarditis,  which  is  often  associated  with  this 
disease,  marked  thickening  of  the  valves  occurs,  clue  to  the  growth  of  connect- 
ive tissue.  There  are  also  changes  in  the  way  of  contraction,  adhesion,  and 
finally  often  of  considerable  calcification.  The  unavoidable  result  of  all  these 
processes  is  that  the  altered  valves  are  rendered  incapable  of  fulfilling  their 
physiological  function  of  regulating  the  circulation.  Inasmuch  as  the  mitral 
valve  is  most  often  attacked  by  endocarditis  when  associated  with  acute  articu- 
lar rheumatism,  we  find  mitral  disease  predominating  among  rheumatic  valv- 
ular troubles;  but  lesions  of  the  aortic  valves,  rheumatic  in  their  origin,  are 
by  no  means  rare. 

If  we  find  a  valvular  lesion  in  a  patient  who  has  never  suffered  from  articu- 
lar rheumatism  or  chorea,  we  may,  in  some  cases,  be  able  to  refer  the  origin 
of  the  valvular  trouble  to  a  previous  attack  of  acute  endocarditis,  excited  by 
one  of  the  other  causes  above  mentioned.  Thus  it  is  well  known  that  acute 
endocarditis  may  occur  in  the  course  of  scarlet  fever,  diphtheria,  and  typhoid 
fever,  and  eventuate  in  chronic  disease,  but  this  is,  according  to  our  experience, 
very  rare. 

In  quite  a  large  number  of  cases  of  heart  disease,  however,  we  cannot  ob- 
tain a  history  of  acute  endocarditis.  We  have  to  do  here  with  an  endocarditis 
which  is  chronic  from  the  start,  which  also  leads  gradually  to  thickening,  con- 
traction, adhesion,  and  calcification  of  the  valves. 

The  causes  of  this  chronic  fibrous  endocarditis  are  probably  the  same  as  of 
acute  articular  rheumatism,  but  in  such  cases  they  act  from  the  start  in  a 
chronic  manner.  Perhaps  often  there  may  have  been  an  incipient  acute  endo- 
carditis, whose  course  was  unperceived.  We  not  infrequently  learn  from  pa- 
tients with  chronic  heart  disease,  who  have  never  had  an  attack  of  acute 
articular  rheumatism,  that  in  former  years  they  did  suffer  repeatedly  from 
mild  rheumatic  pains,  to  which  they  paid  little  attention.    Furthermore,  it  is 


VALVULAR  DISEASE  OF  'JUL   HEART  377 

by  no  means  exceptional  to  observe  thai  such  patients  with  a  well-developed 
cardiac  valvular  lesion  later  od  undergo  one  or  more  attacks  of  acute  poly- 
arthritis. Heart  disease.'  is  also  rarely  associated  with  genuine  chronic  ar- 
thritis deformans.  In  other  cases  of  valvular  disease  we  must  consider  the  pos- 
sibility of  other  lesions,  some  infectious,  some  perhaps  of  a  chemical  and 
mechanical  nature.  Here  belong,  in  the  first  place,  those  cases  of  cardiac 
disease  which  are  associated  with  general  arteriosclerosis  (atheroma  of  the 
blood  vessels).  Indeed,  atheromatous  degeneration  of  the  aorta  seems  some- 
times to  extend  directly  to  the  aortic  valves,  and  thus  cause  a  valvular  lesion. 
Every  ^etiological  factor  favorable  to  general  arteriosclerosis  is,  therefore,  im- 
portant in  the  aetiology  of  valvular  disease.  This  includes  advanced  life,  excess- 
ive physical  labor,  alcoholism,  and  genuine  gout.  Another  important  cause 
is  syphilis.  Of  late  years,  since  we  have  paid  more  attention  to  this  last  factor 
than  formerly,  we  have  observed  many  cases  of  valvular  disease  which  were 
almost  certainly  of  syphilitic  origin.  In  particular,  lesions  of  the  aortic  valves, 
when  there  is  no  evidence  of  other  causation,  must  awaken  our  suspicion  of 
syphilis.  There  remains  to  be  mentioned  the  influence  of  chronic  nephritis 
upon  the  development  of  cardiac  valvular  disease,  although  in  the  not  infre- 
quent cases  in  which  chronic  nephritis,  particularly  of  the  interstitial  variety, 
is  associated  with  chronic  endocarditis,  it  is  not  always  eas}^  to  determine 
whether  both  conditions  are  related  in  the  way  of  cause  and  effect,  or  whether 
they  are  both  secondary,  and  both  alike  the  result  of  some  third  unfavorable 
influence.  A  hereditary  predisposition  to  heart  disease  is  not  very  frequent, 
but  }^et  it  can  be  made  out  with  certainty  in  many  cases.  We  have  ourselves 
seen  five  members  of  the  same  family  who  have  suffered  from  chronic  heart 
disease,  some  from  pure  valvular  disease  and  some  from  severe  so-called  idio- 
pathic hypertrophy.  Perhaps  the  very  frequent  occurrence  of  heart  disease  in 
many  families  is  also  connected  with  a  special  family  predisposition  to  rheu- 
matic affections,  the  occurrence  of  which  predisposition  cannot,  in  our  opinion, 
be  denied.  Finally,  a  small  number  of  cases  of  heart  disease,  especially  in  the 
right  side  of  the  heart,  depend  upon  anomalies  of  development  of  the  heart — 
congenital  heart  disease. 

Valvular  disease  of  the  heart  occurs  at  every  age  of  life.  The  time  of  origin 
of  most  cases,  corresponding  in  part  to  the  occurrence  of  acute  articular  rheu- 
matism, falls  in  youth  and  middle  age,  somewhere  between  eighteen  and  forty ; 
but  severe  valvular  disease  is  not  infrequent  even  in  children ;  while  late  in  life 
the  clinical  picture  of  valvular  disease  is  often  confused  by  the  simultaneous 
presence  of  general  arteriosclerosis,  pulmonary  emphysema,  or  kidney  trouble. 
Heart  disease  is  said  to  be  rather  mere  frequent  in  the  female  sex  than  in  the 
male.  Women  with  heart  disease  not  infrequently  date  their  symptoms  from 
pregnancy  and  the  puerperium. 

GENERAL  PATHOLOGY  OF  VALVULAR  DISEASE   OF  THE 

HEART 

Every  valve  of  the  heart,  in  order  to  fulfill  its  physiological  task,  must, 
on  the  one  hand,  open  perfectly  at  the  right  time  in  order  to  furnish  a  free 
passage  to  the  blood  current  through  the  appropriate  orifice,  and  must,  on  the 
other  hand,  close  firmly  and  perfectly  at  the  right  time  in  order  to  make  any 


378  DISEASES   OF  THE   CIRCULATORY   ORGANS 

abnormal  backward  flow  of  blood  impossible.  In  both  relations  the  function 
of  the  valves  may  be  disturbed  by  chronic  endocarditis,  the  disturbance  being 
the  result  of  their  anatomical  changes.  If  the  tips  of  the  valves  are  shortened 
on  their  free  edges  by  contraction,  or  if  the  complete  unfolding  of  the  auriculo- 
ventricular  valves  is  hindered  by  a  shortening  of  their  chordae  tendinae,  the 
closure  of  the  valve  cannot  be  complete.  At  the  moment  when  the  closure 
of  the  valve  is  necessary  a  fissure  remains  open  between  its  apices.  We  call 
this  condition  an  insufficiency  of  the  valve.  On  the  other  hand,  the  valves 
may  lose  their  capability  of  free  and  sufficient  separation  from  one  another,, 
as  a  result  of  thickening  and  calcification  of  the  connective  tissue,  and  also 
as  a  result  of  adhesions  of  the  points  of  the  valves  with  one  another.  At  the 
moment  when  the  blood  current  should  pass  freely  through  the  open  orifice, 
the  valve  remains  a  stiff,  narrow  ring,  through  which  the  blood  must  force  its; 
way — stenosis  of  the  orifice.  The  changes  in  the  valves  are  often  of  such  a 
sort  that  they  cause  at  the  same  time  both  an  insufficiency  of  the  valve  and  a 
stenosis  of  the  orifice.  The  thickening  and  calcification  of  the  valves  in  steno- 
sis cause,  as  a  rule,  a  valvular  insufficiency  at  the  same  time;  but  an  insuffi- 
ciency, set  up  by  a  contraction  of  the  edges  of  the  valves,  may  occur  without  a 
coincident  stenosis  of  the  orifice. 

The  abnormal  and  injurious  effect  of  a  valvular  lesion  upon  the  circulation 
in  the  heart  is  felt  in  two  directions.  Either  the  obstacles  to  the  circulation  are 
increased  in  certain  places,  or  there  is  a  greater  diastolic  distention  of  certain 
portions  of  the  heart.  Both  circumstances  of  course  demand  greater  cardiac 
effort.  If  the  heart  were  to  labor  with  only  the  same  degree  of  energy  as  under 
normal  conditions,  in  spite  of  the  increased  resistance,  or  in  spite  of  the  greater 
distention,  there  would  speedily  be  an  imjmirment  of  circulation,  incompatible 
with  the  continuance  of  life ;  for,  if  the  increased  resistance  were  not  overcome, 
or  if  the  abnormally  distended  cavity  were  not  properly  emptied,  there  would  at 
once  be  a  rapidly  increasing  congestion  behind  the  diseased  valve,  and  beyond 
it  a  constantly  diminishing  pressure.  We  can  speak  of  a  circulation  of  the 
blood  only  when,  in  a  given  interval  of  time,  exactly  as  much  blood  is  driven 
out  of  the  heart  as  flows  into  it.  The  slightest  difference  in  this  regard  would, 
in  a  very  brief  period,  produce  such  a  congestion  of  blood  in  the  veins  and  such 
a  diminution  of  blood  in  the  arteries  that  the  demand  of  the  tissues  for  oxygen 
could  no  longer  be  satisfied,  and  death  would  be  the  necessary  result.  A  nor- 
mal circulation  is  maintained  so  long  as  the  rapidity  (the  momentum)  of  the 
blood  stream,  as  well  as  the  amount  of  arterial  blood,  which  flows  into  the 
organs  in  a  given  interval  of  time,  is  sufficiently  great.  Withal,  the  circulation 
must  at  any  time  be  capable  of  immediate  adaptation  to  any  temporary  in- 
crease in  the  demands  of  the  organs,  as,  for  example,  when  there  is  bodily 
exertion.  The  amount  of  blood  flowing  through  the  organs  in  a  given  time 
depends  upon  the  degree  of  distention,  the  frequency  of  contraction,  and  the 
complete  emptying  of  the  left  side  of  the  heart.  This  amount  ("the  size  of 
the  circulation  ")  may  be  diminished,  and  yet  the  circulation  continue  as  such; 
but  that  the  circulation  can,  in  spite  of  the  disturbance  occasioned  by  a  valv- 
ular lesion,  still  be  maintained  in  a  satisfactory  manner  is  due  to  the  capa- 
bility of  the  heart  of  overcoming  the  obstacles  to  the  circulation  by  means  of 
increased  work.  It  is  one  of  the  wisest  contrivances  in  our  organism,  that  the 
heart  has  control  of  a  reserve  fund  of  strength,  which  comes  into  action,  if. 


VALVULAR   DISEASE  OF  THE   HEART  379 

need  be,  in  a  way  to  compensate  as  far  as  possible  for  any  disturbance  of  the 

circulation.  This  explains  why  a  man  with  valvular  disease  of  the  hear!  may 
be  almost  perfectly  well  for  a  Long  time,  while  tin-  increased  work  of  certain 
portions  of  his  heart  suffices  Id  keep  up  an  approximately  normal  circulation 
in  spite  of  the  existing  valvular  disease.  We  call  a  heart  disease,  in  which 
there  is  at  least  no  marked  disturbance  of  circulation,  a  compensated  hear! 
disease. 

The  abnormal  increase  in  functional  activity  of  certain  portions  of  the 
heart,  associated  with  every  cardiac  lesion,  and  referable  in  every  case,  as  we 
have  said,  either  to  increased  resistance  or  to  increased  distention,  results  in 
a  hypertrophy  of  those  particular  portions  of  the  heart,  just  as  in  the  case  of 
any  other  muscle.  The  development  of  this  hypertrophy  may  he  explained 
by  the  fact  that  the  increased  labor  involves  a  greater  catabolism  in  the  cardiac 
muscle,  and  this  in  turn  is  followed  by  an  increased  tendency  to  assimilation 
and  growth  of  the  muscle.  The  hypertrophy  does  not  consist  of  an  increase  in 
thickness  of  the  individual  muscular  fibers,  but  chiefly  of  an  increase  in  num- 
ber. The  total  bulk  of  the  cardiac  muscle  increases,  and  thus  its  capacity  for 
work  naturally  becomes  greater.  It  goes  without  saying  that  increased  nutri- 
tive processes  and  a  large  supply  of  nourishment  for  the  heart  are  necessary 
to  bring  about  such  a  hypertrophy,  by  which  alone  a  compensation  of  the  heart 
disease  is  possible  for  any  length  of  time.  Hence  we  find  the  secondary  hyper- 
trophy of  the  heart  absent,  or  at  least  only  imperfectly  developed,  in  feeble 
individuals,  especially  in  those  who  have  suffered  from  some  other  chronic 
wasting  disease  besides  the  heart  disease,  such  as  phthisis  or  carcinoma.  With 
this  hypertrophy  of  the  cardiac  muscle,  however,  there  is  also  associated  a  per- 
manent dilatation  of  those  heart  cavities  which  have  to  take  up  increased 
amounts  of  blood  during  their  diastole.  To  the  extent  to  which  this  dilatation 
aids  the  circulation,  it  may  be  termed  compensatory  dilatation. 

Although  the  compensatory  processes  in  the  heart  may  prevent  for  a  long 
time  any  marked  disturbance  of  the  circulation,  the  already  overburdened 
heart  can  no  longer  completely  satisfy  any  excessive  demands  upon  it,  even  in 
a  compensated  heart  disease.  Hence  patients  with  a  compensated  heart  disease 
are  free  from  subjective  disturbance  only  when  they  remain  at  rest,  while  the 
signs  of  a  disturbed  circulation  usually  become  quite  apparent  on  slight  physi- 
cal exertion. 

The  hypertrophied  cardiac  muscle  can  seldom  supply  permanently  the  ab- 
normally great  drafts  made  upon  it.  There  finally  comes  a  condition  of  "  fa- 
tigue," of  "  cardiac  insufficiency/'  The  cause  lies  either  in  the  increase  of 
the  valvular  disease,  so  that  the  hindrance  to  the  blood  current  caused  by  it  can 
no  longer  be  completely  overcome,  or  in  the  fact  that  the  nervous  and  muscular 
elements  in  the  heart  have  their  powers  gradually  impaired  by  a  disturbance  of 
circulation  in  the  heart  itself. 

Very  often  a  chronic  myocarditis  becomes  associated  with  the  valvular 
lesion  (chronic  endocarditis),  and,  naturally,  further  diminishes  the  working 
capacity  of  the  heart.  In  consequence,  the  cardiac  muscle  loses  its  tone,  the 
heart  chambers  can  no  longer  completely  empty  themselves,  and  as  a  result 
of  the  stasis  there  is  a  gradually  increasing  filling  up,  until  a  condition  of 
overdistention  or  of  so-called  congestive  dilatation  supervenes.  In  short,  in 
every  heart  disease  the  moment  may  finally  come  when  the  capacity  of  the  heart 


380  DISEASES   OF  THE   CIRCULATORY  ORGANS 

has  reached  its  limit,  and  hence  the  compensation  of  the  heart  disease  ceases. 
The  results  of  stasis  now  appear  with  increasing  severity  in  the  different 
organs,  as  we  shall  learn  to  recognize  later  on,  and  the  patient  finally  succumbs 
to  them,  unless  some  intercurrent  event  puts  an  end  to  life. 

After  these  general  remarks,  which  will  be  understood  better  on  reading 
what  follows,  we  will  pass  on  to  the  special  description  of  the  different  forms 
of  heart  disease  and  their  physical  signs. 

VARIOUS  FORMS   OF   HEART   DISEASE   AND   THEIR 
PHYSICAL   SIGNS 

1.  Insufficiency  of  the  Mitral  Valve. — Mitral  insufficiency  is  one  of  the  most 
frequent  forms  of  heart  disease.  It  develops  in  acute  or  chronic  endocarditis 
•of  the  mitral  valve,  from  contraction  of  the  free  edges  of  the  valve  or  from 
shortening  of  the  chordae  tendinne.  In  rare  cases  it  comes  on  from  partial 
adhesion  of  the  valves  to  the  walls  of  the  ventricle. 

The  closure  of  the  mitral  valve  occurs  normally  at  each  systole  of  the  left 
ventricle.  It  prevents  the  return  of  blood  from  the  left  ventricle  to  the  left 
auricle.  If  the  mitral  valve  is  insufficient  and  its  closure  is  incomplete,  at 
every  systole  of  the  left  ventricle  a  part  of  the  blood  is  thrown  back  from  it 
into  the  left  auricle  through  the  open  space  of  the  ostium  venosum.  This 
abnormal  backward  wave  encounters  the  blood  current  coming  in  an  opposite 
direction  into  the  left  auricle  from  the  pulmonary  veins.  The  meeting  of  these 
two  opposing  currents,  as  well  as  the  stream  of  regurgitant  blood  pressing 
through  the  open  chink  in  the  mitral  valves,  sets  the  blood  in  a  whirl,  and 
this  impinging  upon  the  tense  edges  of  the  valves  produces  a  loud,  blowing, 
systolic  murmur.  We  hear  this  murmur  loudest  at  the  apex  of  the  heart, 
corresponding  to  the  laws  of  conduction  in  the  thorax ;  yet  it  usually  is  propa- 
gated so  far  that  it  may  often  be  heard  at  the  other  cardiac  orifices,  although 
not  so  distinctly.  A  loud  systolic  mitral  murmur  can  also  be  heard  sometimes 
in  the  back,  on  the  left,  and  occasionally  on  the  right.  In  some  few  cases 
the  systolic  murmur  of  mitral  insufficiency  is  heard  best  in  the  second  left 
intercostal  space.  This  is  said  to  be  due  to  the  fact  that  the  murmur  occa- 
sioned by  the  commotion  in  the  left  ventricle  is  especially  well  conducted  by 
the  left  auricular  appendix  which  is  near  to  the  anterior  chest  wall  (Kaunyn). 
Curschmann  has  pointed  out  that  this  is  particularly  apt  to  happen  in  cases 
of  incipient  mitral  insufficiency ;  but,  as  a  rule,  even  in  these  cases,  the  mur- 
mur is  found  at  the  apex  of  the  heart.  In  most  instances  the  systolic  muscle 
sound  of  the  left  ventricle,  the  so-called  first  sound  of  the  heart,  can  also 
be  heard  besides  the  systolic  murmur.  It  can  be  heard  rather  better  if  the 
ear  is  slightly  removed  from  the  ear  piece  of  the  stethoscope  [meaning  the 
monaural  instrument].  Exceptionally  the  sound  may  be  completely  obscured 
by  the  murmur.  The  second  sound  is  often  not  to  be  heard  at  the  apex,  prob- 
ably because  it  is  obscured  by  the  relatively  protracted  murmur. 

Since  the  left  auricle,  at  each  systole  of  the  ventricle,  receives  blood  from 
two  sides — its  normal  quantity  from  the  pulmonary  veins,  and,  besides  that, 
the  abnormal  blood  wave  from  the  left  ventricle — it  becomes  much  dilated. 
At  the  next  diastole  of  the  left  ventricle  the  whole  amount  of  blood  collected 
in  the  auricle  under  increased  pressure  pours  into  the  left  ventricle  through 


VALVULAR    DISEASE   OF   THE    HEART  I^Sl 

the  mitral  valve,  which  is  now  wide  open  (supposing  a  pure  insufficiency  of  the 
valve  without  any  stenosis).  We  sec,  then,  that  in  pure  mitral  insufficiency 
the  left  ventricle  must  be  filled  beyond  the  normal  amount  during  the  diastole. 

The  left  ventricle  must  also  expel  in  the  following  systole  an  abnormally  large 
amount  of  blood.  Although  by  this  contraction  only  a  part  of  the  blood  reaches 
the  aorta  in  the  direction  of  the  normal  blood  current  while  a  part  pours  back 
into  the  auricle,  the  work  of  the  left  ventricle  is,  of  course,  excessive.  Thus, 
in  pure  mitral  insufficiency,  the  left  ventricle  is  dilated  as  a  result  of  its 
increased  filling  in  diastole,  ami  is  hypertrophied  as  a  result  of  its  increased 
labor.  The  general  arterial  tension  remains  approximately  normal.  It  is  not 
increased,  since  a  part  of  the  abnormal  amount  of  hlood,  which  pours  out 
of  the  left  ventricle  at  every  systole,  flows  backward  into  the  auricle.  So  long 
as  the  left  ventricle  is  completely  emptied  by  vigorous  contractions,  the  aorta 
receives  about  the  normal  amount  of  blood,  and  the  radial  pulse  remains,  there- 
fore, in  cases  of  pure  mitral  insufficiency,  of  about  the  normal  strength  and 
tension. 

The  anomalies  in  the  movements  of  the  blood  in  mitral  insufficiency  pro- 
duce still  other  effects.  We  have  already  seen  that  the  left  auricle  is  dilated 
from  its  overfilling.  It  also  becomes  hypertrophied,  so  far  as  its  weak  muscu- 
lar structure  permits,  but  it  is  not  in  itself  capable  of  compensating  for  the 
disturbance  which  the  pulmonary  circulation  suffers  from  the  mitral  insuffi- 
ciency, for  the  back  current  from  the  left  ventricle,  and  the  consequent  high 
pressure  in  the  left  auricle,  must  plainly  offer  an  abnormal  hindrance  to  the 
flow  of  blood  from  the  pulmonary  veins.  This  stasis  sets  back  through  the 
pulmonary  capillaries  and  arteries  into  the  right  ventricle.  This  may  be 
recognized,  on  physical  examination,  by  the  change  in  the  pulmonic  second 
sound,  which  is  louder,  more  valvular,  and  "  accentuated,"  since  the  closure 
■of  the  semilunar  valves  in  the  pulmonary  artery  now  takes  place  under  the 
abnormally  high  pressure  which  prevails  in  the  arteries  of  the  lungs.  The 
right  ventricle  has  the  task  of  overcoming  this  abnormal  stasis  in  the  pulmo- 
nary circulation.  It  can  overcome  the  abnormal  resistance  in  the  pulmonary 
circulation  by  increased  work,  and  as  a  result  it  becomes  hypertrophied.  So 
long  as  the  hypertrophy  of  the  right  ventricle  suffices  to  maintain  the  normal 
pulmonary  circulation,  the  stasis  extends  no  farther  backward,  but  in  the 
later  stages  of  heart  disease  we  see  the  right  ventricle  becoming  paralyzed, 
and  more  and  more  dilated  as  a  result  of  stasis.  The  flow  of  venous  blood 
from  the  body  into  the  right  auricle  and  ventricle  is  now  rendered  more 
difficult.  The  signs  of  venous  stasis  become  manifest;  the  patient  has  a 
.cyanotic  hue,  congestive  oedema  appears  in  the  face  and  the  extremities,  symp- 
toms of  passive  congestion  of  the  liver,  spleen,  and  kidneys  appear,  and,  in 
short,  there  is  developed  the  picture  of  an  uncompensated  heart  disease. 

If  we  now  sum  up  the  physical  signs  of  mitral  insufficiency,  the  different 
methods  of  investigation  give  the  following  results : 

Inspection. — The  cardiac  region  often  seems  rather  prominent,  as  a  re- 
sult of  the  hypertrophy  of  the  heart.  This  protrusion  is  most  marked  in  young 
persons  with  a  yielding  thorax.  The  apex  beat  is,  as  a  result  of  the  dilatation 
and  hypertrophy  of  the  left  ventricle,  displaced  toward  the  left  and  sometimes 
downward  into  the  sixth  intercostal  space.  It  is  more  extensive  and  stronger 
than  normal  ("heaving").    The  apex  beat  is  somewhat  displaced  toward  the 


382  DISEASES   OF   THE   CIRCULATORY  ORGANS 

left  as  a  result  of  the  hypertrophy  and  dilatation  of  the  left  ventricle,  and  it 
is  quite  marked.  Besides  that,  we  often  see  a  diffuse  pulsation  in  the  whole 
cardiac  region.  In  the  epigastrium  we  sometimes  see  an  epigastric  pulsation 
proceeding  from  the  hypertrophied  right  ventricle.  In  cases  which  are  no 
longer  perfectly  compensated  the  stasis  in  the  veins  of  the  body  is  rendered 
apparent  by  the  general  cyanotic  appearance  of  the  patient  and  the  marked 
filling  of  the  jugular  veins  in  the  neck.  Undulatory  or  pulsating  movements 
often  occur  in  the  latter  (see  tricuspid  insufficiency,  below). 

Palpation. — By  palpation  likewise  we  perceive  the  abnormal  vigor  and 
extent  of  the  apex  beat,  and  the  displacement  of  the  same  toward  the  left ;  and 
often,  also,  an  extensive  diffuse  pulsation  over  the  cardiac  region,  and  in  par- 
ticular a  distinct  epigastric  pulsation  due  to  the  right  ventricle.  We  often 
feel  a  systolic  thrill  at  the  apex  of  the  heart — a  "  cat's  purr  " — by  laying  the 
hand  flat  on  the  chest.  The  same  whirl  of  blood,  which  is  audible  as  a  mur- 
mur, may  be  perceived  as  a  fine  tremor  of  the  chest  wall. 

The  radial  pulse  is  quite  strong  and  usually  regular.  The  sphvgmo- 
graphic  tracing  of  it  shows  nothing  characteristic  in  mitral  insufficiency. 

Percussion. — This  usually  gives  at  first  only  a  moderate  increase  of  the 
heart's  dullness  to  the  left  (vide  illustration  on  page  381,  showing  the  position 
of  the  different  heart  segments),  but  in  the  later  stages  there  is  at  the  same 
time  an  increase  of  the  heart's  dullness  to  the  right,  caused  by  hypertrophy 
and  dilatation  of  the  right  ventricle.  The  whole  area  of  cardiac  dullness  may 
finally  extend  two  fingers'  breadth  beyond  the  right  edge  of  the  sternum,  and 
to  the  left  it  may  reach  the  mammillary  line,  or  even  pass  far  beyond  it. 

Auscultation. — At  the  apex  of  the  heart  we  hear  a  loud,  quite  long,  pure 
systolic  blowing  murmur,  limited  to  the  systole,  either  replacing  the  first 
sound  or  accompanying  it.  The  second  sound  is  often  obscure  or  inaudible  at 
the  apex,  but  the  pulmonic  second  sound  is  increased  and  accentuated.  Aus- 
cultation of  the  vessels  gives  nothing  characteristic. 

2.  Stenosis  of  the  Mitral  Orifice  (Mitral  Stenosis). — Mitral  stenosis  often 
develops  in  chronic  endocarditis  of  the  mitral  valve,  as  a  sequel  to  a  previous 
insufficiency.     The   valve  constantly  grows   stiffer  and  more  rigid,  and  the 


Fig.  60. — Pulse  curve  in  marked  mitral  stenosis. 

signs  of  stenosis  gradually  predominate  over  those  of  insufficiency.  Hence 
we  very  often  find  stenosis  and  insufficiency  of  the  mitral  valve  combined, 
but  often  the  signs  of  stenosis  are  so  much  more  prominent  that  we  can  prop- 
erly speak  of  a  pure  mitral  stenosis. 

The  disturbance  which  the  circulation  suffers  in  mitral  stenosis  is  much 
greater  than  in  mitral  insufficiency.  In  mitral  stenosis  the  orifice  may  finally 
become  so  narrow  that  it  scarcely  admits  an  ordinary  lead  pencil.  The  influx 
of  blood  into  the  left  ventricle  is  accordingly  much  impeded.  During  the 
diastole  of  the  left  ventricle  the  blood  must  force  its  way  through  the  stiff  and 
narrow  ring  of  the  mitral  valve.     In  this  way,  each  time  there  are  caused 


VALVULAR   DISEASE   OF  THE   HEART  383 

irregular  whirling  movements  in  the  blood,  and  abnormal  vibrations  of  the 
mitral  valve,  giving  rise  in  rriosl  cases  to  an  audible  diastolic  murmur.  In 
mitral  stenosis  the  Left  ventricle  receives  less  than  its  normal  amount  of 
blood,  and  therefore  it  lias  no  direct  occasion  for  hypertrophy,  and  in  fact 
it  is  sometimes  found  at  the  autopsy  to  be  comparatively  small  and  to  be 
crowded  backward  by  the  enormously  dilated  and  hypertrophied  right  heart. 
If,  nevertheless,  we  often  find  hypertrophy  of  the  left  ventricle  in  cases  of 
mitral  stenosis,  it  is  for  tbe  reason  that  mitral  stenosis  usually  develops 
gradually  from  a  previous  insufficiency  of  the  valves.  That  is,  the  chronic 
endocarditis  occasions,  probably  in  every  case,  first,  an  insufficiency  of  the 
valve,  which  is  later  followed  by  stenosis  as  the  change  progresses.  As  insuf- 
ficiency of  the  mitral  valve  leads  to  hypertrophy  of  the  left  ventricle  (vide 
supra),  we  find  it  to  persist  even  at  a  time  when  stenosis  has  become  the 
prominent  lesion.  In  other  cases  of  stenosis,  hypertrophy  of  the  left  ventricle 
is  due  to  certain  associated  conditions,  such  as  arteriosclerosis  or  chronic 
nephritis.  And  finally  we  should  also  consider  Friedreich's  theory,  that  ex- 
treme venous  congestion  may  extend  into  the  capillaries,  and  thence  finally 
occasion  abnormal  resistance  to  the  arterial  circulation. 

The  radial  pulse  in  mitral  stenosis  is  approximately  normal,  as  long  as 
the  ventricle  is  sufficiently  filled  with  blood  during  diastole.  In  spite  of  the 
stenosis  of  the  mitral  valve,  the  left  ventricle  may  be  satisfactorily  filled,  and 
this  is  more  likely  if  the  action  of  the  heart  is  slow,  allowing  a  longer  dias- 
tole; and  if,  also,  the  left  auricle  is  still  capable  of  vigorous  contraction.  If, 
however,  the  action  of  the  heart  is  hurried,  and  the  left  ventricle  is  no  longer 
sufficiently  distended  with  blood  during  the  diastole,  the  radial  pulse  becomes 
small  and  of  low  tension.  Marked  arrhythmia  is  very  often  present  in  mitral 
stenosis,  probably  because  of  the  insufficient  amount  of  arterial  blood  supplied 
to  the  myocardium  and  its  ganglia,  or  because  of  a  concomitant  myocarditis. 

The  hindrance  to  the  flow  into  the  left  ventricle  in  mitral  stenosis  soon 
leads  to  a  marked  stasis,  which  extends  to  the  right  side  of  the  heart  through 
the  left  auricle,  and  the  pulmonary  veins,  capillaries,  and  arteries.  The  left 
auricle  is  dilated  first  (often  to  an  enormous  extent),  and  its  walls  are  hyper- 
trophied, but  it  can  overcome  only  a  very  small  part  of  the  resistance  at  the 
mitral  orifice.  The  right  ventricle  can,  by  more  work,  so  increase  the  pres- 
sure in  the  pulmonary  vessels  that,  in  spite  of  the  narrowed  orifice,  an  approx- 
imately sufficient  quantity  of  blood  may  pour  into  the  left  ventricle.  Hence 
we  find  in  mitral  stenosis  a  very  marked  hypertrophy  and  dilatation  of  the 
right  ventricle.  The  stasis  in  the  pulmonary  circulation,  manifested  objec- 
tively by  the  accentuation  of  the  pulmonic  second  sound,  has  as  a  result  a 
gradually  developing  ectasis  of  the  pulmonary  capillaries.  Thickening  of  the 
intima  of  the  pulmonary  arteries  and  veins  also  usually  develops.  (See  the 
chapter  on  Brown  Induration  of  the  Lungs.) 

The  results  of  physical  examination  are  as  follows : 

Inspection. — The  whole  cardiac  region  may  seem  slightly  prominent, 
as  a  result  of  the  hypertrophy  of  the  heart.  This  protuberance  is  most  marked 
in  children  with  their  yielding  thoracic  walls.  The  heart's  action  is  usually 
extended  over  a  larger  area,  but  in  pure  mitral  stenosis  the  apex  beat  is  no 
stronger  than  usual,  though  often  displaced  to  the  left.  We  frequently  notice 
a  marked  pulsation  in  the  epigastrium,  produced  by  the  right  side  of  the 


384 


DISEASES  OF  THE   CIRCULATORY   ORGANS 


heart.     The  jugular  veins  are  apt  to  be  prominent,  and  show  the  different 
forms  of  undulatory  and  pulsating  movement. 

Palpation. — This  also  gives  signs  corresponding  to  the  enlargement 
of  the  heart  (sternal  and  epigastric  pulsation).  We  sometimes  feel  the  pul- 
sation of  the  dilated  right  auricle  (vide  infra)  even  to  the  right  of  the 
sternum.  In  some  cases  we  feel  a  diastolic  thrill  at  the  apex  of  the  heart,, 
which  alone  may  almost  establish  the  diagnosis  of  mitral  stenosis.  This  thrill 
arises  from  the  same  vertiginous  currents  in  the  blood  which  form  the  basis 
of  the  diastolic  murmur  (vide  infra).  The  radial  pulse  is  small  in  every 
case  of  severe  mitral  stenosis,  and  is  very  often  irregular. 

Pekcussion. — Percussion  shows,  in  the  first  place,  an  extension  of  cardiac 
dullness  toward  the  right,  reaching  to  the  right  edge  of  the  sternum,  or  far 
beyond.  Dullness  also  extends,  as  a  rule,  farther  to  the  left  than  normal. 
This  is  in  part  due  to  the  hypertrophy  of  the  left  ventricle  (vide  supra),  in 
part  to  a  dilatation  of  the  right  side  of  the  heart,  so  great  as  to  push  the  left 

ventricle  backward  and 
to  the  left.  The  great 
distention  of  the  right 
ventricle  causes  an  en- 
largement of  the  car- 
diac dullness  upward. 

We  have  often  been 
able  to  convince  our- 
selves by  autopsies  that 
the  extension  of  cardiac 
dullness  upward  (abso- 
lute dullness  beginning 
about  the  third  rib),  in 
mitral  stenosis  as  well 
as  in  almost  all  other 
hypertrophies  of  the 
right  ventricle,  usually 
results  from  the  right 
ventricle  itself,  and 
more  especially  from 
the  dilatation  of  the 
right  conus  arteriosus. 
A  marked  extension  of 
cardiac  dullness  toward 
the  right  and  beyond 
the  right  sternal  edge 
is  almost  without  excep- 
tion ascribable  to  dila- 
tation of  the  right  auricle.  The  right  auricle,  as  is  not  always  remembered,  lies 
not  above,  but  to  the  right  of  the  right  ventricle.  In  hearts  with  enlarged  right 
ventricle,  the  right  atrioventricular  boundary  almost  always  runs  perpendicu- 
larly, so  that  the  base  of  the  heart  is  formed  by  the  right  auricle  and  the  right 
ventricle.  In  the  adjoining  sketch  (Fig.  61)  the  position  of  the  various  car- 
diac segments  is  demonstrated  as  found  in  almost  all  mitral  lesions,  especially 


Fig.  61.— The  position  of  the  various  cardiac  segments  in  mitral 
stenosis,  r.  Vo.  is  the  dilated  right  auricle;  r.  Ve,  the  di- 
lated right  ventricle;  Con.  a,  the  right  conus  arteriosus;  P., 
the  pulmonary  artery;  A,  the  aorta;  I.  Ve.,  the  left  ventri- 
cle pushed  toward  the  left  and  backward. 


VALVULAR   DISEASE   OF  THE   HEART 

in  mitral  stenosis.  The  relations  of  the  various  portions  to  the  enlarged  cardiac 
dullness  are  easily  recognized.  Only  exceptionally  are  the  relations  otherwise. 
Thus,  we  once  saw  a  case  of  mitral  stenosis  in  which  the  left  auricle  wa- 
enormously  dilated  that  it  extended  toward  the  right  behind  and  beyond  the 
right  auricle,  and  was  a  prominent  factor  in  the  increase  of  cardiac  dullness 
toward  the  right,  ohserved  during  life.  At  times  the  upward  increase  in  heart 
dullness  is  also  caused  by  a  distended  right  auricle. 

Auscultation. — The  characteristic  auscultatory  sign  of  mitral  stenosis  is 
the  diastolic  [presystolic]  murmur  at  the  apex.  This  is  never  so  loud  and 
blowing  as  the  systolic  murmur  of  insufficiency,  but  it  usually  sounds  more 
rolling  or  rippling.  It  is  loudest  at  the  apex,  and  it  is  transmitted  only 
slightly  toward  the  base.  Since,  as  has  been  said,  the  left  ventricle  in  mitral 
stenosis  is  sometimes  pushed  to  the  left  and  backward  by  the  very  much 
enlarged  right  ventricle,  in  looking  for  the  murmur  we  must  often  go  far  to 
the  left,  in  order  not  to  auscult  the  right  ventricle  only. 

The  origin  of  the  murmur  is  easily  explained.  In  the  diastole  of  the  left 
ventricle  the  blood  current  must  force  its  way  through  the  narrow  mitral 
orifice,  whence  vertiginous  movements  arise  in  the  blood,  and  produce  the 
murmur.  Since  the  blood  flowing  through  the  narrow  orifice  has  a  current  of 
relatively  slight  intensity,  the  murmur  produced  by  it  cannot  be  very  loud. 
Indeed,  in  the  most  extreme  cases  of  mitral  stenosis,  the  murmur  is  particu- 
larly apt  to  be  very  faint,  and  when  the  heart's  action  is  hurried  and  irregular, 
entirely  inaudible.  Not  infrequently  the  murmur  is  not  heard  until  the 
second  half  of  diastole,  that  is,  when  the  contraction  of  the  left  auricle  gives 
a  fresh  impulse  to  the  current  of  blood  streaming  through  the  stenosed  orifice. 
A  murmur  of  this  sort,  which  is  audible  only  at  the  end  of  diastole,  and  passes 
with  a  distinct  crescendo  directly  into  the  loud  systolic  sound  and  ter- 
minates with  this,  is  called  a  presystolic  murmur.  This  murmur  can  often 
be  plainly  felt  if  the  hand  is  laid  upon  the  apex  of  the  heart,  as  a  presystolic 
thrill. 

It  is  not  very  exceptional  to  find  no  murmur  audible  in  cases  of  extreme 
mitral  stenosis.  If  such  cases  do  not  come  under  observation  till  the  last 
stage  of  the  disease,  the  mitral  stenosis  may  readily  be  overlooked.  We  have 
ourselves  repeatedly  found,  in  cases  of  mitral  stenosis,  that  as  the  lesion  grew 
worse  the  distinct  diastolic  or  presystolic  murmur  gradually  and  completely 
disappeared.  This  is  explained  by  the  fact  that  as  the  chink  in  the  valve 
grows  narrower  and  the  weakness  of  the  heart  greater,  the  blood  is  not  forced 
through  the  narrow  orifice  with  sufficient  vigor  to  cause  audible  vibrations  of 
the  thickened  valves.  If  the  left  ventricle  is  wholly  displaced  backward  by 
the  enormous  increase  in  size  of  the  right  ventricle,  we  have  also  less  favorable 
conditions  for  the  propagation  of  the  waves  of  sound  from  the  mitral  valve 
to  the  ear. 

The  first  sound  at  the  apex  is  maintained  in  pure  mitral  stenosis.  Indeed, 
it  is  often  noticeably  loud  and  valvular.  All  the  later  observations  confirm 
the  view  that  the  systolic  sound  is  a  muscle  sound,  and  consequently  it  is 
probable  that  this  vigorous  first  sound  is  due  to  the  contraction  of  the  left 
ventricle,  which  is  often  hypertrophied  (vide  supra,  page  383),  but  never- 
theless, as  a  result  of  the  stenosis,  only  imperfectly  filled.  The  strength  of 
the  first  ventricular  sound  in  mitral  stenosis  affords,  at  any  rate,  a  marked 


386  DISEASES   OF   THE   CIRCULATORY   ORGANS 

contrast  to  its  weakness  in  aortic  insufficiency  (vide  infra).  We  have  a 
strong  sound  when  the  ventricle  is  little  filled,  diminution  and  dullness  of 
sound  when  the  ventricle  is  overfilled.  If  insufficiency  of  the  valve  coexists, 
we  hear  a  systolic  murmur  usually  along  with  the  first  sound.  In  mitral  ste- 
nosis there  is  often  a  very  marked  accentuation  of  the  pulmonic  second  sound, 
the  result  of  the  abnormally  high  tension  in  the  pulmonary  artery.  The 
pulmonic  second  sound  is,  however,  very  often  only  slightly  accentuated 
without  our  being  able  always  to  assign  a  real  cause  therefor.  Perhaps  there 
is  a  difference  in  the  vibratory  power  of  the  valves.  In  ansemic,  sickly  indi- 
viduals, and  also  in  cases  of  simultaneous  insufficiency  of  the  tricuspid  valve 
(vide  infra),  there  is  no  accentuation  of  the  second  pulmonic  sound.  Some- 
times, as  a  result  of  extensive  congestion  in  the  systemic  veins,  the  pressure 
in  the  pulmonary  artery,  and  with  it  the  accentuation  of  the  second  pul- 
monic sound,  appear  to  lessen.  Very  often  the  second  sound  at  the  base  of 
the  heart  is  "split"  (reduplicated).  The  closure  of  the  semilunar  valves  in 
diastole  does  not  happen  at  the  same  time  in  the  pulmonary  artery  and  in  the 
aorta,  on  account  of  the  unequal  tension  in  the  two  vessels,  so  that  conse- 
quently the  two  sounds  are  heard,  one  shortly  after  the  other.  But  other, 
still  unknown,  factors  may  operate.  At  times  we  may  hear  no  murmur  in 
mitral  stenosis  (vide  supra),  but  only  a  loud  valvular  systolic  and  diastolic 
■  sound. 

Mitral  stenosis  is  one  of  the  severest  forms  of  heart  disease.  It  almost  always 
causes  greater  subjective  disturbance  than  mitral  insufficiency.  Hypertrophy 
of  the  right  ventricle  ma}',  indeed,  maintain  for  a  time  an  approximately  com- 
plete compensation,  but  the  signs  of  marked  stasis  in  the  pulmonary  circula- 
tion, and  further,  in  the  veins  of  the  body,  are  apt  to  appear  quite  early.  The 
disturbances  of  compensation  which  occur  in  mitral  stenosis  are,  indeed,  par- 
ticularly susceptible  of  treatment,  so  that  for  many  years  there  may  be  times 
of  improvement,  alternating  with  times  of  general  circulatory  disturbance 
and  marked  subjective  symptoms.  But  at  last  it  becomes  impossible  to  regu- 
late the  circulation.  The  dyspnoea  grows  worse,  and  finally  death  occurs, 
usually  ushered  in  by  increasing  dropsy. 

3.  Insufficiency  of  the  Semilunar  Valves  of  the  Aorta. — Insufficiency  of  the 
aortic  valves  is  due  most  frequently  to  contraction  of  the  free  edges  of  the 
valves.  Tears,  perforations,  or  adhesions  of  the  valve  to  the  wall  of  the 
vessel  more  rarely  lead  to  insufficiency.  The  cause  of  all  these  changes  is 
either  a  valvular  endocarditis,  which  is  usually  a  sequel  of  articular  rheuma- 
tism, or  a  general  arterial  atheroma,  which  extends  gradually  from  the  intima 
of  the  aorta  to  the  valves.  We  have  already  referred  to  syphilis  as  a  not  very 
infrequent  cause  of  aortic  lesions.  A  question  of  practical  importance  is 
whether  violent  bodily  exertion  may  suddenly  occasion  the  partial  lacera- 
tion of  an  aortic  valve.  Many  clinical  observations,  including  a  recent 
case  of  the  author's,  seem  to  show  the  possibility  of  this  extremely  rare 
occurrence. 

The  function  of  the  aortic  valves  is  to  close  tightly  at  the  time  of  diastole 
of  the  left  ventricle,  in  order  to  prevent  any  return  of  blood  from  the  aorta 
into  the  ventricle.  If  these  valves  are  insufficient- — that  is,  if  they  do  not 
close  perfectly  at  each  diastole — there  is  a  return  current  of  blood  from  the 
aorta  into  the  left  ventricle. 


VALVULAR   QISEASE   OF  THE   HEART 

This  regurgitant  diastolic  wave  sets  the  tense  edges  of  the  valve  in  vibra- 
tion as  it  passes  over  them.  Furthermore,  the  two  currents  of  blood  imping- 
ing upon  each  other  in  the  lefi  ventricle,  the  one  an  abnormal  regurgitation 
from  the  aorta,  the  other  the  normal  stream  from  the  Lefi  auricle,  prod 
irregular  whirling  motions  in  the  blood.  All  these  vibrations  are  propagated 
to  the  surrounding  structures,  and  produce  the  Long-continued,  blowing,  dias- 
tolic, and  remarkably  characteristic  murmur  of  aortic  insufficiency. 

Aortic  insufficiency  causes  an  immediate  and  greal  increase  in  the  de- 
mands upon  the  left  ventricle,  because  of  its  abnormal  distention,  for  it  re- 
ceives, as  we  have  already  said,  not  merely  its  uormal  quantum  of  blood  from 
the  left  ventricle,  but  also  the  blood  which  regurgitates  through  the  leaking 
valves  of  the  aorta.  It  is  consequently  overfilled  at  cwvy  diastole,  and  finally 
becomes  permanently  distended.  Dilatation  of  the  lefi  ventricle  Forms  a  con- 
stant anatomical  lesion  in  every  case  of  aortic  insufficiency,  and  is  shown  not 
only  in  the  dilatation  of  the  whole  ventricular  cavity,  but  also  in  the  very 
characteristic  flattening  of  the  trabecule  and  of  the  papillary  muscles.  There 
is  usually  some  fibrous  thickening  of  the  endocardium  at  the  spot  upon  which 
the  regurgitant  blood  current  is  continually  impinging.  The  left  ventricle 
possesses  sufficient  reserve  strength  to  discharge  its  content-  completely 
for  a  long  period  by  means  of  increased  effort.  This  is  indeed  a  task  like 
that  of  Sisyphus,  since  the  portion  of  the  blood  which  is  thrown  into  the  aorta 
is  constantly  rolling  back  into  the  ventricle.  The  increased  demands,  however, 
lead  necessarily  at  last  to  a  hypertrophy  of  the  left  ventricle,  often  greater 
than  is  seen  under  any  other  conditions. 

From  the  facts  enumerated  Ave  can  easily  understand  the  physical  signs  of 
insufficiency  of  the  aortic  valves. 

Inspection. — The  great  dilatation  of  the  left  ventricle  often  causes  a 
marked  protrusion  of  the  whole  cardiac  region.  The  diffuse  and  very  strong 
apex  beat,  displaced  downward  and  to  the  left,  is  especially  striking.  It  may 
usually  be  seen  in  the  sixth  intercostal  space,  outside  the  left  mammillary 
line,  and  sometimes  even  at  the  anterior  axillary  line.  Besides,  we  often  see 
a  marked  diffuse  tremor  of  the  whole  cardiac  region.  There  is  marked  pul- 
sation of  the  carotid  arteries  in  the  neck.  The  jugular  veins  show  undula- 
tion and  pulsation,  when  at  last  compensation  begins  to  fail. 

Palpation. — We  can  appreciate  the  heart's  action  to  a  still  greater  extent 
by  palpation  than  by  inspection.  The  apex  beat  is  very  resistant,  massive,  and 
plainly  heaving — that  is,  the  finger  or  stethoscope  applied  to  the  apex  is  lifted 
by  the  beat  at  every  systole.  In  rare  cases  a  diastolic  thrill,  corresponding  to 
the  diastolic  murmur,  can  be  felt  over  the  base  of  the  heart.  In  two  such  cases 
observed  by  us  the  murmur  had  a  marked  musical  character  (vide  infra). 
The  appearances  in  the  arteries  are  given  below. 

Percussion. — Percussion  gives  an  extension  of  the  cardiac  dullness  to  the 
left,  beyond  the  left  mammillary  line  and  even  to  the  anterior  axillary  line, 
caused  by  the  hypertrophy  and  dilatation  of  the  left  ventricle.  The  upper 
boundary  of  the  cardiac  dullness  is  normal,  or  it  may  extend  up  to  the  third 
rib.  The  right  boundary  is  in  its  normal  place  at  the  left  border  of  the 
sternum,  but  it  may  also  be  pushed  farther  to  the  right,  either  because  the  large 
left  ventricle  of  itself  causes  an  extension  of  the  whole  heart  to  the  right,  or 
because  the  right  ventricle  is  also  hypertrophied.     The  latter  change  occurs 


388  DISEASES  OF  THE  CIRCULATORY  ORGANS 

in  pure  aortic  insufficiency  when  the  compensation  is  no  longer  complete,  and 
the  stasis  extends  backward  from  the  left  ventricle,  through  the  pulmonary 
circulation,  into  the  right  side  of  the  heart. 

It  may  also  be  remarked  here  that,  in  insufficiency  of  the  aortic  valves,  the 
ascending  aorta  is  often  considerably  dilated  by  the  marked  impulse  of  the 
volume  of  blood  pouring  into  it.  A  moderate  degree  of  dullness  is  found  over 
the  dilated  aorta,  which  may  sometimes  be  made  out  at  the  sternal  end  of  the 
second  right  intercostal  space. 

Auscultation. — Insufficiency  of  the  aortic  valves  is  characterized  by  a 
long-drawn,  loud,  blowing,  diastolic  murmur,  the  origin  of  which  has  been 
explained  above.  The  place  in  which  the  murmur  is  heard  loudest  is  not  the 
sternal  end  of  the  second  right  intercostal  space,  the  ordinary  point  for  aus- 
cultation of  the  aorta,  but  it  almost  always  lies  farther  to  the  left.  Corre- 
sponding to  the  backward  current  of  blood  toward  the  left  ventricle,  which 
begets  the  murmur,  we  hear  the  latter  loudest  over  the  upper  part  of  the 
sternum  or  even  at  its  left  border.  In  some  cases  the  murmur  assumes  a 
marked  "  musical  character  " — that  is,  there  is  a  definite  high  musical  tone, 
which  is  due  to  a  tendinous  fiber  arising  from  a  wearing  away  of  the  valve, 
and  set  in  vibration  by  the  diastole,  or  to  some  similar  cause.  The  diastolic 
murmur  is  often  audible  at  the  apex,  but  it  is  faint  there.  It  is  only  in  a  few 
exceptional  cases  that  there  is  no  diastolic  murmur  in  aortic  insufficiency. 
Sometimes  we  hear  not  only  the  murmur,  but  also  the  diastolic  sound  of  the 
closing  valve.  During  systole  we  only  rarely  hear  over  the  aorta  a  pure,  loud, 
first  sound,  but  almost  always  a  short  systolic  murmur.  This  murmur  may, 
of  course,  be  due'  to  accompanying  stenosis  of  the  aortic  valves,  but  yet  is  fre- 
quent when  there  is  insufficiency  alone.  It  is  explained  by  0.  Eosenbach  as 
being  clue  to  the  fact  that  at  the  beginning  of  the  systole  of  the  left  ventricle, 
the  diastolic  flow  of  blood  has  not  yet  completely  ceased,  so  that  the  emerging 
blood  stream  encounters  this  opposing  current.  This  meeting  of  the  two 
blood  currents  in  the  root  of  the  aorta  during  systole  causes  the  vibrations 
which  give  rise  to  the  short  systolic  murmur.  It  is  to  be. noted  that  this  cir- 
cumstance also  may  perhaps  have  some  influence  upon  the  development  of  the 
hypertrophy  of  the  left  ventricle. 

It  is  very  interesting  and  important  that,  as  Traube  pointed  out,  we  find 
the  first  sound  at  the  apex  scarcely  ever  loud  and  pure,  but  often  very  indis- 
tinct and  muffled ;  or  else  we  hear  a  short  systolic  murmur  instead  of  it.  This 
veiling  of  the  first  sound  at  the  apex  of  the  heart  has  theoretic  interest,  because 
it  has  been  employed  as  an  argument  against  the  view  that  the  first  mitral 
sound  is  a  muscular  sound;  for  it  is  not,  in  fact,  at  once  apparent  why  the 
hypertrophied  left  ventricle  should  so  often  fail  to  produce  a  distinctly  audi- 
ble tone  by  its  contraction.  But,  as  we  have  already  pointed  out  (see  page 
387),  the  probable  explanation  lies  in  the  previous  overdistention  of  the  left 
ventricle  during  diastole.  This  renders  the  systolic  contraction  difficult  and 
somewhat  slow,  and  may  be  the  cause  of  the  indistinctness  of  the  muscle 
sound.  In  later  stages  of  the  disease  we  may  also  adduce  parenchymatous 
degeneration  of  the  myocardium  as  an  explanation  of  its  feebleness.  The 
systolic  murmur,  often  heard  at  the  apex  in  aortic  insufficiency,  may  depend 
upon  a  coexisting  true  mitral  insufficiency,  but  it  is  probably  often  due  to 
a  relative  insufficiency  of  the  mitral,  since  the  valves,  which  are  normal  in 


VALVULAR   DISEASE   OF  THE   HEAICI 


themselves,  can  no  longer  cause  a  perfect  closure  of  the  left  mitral  orifice  now 
that  the  left  ventricle  is  dilated. 

Symptoms  in  the  Peripheral  Arteries.— Such  remarkable  symptoms 
are  found  in  the  peripheral  arteries  in  aortic  insufficiency  thai  they  demand 
a  brief  special  description.  The  firsl  striking  symptom  is  the  strong  pulsation 
not  only  of  the  larger  but  also  of  the  smaller  arteries,  even  those  the  pul- 
sation of  which  is  not  generally  visible.  We  see  and  feel  not  only  a  strong 
pulsation  in  the  carotids,  but  also  in  the  tortuous  brachial  artery,  in  the  radial, 
ulnar,  temporal,  dorsalis  pedis,  etc.  We  sometimes  feel  an  arterial  puis*;  in 
the  liver  through  the  abdominal  walls. 

The  rapid  decline  of  the  pulse— the  pulsus  cehr  [Corrigan's  pulse] — is 
most  characteristic  of  aortic  insufficiency,  and  is  to  be  felt  especially  in  the 
radial  artery,  but  also  in  the  femoral,  dorsalis  pedis,  and  other  vessels.  An 
abnormally  large  quantity  of  blood  is  thrown  into  the  arteries  from  the  hyper- 
trophied  and  dilated  left  ventricle;  hence  the  high  ascent  of  the  pulse;  but 
since  the  distended  artery  quickly  contracts  again,  and  particularly  as  at  tin- 
next  diastole  of  the  ventricle  the  blood  escapes  in  two  directions,  into  the  capil- 
laries and  back  into 
the  ventricle,  an  ab- 
normally rapid  and 
deep  decline  of  the 
pulse  follows  the  high 
ascent  of  its  wave — 
a  condition  which  ex- 
plains the  "  jump- 
ing," "springing" 
pulse  (pulsus  celer) 
of  aortic  insufficien- 
cy. The  quality  of 
the  pulse  may  be 
plainly  recognized  also  in  its  sphygmographic  tracing  (see  Fig.  62).  The 
abnormal  backward  wave  may  even  be  detected  in  the  capillaries.  We  often 
see  a  marked  pallor  of  the  finger  nails,  or  of  the  skin  of  the  forehead  when 
reddened  by  rubbing,  at  every  diastole  of  the  heart  in  patients  with  aortic 
insufficiency — Quincke's  capillary  pulse. 

The  auscultatory  phenomena  over  the  arteries  are  connected  partly  with 
the  changing  conditions  of  tension  of  the  arterial  walls.  We  very  often  hear 
a  short,  rough,  systolic  murmur  in  the  carotid.  The  second  sound,  which  is 
well  known  to  be  the  transmitted  aortic  second  sound,  is  absent.  Instead  of  it 
we  sometimes  hear  faintly  transmitted  the  aortic  diastolic  murmur.  The  sound 
of  the  medium-sized  and  smaller  arteries  is  very  characteristic.  By  applying 
the  stethoscope  lightly  we  hear  over  the  femoral,  the  brachial,  and  often  over 
the  radial,  the  ulnar,  the  palmar  arch,  and  the  dorsalis  pedis,  a  marked  valvu- 
lar sound,  which  is  changed  by  pressure  on  the  artery,  especially  in  the  larger 
arteries,  to  a  loud  stenotic  murmur.  The  quicker  the  pulse,  the  more  certain 
are  we  to  hear  these  sounds  in  the  arteries.  In  the  most  marked  cases  of 
Corrigan's  pulse  these  vascular  sounds  are  so  loud  that  we  may  hear  almost 
anywhere  below  the  knee,  by  means  of  a  stethoscope,  a  valvular  sound.  The 
double  sound  in  the  femoral  (Traube's  double  sound)  is  quite  a  frequent 
25 


Fig.  62. — Pulse  curve  in  aortic  insufficiency. 


300  DISEASES  OF  THE  CIRCULATORY  ORGANS 

phenomenon,  about  the  origin  and  significance  of  which  there  has  been  much 
discussion.  The  double  sounds  either  follow  each  other  shortly,  so  that  the 
first  seems  something  like  a  preparatory  blow  for  the  second,  or  they  are 
separated  from  each  other  by  a  longer  interval,  like  the  two  sounds  of  the 
heart.  Traube  explained  the  origin  of  the  first  sound  by  the  sudden  tension 
of  the  vessel  wall,  as  in  the  simple  femoral  sound,  and  the  second  sound  by  the 
sudden  relaxation  of  it.  Friedreich  has  pointed  out  in  regard  to  this  that,  in 
coexisting  tricuspid  insufficiency,  a  sound  may  also  be  produced  in  the  femoral 
vein  by  tension  of  the  venous  valves.  The  double  sound  in  the  femoral  may 
probably  have  different  causes  of  origin.  It  is,  of  course,  by  far  the  most 
frequent  in  aortic  insufficiency,  but  it  has  also  been  repeatedly  observed  in 
other  forms  of  heart  disease,  as  in  mitral  stenosis.  The  so-called  Duroziez's 
double  murmur  in  the  femoral  is  more  rare,  and  it  is  noticed  almost  exclu- 
sively in  aortic  insufficiency.  By  pressing  the  stethoscope  on  the  femoral,  we 
hear  two  murmurs  plainly  distinct  from  each  other,  of  which  the  first  comes 
from  the  passage  of  the  systolic  blood  wave,  and  the  second  from  the  passage 
of  the  abnormal  backward  wave  coming  from  the  periphery  of  the  vascular 
system  through  the  artificially  contracted  vessel. 

While  the  well-marked  Corrigan's  pulse  and  the  arterial  sounds  associated 
with  it  are  so  characteristic,  they  appear  with  great  distinctness  only  in  some 
cases  of  aortic  insufficiency ;  while  in  other  and  often  apparently  similar  cases 
they  are  indistinct  or  quite  absent.  Probably  this  difference  depends  at  least 
in  part  upon  a  difference  in  the  elasticity  of  the  arterial  walls.  At  any  rate, 
we  have  seen  well-marked  Corrigan's  pulse  and  sounding  arteries  in  youthful 
patients;  while  in  elderly  persons  with  accompanying  arteriosclerosis  or  sim- 
ilar changes,  these  phenomena  are  not  apt  to  be  striking. 

Aortic  insufficiency  is  a  comparatively  favorable  form  of  heart  disease, 
since  it  may  be  almost  perfectly  compensated  for  years  by  hypertrophy  of  the 
left  ventricle.  Many  patients  with  moderate  aortic  insufficiency  feel  perfectly 
well,  and  are  even  capable  of  quite  hard  work.  They  have  not  the  slightly 
cyanotic  hue  which  almost  all  patients  with  mitral  disease  exhibit,  but  they 
have  a  normal  or  even  a  pale  complexion.  If,  however,  the  signs  of  dis- 
turbed compensation  once  appear  in  aortic  insufficiency  the  severest  sequela? 
may  develop  quite  rapidly.  In  aortic  insufficiency  it  is  exceptional  to  see 
such  repeated  changes  from  bad  to  good,  and  good  to  bad,  as  are  often  ob- 
served, for  instance,  in  mitral  stenosis.  If  the  left  ventricle  becomes  enfeebled, 
it  can  no  longer  satisfy  the  excessive  demands  made  upon  it.  Passive  con- 
gestion ensues,  extending  backward  through  the  pulmonary  circuit  into  the 
systemic  veins,  even  while  the  pulse  may  still  seem  to  be  powerful.  The  aver- 
age arterial  tension  becomes  subnormal,  dyspnoea  increases,  and  there  are 
attacks  of  cardiac  asthma.  (Edema  appears,  and  the  patient  dies  with  the 
symptoms  of  anasarca.  We  will  speak  more  fully  below  of  certain  intercur- 
rent events  in  aortic  insufficiency,  such  as  cerebral  hemorrhage  and  peri- 
carditis. 

4.  Stenosis  of  the  Aortic  Orifice. — Except  for  the  mild  forms  of  aortic  ste- 
nosis, which  often  come  on  with  aortic  insufficiency,  aortic  stenosis  is  a  rare 
disease.  It  arises  from  marked  thickenings  and  calcifications,  and  especially 
from  adhesions  of  the  aortic  valves  to  one  another.  The  stenosis  may  become 
so  considerable  that  the  orifice  is  finally  reduced  to  a  mere  fissure,  through 


VALVULAR  DISEASE  OF  'J' HE   HEART  391 

which  the  left  ventricle  must  force  the  blood  at  Its  systole.  The  fluttering  of 
the  valves  and  the  vertiginous  movements  in  the  blood  thus  arising  produce  a 

loud  systolic  murmur.  The  left  ventricle  is  compelled  to  do  greater  work- 
in  consequence  of  the  increased  resistance  of  the  aortic  orifice,  and  hence 
becomes  hypertrophied.  In  spite  of  the  increased  effort,  however,  compara- 
tively little  blood  reaches  the  arterial  system,  and  consequently  the  radial  pulse 
is  small  and  the  arteries  contracted. 

Inspection  and  Palpation. — Upon  physical  examination  of  the  heart  we 
find,  in  the  first  place,  the  apex  beat  displaced  outward  as  a  result  of  the 
hypertrophy  of  the  left  ventricle,  and  also  often  more  powerful  than  normal. 
It  may,  however,  be  noticeably  feeble,  perhaps  because  of  the  slowness  of  the 
systole.  A  former  explanation  of  this  feebleness  was  the  diminution  of  the 
recoil  of  the  apex  (the  Gutbrod-Skoda  theory  of  the  apex  beat). 

Percussion. — Percussion  gives  an  extension  of  the  heart's  dullness  to  the 
left.  The  right  ventricle  is  also  dilated  and  hypertrophied  to  a  moderate 
degree  in  the  later  stages,  if  the  stasis  extends  backward  through  the  pulmo- 
nary circulation. 

Auscultation. — On  auscultation,  we  hear  over  the  aorta  a  very  loud 
"  sawing,"  long-drawn,  systolic  murmur,  which  is  usually  transmitted  to  the 
right,  corresponding  to  the  course  of  the  aorta,  in  distinction  from  the  diastolic 
murmur  of  aortic  insufficiency.  It  is  usually  to  be  heard  loudest  at  the  sternal 
end  of  the  second  right  intercostal  space,  but  it  is  audible  to  a  lesser  extent 
over  almost  the  whole  heart.  It  is  usually  quite  loud  over  the  carotids.  The 
systolic  sound  at  the  apex  is  apt  to  be  feeble.  The  second  aortic  sound  is 
likewise  faint  or  even  inaudible.  If  there  is  coexisting  insufficiency  of  the 
valve,  the  second  aortic  sound  is  replaced  by  a  diastolic  murmur. 

The  pulse  has  been  already  described.  It  is  small,  and  often  surprises 
one  by  its  contrast  with  the  strength  of  the  apex  beat.  In  well-compensated 
cases  it  is  regular,  and  often  moderately  or  even  extremely  slow.  This  slow 
pulse  of  aortic  stenosis  is  often  explained  as  a  compensatory  change  in  the 
heart's  action,  appropriate  to  the  existing  lesion — the  systole  being  lengthened, 
an  increased  amount  of  blood  can  be  driven  through  the  narrow  aortic  orifice. 
But  the  slowing  of  the  cardiac  action  is  really,  in  main  part,  a  prolongation 
of  the  diastole,  and  therefore  the  slow  pulse  is  probably  due  chiefly  to  the  fact 
that  the  wall  of  the 
left  ventricle  is  ill 
supplied  with  blood, 
just  as  in  the  case  of 

sclerosis   of  the   COrO-  Fig.  63.— Pulse  curve  in  stenosis  of  the  aortic  orifice, 

nary     arteries.      The 

sphygmographic  tracing  of  the  radial  pulse  (see  Fig.  63)  shows  a  low  wave 
and  a  comparatively  slow  rise  and  fall. 

Aortic  stenosis  of  slight  or  moderate  degree  may  be  tolerably  well  borne 
by  the  patient.  We  have  even  seen  a  man  with  well-marked  aortic  stenosis 
who  for  years  did  not  have  the  slightest  subjective  symptoms  of  heart  disease, 
until  he  finally  died  with  an  acute  recurrent  endocarditis.  When  the  stenosis 
is  more  complete  we  sometimes  have  a  most  peculiar  clinical  picture.  The 
pulse  is  very  infrequent,  as  low  as  thirty  to  twenty-four  beats  in  a  minute. 
From  time  to  time  there  are  attacks  of  vertigo  or  syncope,  the  patient  often 


392  DISEASES  OF  THE  CIRCULATORY  ORGANS 

falls,  and  has  epileptiform  attacks.  These  seizures,  which  may  be  repeated 
for  months  or  even  for  some  years,  are  probably  connected  with  a  sudden 
anaemia  of  the  heart  and  brain.  We  have  observed  this  remarkable  group  of 
symptoms  particularly  in  elderly  persons  with  aortic  stenosis,  due  to  arterio- 
sclerosis (vide  infra,  page  417).  In  other  respects  the  course  of  aortic  steno- 
sis is  similar  to  that  of  the  acute  valvular  diseases,  and  in  the  same  way  termi- 
nates in  general  circulatory  derangement  with  its  results. 

5.  Insufficiency  of  the  Tricuspid  Valve. — Insufficiency  of  the  tricuspid  valve 
is  extremely  rare  as  an  independent  disease  of  the  heart,  but  a  secondary  insuf- 
ficiency of  the  tricuspid  is  quite  frequent,  and  is  therefore  of  practical  inter- 
est, as  it  complicates  other  already  existing  valvular  diseases  in  the  left  side  of 
the  heart.  It  arises  either  from  a  secondary  endocarditis,  affecting  the  tri- 
cuspid, in  quite  an  analogous  manner  with  mitral  insufficiency,  or  it  is  a  so- 
called  relative  insufficiency.  This  name  we  give  to  that  form  of  insufficiency 
which  develops  when  the  edges  of  the  tricuspid  valve,  normal  in  themselves, 
at  last  fail  to  meet  one  another,  from  the  increasing  dilatation  of  the  right 
ventricle,  or  at  any  rate  from  the  inability  of  the  enfeebled  right  ventricle 
properly  to  close  the  valve. 

The  necessary  result  of  tricuspid  insufficiency  is,  that  in  every  systole  of 
the  right  ventricle  a  backward  current  passes  through  the  open  tricuspid  ori- 
fice into  the  right  auricle,  and  thence  into  the  veins  of  the  body.  The  tricuspid 
insufficiency  ensuing  in  other  forms  of  heart  disease  must  therefore  increase 
the  stasis  in  the  veins  of  the  body,  and  it  is  thus  far  an  unfavorable  complica- 
tion. It  has  a  compensatory  significance  only  as  it  affords  relief  to  the  pulmo- 
nary circulation.  Since  a  part  of  the  blood  passes  back  from  the  right  ven- 
tricle into  the  veins,  less  blood  than  usual  must  reach  the  pulmonary  arteries. 
The  decrease  in  tension  thus  produced  in  these  arteries  makes  itself  apparent 
on  auscultation,  since  the  accentuation  of  the  pulmonic  second  sound  in 
valvular  disease  of  the  mitral  orifice  diminishes  when  tricuspid  insufficiency 
takes  place. 

That  tricuspid  insufficiency  must  result  in  a  hypertrophy  of  the  right  ven- 
tricle is  explained  in  just  the  same  way  as  the  hypertrophy  of  the  left  ventricle 
in  mitral  insufficiency,  from  the  increased  influx  of  blood  at  increased  tension 
into  the  right  ventricle  during  diastole;  but  this  effect  of  tricuspid  insuffi- 
ciency can  rarely  be  made  out  in  any  individual  case,  since  the  right  ventricle 
is  usually  already  hypertrophied  as  a  result  of  the  disease  in  the  left  side  of 
the  heart. 

The  most  important  symptom  from  which  we  can  diagnosticate  tricuspid 
insufficiency  is  the  venous  pulse.  The  cause  of  this  is  the  backward  wave  of 
blood  produced  at  each  systole  of  the  right  ventricle.  So  long  as  the  venous 
valve  above  the  bulbus  jugularis  is  closed,  we  usually  see  only  a  "  bulbar 
pulse,"  but  very  soon  this  valve  also  yields  to  the  continued  impulse  of  the 
blood,  and  then  a  strong,  purely  venous  pulse  is  visible  along  the  whole  course 
of  the  jugular  vein  up  to  the  vicinity  of  the  mastoid  process.  The  contraction 
of  the  right  auricle  very  often  causes  a  decidedly  weaker  elevation  of  the  vein, 
which  just  precedes  the  marked  pulsation  caused  by  the  ventricular  systole 
(anadicrotic  venous  pulse).  On  account  of  the  straighter  course  of  the  right 
innominate  vein,  the  jugular  venous  pulse  is  often  stronger  on  the  right  side 
than  on  the  left.     We  must  state,  however,  that  the  jugular  venous  pulse  is 


VALVULAR   DISEASE   OF  THE   HEART  393 

not  an  absolutely  certain  sign  of  tricuspid  insufficiency,  sine"  it  may  arise  in 
hypertrophy  of  the  right  side  of  the  heart  without  any  insufficiency  of  the 
tricuspid   from  the  closure  of  the  valves. 

If  there  is  pulsation  in  the  bulb  of  the  jugular  vein  and  the  jugular  valve 
is  still  capable  of  closing,  a  low,  audible,  venous,  valvular  sound  may  be  pro- 
duced by  its  closure.  A  sound  may  also  arise  in  tricuspid  insufficiency,  as  has 
been  already  said,  from  the  tension  of  the  valves  in  the  femoral  vein.  A 
visible  pulsation  in  the  larger  veins  of  the  extremities  is  very  rare,  but  in 
tricuspid  insufficiency  we  quite  frequently  feel  a  venous  pulsation  in  the 
liver,  which  organ  is  usually  enlarged  by  passive  congestion.  This  may  be 
quite  apparent  even  in  many  cases  in  which  the  jugular  venous  pulse  is  absent, 
because  the  veins  in  the  liver  are  without  valves.  [It  is  best  appreciated  by 
means  of  bimanual  palpation.] 

Auscultation  over  the  right  side  of  the  heart  gives  a  systolic  murmur  in 
insufficiency  of  the  tricuspid,  arising  from  the  regurgitating  blood  current. 
This  may  be  heard  loudest  over  the  lower  part  of  the  sternum,  or  at  the 
sternal  end  of  the  right  fifth  rib.  The  significance  of  this  murmur  in  diagno- 
sis, however,  is  impaired  by  the  fact  that  it  cannot  always  be  separated  from 
the  systolic  mitral  murmur  that  often  coexists. 

6.  Stenosis  of  the  Tricuspid  Orifice. — Stenosis  of  the  tricuspid  orifice  is 
an  extremely  rare  disease,  and.  hence  it  is  without  practical  significance.  It 
has  usually  been  observed,  up  to  the  present  time,  as  a  congenital  form  of 
heart  disease,  almost  always  combined  with  other  anomalies  of  development 
in  the  heart. 

The  physical  signs  of  tricuspid  stenosis  can  easily  be  constructed  theoret- 
ically. The  first  result  must  be  a  marked  dilatation  of  the  right  auricle,  and 
the  occurrence  of  a  diastolic  or  presystolic  murmur  over  the  right  side  of  the 
heart.  From  the  rarity  and  complex  character  of  the  cases,  however,  we  have 
so  far  seldom  had  an  opportunity  to  confirm  these  theories  at  the  bedside. 

The  prognosis  of  this  form  of  heart  disease  is  very  unfavorable,  since  a 
long-continued  compensation  by  increased  labor  on  the  part  of  the  right  auri- 
cle is  scarcely  conceivable. 

[Seventy  cases  of  tricuspid  stenosis  have  been  collected  by  Bedford  Fen- 
wick,  whose  analysis  affords  good  grounds  for  thinking  that  the  lesion  is  often 
acquired.  In  fifty  per  cent  of  the  cases  there  was  a  clear  history  of  rheuma- 
tism, and  nearly  all  of  the  patients  were  more  than  twenty  years  of  age  at 
the  time  of  death. 

This  lesion  is  rarely  found  alone,  being  almost  invariably  combined  with 
mitral  stenosis ;  all  but  eight  of  the  cases  were  in  women.  Fenwick  thinks  that 
the  influence  of  sex  lies  in  the  less  onerous  nature  of  the  work  of  women  than 
of  men,  the  granulating  edges  of  the  valves  being  kept  more  in  apposition, 
thus  healing  with  adhesion  and  causing  obstructions  at  the  orifice.] 

7.  Insufficiency  of  the  Pulmonary  Valve. — Insufficiency  of  the  pulmonary 
valve  is  also  a  very  rare  form  of  heart  disease.  It  occurs  as  a  congenital  anom- 
aly, often  combined  with  other  failures  of  development,  or  as  a  disease 
acquired  after  birth.  The  anatomical  changes  in  the  valves,  which  lead  to 
insufficiency,  are  precisely  analogous  to  those  which  cause  insufficiency  of  the 
aortic  valve. 

The  physical  signs  of  this  form  of  valvular  disease  consist  chiefly  of  a 


394  DISEASES  OF  THE  CIRCULATORY  ORGANS 

marked  dilatation  and  hypertrophy  of  the  right  ventricle,  to  be  made  out  by 
percussion,  and  of  a  loud  diastolic  murmur  over  the  pulmonary  valve.  These 
signs  are  explained  in  just  the  same  way  as  the  precisely  analogous  signs  in 
the  left  ventricle  in  aortic  insufficiency. 

In  general,  pulmonary  insufficiency,  like  aortic  insufficiency,  seems  to  be 
compensated  quite  well  for  a  long  time  by  hypertrophy  of  the  right  ventricle. 
In  many  cases  a  coexisting  patency  of  the  foramen  ovale  also  seems  to  be  of 
favorable  influence,  as  it  lessens  the  stasis  in  the  right  auricle  and  the  veins 
of  the  body,  while  it  renders  easier  the  filling  of  the  left  ventricle. 

8.  Stenosis  of  the  Pulmonary  Orifice  (Pulmonary  Stenosis)  and  the  other 
Congenital  Diseases  of  the  Heart. —  (1)  Congenital  Pulmonary  Stenosis. 
— While  the  stenosis  of  the  pulmonary  orifice  acquired  in  later  life  is  so  rare 
that  it  has  only  slight  practical  significance,  the  congenital  pulmonary  stenosis 
is  of  far  greater  importance.  It  is,  on  the  whole,  the  most  frequent  of  the 
congenital  forms  of  heart  disease.  Its  origin  is  to  be  referred  either  to  an 
endocarditis  of  the  pulmonary  valves  during  fetal  life,  or  to  anomalies  in  the 
development  of  the  heart.  The  stenosis  is  often  situated  not  merely  at  the 
pulmonary  orifice  itself,  but  farther  back  in  the  conus  arteriosus,  which  seems 
to  be  narrowed  by  the  formation  of  myocardial  cicatrices.  The  pulmonary 
artery  is  often  also  narrowed  as  a  whole.  In  the  majority  of  cases  we  find,  in 
addition,  other  anomalies  of  development  in  the  heart,  especially  patency  of 
the  foramen  ovale,  great  defects  in  the  ventricular  septum,  and  in  about  half 
the  cases,  patency  of  the  ductus  Botalli,  etc. 

The  symptoms  of  congenital  pulmonary  stenosis  sometimes  appear  soon 
after  the  birth  of  the  child.  The  first  thing  that  strikes  us  is  the  marked 
cyanosis,  which  is  constant,  or  else  comes  on  with  crying,  or  with  movements 
of  the  body.  Many  children,  however,  reach  a  fair  age,  five  or  ten  years,  or 
even  fifteen.  In  some  cases  the  heart  disease  may  be  so  perfectly  compensated 
that  the  child  may  be  comparatively  well  for  a  time,  and  severe  disturbances 
may  not  appear  for  several  years. 

As  a  rule,  children  with  congenital  pulmonary  stenosis  present  a  very  strik- 
ing appearance.  The  cyanosis  is  especially  noticeable  in  the  face,  the  lips,  the 
nose,  and  the  hands  and  nails.  The  parts  mentioned  feel  cool.  The  eyes  are 
often  somewhat  prominent,  and  there  is  a  slight  cedematous  swelling  about 
them.  The  peculiar  club-like  thickening  of  the  terminal  phalanges  of  the 
fingers  and  toes,  a  result  of  stasis,  as  seen  also  in  many  cases  of  bronchiectasis, 
is  very  characteristic.  The  nails  also  present  a  characteristic  claw-like  curva- 
ture. 

The  whole  development  of  the  child  is  remarkably  retarded.  It  often 
seems  several  years  younger  than  it  is.  The  muscles  and  fatty  layer  are  slight. 
The  gums  are  sometimes  very  spongy  and  disposed  to  bleed.  In  severe  cases 
the  child  suffers  from  faintness,  vertigo,  etc. 

On  physical  examination  of  the  heart,  we  usually  find  the  cardiac  region 
rather  prominent.  Percussion  gives  an  increase  of  the  heart's  dullness,  espe- 
cially toward  the  right.  This  extension  of  the  dullness  is  due  to  the  hyper- 
trophy of  the  right  ventricle,  which  must  arise  in  the  same  way  as  hypertrophy 
of  the  left  ventricle  in  aortic  stenosis..  On  auscultation,  we  hear  a  loud  sys- 
tolic murmur,  which  is  perceptible  over  the  whole  heart,  but  which  has  its 
greatest  intensity  at  the  sternal  end  of  the  second  left  intercostal  space.     The 


VALVULAR  DISEASE   OF  THE   HEART  395 

eddies  of  blood,  which  produce  the  murmur,  may  also  often  be  felt  by  the 
hand  as  a  systolic  thrill.  In  some  cases,  however,  we  miss  the  murmur  in 
pulmonary  stenosis,  just  as  in  mitral  stenosis.  The  pulmonic  second  sound 
is  weak  or  inaudible,  or  it  is  replaced  by  a  murmur  if  there  is  also  insuffi- 
ciency of  the  valves. 

The  course  of  congenital  pulmonary  stenosis  is  always  unfavorahle.  As  has 
been  implied,  few  children  get  beyond  the  age  of  fifteen  years.  Death  ensues, 
either  with  general  disturbances  of  compensation  evidenced  by  dyspnoea  and 
dropsy,  as  in  every  other  form  of  heart  disease,  or  from  complications.  Among 
the  latter,  we  may  mention  especially  phthisis,  which,  probably  because  of  the 
deficient  blood  supply,  strikingly  often  develops  in  children  with  congenital 
pulmonary  stenosis. 

(2)  The  Kemaining  Congenital  Lesions  of  the  Heart. — Inasmuch 
as  other  congenital  lesions  than  pulmonary  stenosis  have  but  slight  clinical 
importance,  we  will  limit  ourselves  here  to  a  brief  review  of  the  same.1 

(a)  Patency  of  the  foramen  ovale  is  a  comparatively  frequent  lesion, 
whether  alone  or  combined  with  others.  Physical  signs  are  mostly  absent.  In 
a  few  cases  a  presystolic  murmur  has  been  heard.  When  mitral  insufficiency 
coexists  with  a  patent  foramen  ovale,  venous  pulsation  may  be  caused. 

(b)  Defects  in  the  septum  between  the  ventricles.  These  are  most  fre- 
quently situated  in  the  posterior  section  of  the  anterior  septum,  and  they  like- 
wise are  associated  with  other  anomalies,  such  as  abnormal  distribution  of  the 
arteries,  pulmonary  stenosis,  or  defects  in  the  septum  between  the  auricles. 
Sometimes  the  patency  of  the  septum  gives  rise  to  a  systolic  murmur,  but  a 
diagnosis  of  the  condition  during  life  is  scarcely  ever  possible. 

(c)  Persistence  of  the  ductus  Botalli.  Inasmuch  as  this  contributes  blood 
from  the  aorta  to  the  pulmonary  circulation  the  pressure  in  the  latter  is  raised, 
hence  there  is  to  be  observed  accentuation  of  the  second  pulmonic  sound  and 
hypertrophy  of  the  right  ventricle.  There  is  sometimes  also  a  loud  systolic 
murmur. 

(d)  We  have  already  spoken  of  congenital  stenosis  of  the  tricuspid  valve. 
Congenital  narrowing  of  the  mitral  valve  and  of  the  aortic  valves  may  also 
occur,  but  they  are  extremely  rare. 

9.  Combined  Valvular  Diseases  of  the  Heart. — Although  in  what  has  pre- 
ceded we  have  dealt  with  the  several  forms  of  valvular  disease  of  the  heart 
separately,  in  order  to  present  them  in  a  general  way,  yet  in  reality  combina- 
tions of  them  often  occur  in  great  variety.  We  find  especially,  as  has  already 
been  mentioned,  stenosis  of  an  orifice  coexisting  with  insufficiency  of  the 
accompanying  valve;  but  diseases  of  two  or  more  different  valves  are  not 
infrequent,  combined  in  the  most  diverse  manners.  The  physical  signs  of  these 
"  combined  forms  of  heart  disease "  may,  of  course,  be  inferred  from  the 
signs  of  anomalies  of  single  valves,  but  the  phenomena  are  often  so  compli- 
cated that  the  diagnosis  of  combined  heart  disease  is  generally  much  harder 
than  that  of  the  simple  forms.  Sometimes  the  single  forms  neutralize  one 
another  in  their  action.  For  example,  the  left  ventricle  is  usually  small  in 
pure  mitral  stenosis,  but,  if  aortic  insufficiency  be  also  present,  it  is  neverthe- 

1  A  more  extensive  presentation  of  the  subject  can  be  found  in  the  article  by  Rauchfuss  in  Ger- 
hardt's  "  Hand buch  der  Kinderkrankheiten, "  vol.  ivT  and  in  text-books  on  pathological  anatomy 
■ — for  example,  Orth's, 


396 


DISEASES  OF  THE  CIRCULATORY  ORGANS 


General    Comparison    of   the    Most    Important    Physical   Signs    in    Valvular 

Disease  op  the  Heart 


FOBM  OP 

Heart  Disease. 

Inspection. 

Palpation. 

Percussion. 

Auscultation. 

1.  Mitral  in- 

Strong apex  beat, 

Systolic  thrill  at 

Hypertrophy    of 

Loud   systolic  murmur 

sufficiency. 

often  somewhat 

the  apex.  Quite 

the   left,   later 

at     the    apex.     Pul- 

displaced      out- 

strong      radial 

of    the    right, 

monic  second   sound 

ward. 

pulse. 

ventricle. 

accentuated. 

2.  Mitral 

Area  of  cardiac  im- 

Diastolic     thrill 

Hypertrophy    of 

Diastolic       or    presys- 

stenosis. 

pulse     enlarged, 

at     the     apex. 

the  right  ven- 

tolic murmur  at  the 

epigastric  pulsa- 

Small   and    of- 

tricle. 

apex.       First    sound 

tion. 

ten       irregular 
pulse. 

sometimes  loud.  Pul- 
monic second  sound 
accentuated,  and 
sometimes  double. 

3.  Aortic  in- 

Apex    beat    very 

Very   strong, 

Marked      hyper- 

Loud   diastolic    aortic 

sufficiency. 

strong,  displaced 

heaving     apex 

trophy    of   the 

murmur,     especially 

downward     and 

beat.        Pulsus 

left  ventricle. 

over  the  upper  part 

to  the  left.    Vis- 

celer. 

of        the       sternum. 

ible  pulsation  of 

Sounds     in    the    ar- 

the     medium- 

teries    (femoral    and 

sized  and  smaller 

brachial  sounds,  etc.). 

arteries. 

Sometimes  a  double 
sound  or  double  mur- 
mur in  the  femoral. 

4.  Aortic 

Apex     beat     dis- 

Heart's     action 

Hypertrophy    of 

Loud     systolic    aortic 

stenosis. 

placed     to     the 

not  very  strong. 

the    left    ven- 

murmur, transmitted 

left. 

Pulse  small,  in- 
frequent, some- 
times slow. 

tricle. 

to  the  right. 

less  found  dilated,  at  least  to  a  certain  degree.  The  influence  of  an  absolute 
or  relative  tricuspid  insufficiency  on  the  action  of  mitral  disease,  especially 
the  decrease  in  tension  in  the  pulmonary  vessels  caused  by  it,  and  also  the 
diminished  accentuation  of  the  pulmonic  sound,  have  been  mentioned  above. 

In  reference  to  the  clinical  symptoms  of  combined  heart  disease  we  may 
say,  on  the  whole,  that,  in  a  large  number  of  cases,  the  disease  of  one  valve 
stands  out  as  predominant  in  the  whole  picture  of  the  disease.  The  other 
anomalies  are  only  slightly  noticeable,  and  often  of  later  date.  Hence,  we 
may  find  at  the  autopsies  of  patients,  who  during  life  have  shown  the  symp- 
toms of  disease  of  only  one  particular  valve,  unimportant  changes  on  the  other 
valves,  which  have  been  without  clinical  significance. 

[Bramwell  reports  that  of  131  cases  with  macroscopic  valvular  lesion,  the 
tricuspid  was  implicated  in  33.58  per  cent:  in  all  but  12  per  cent  of  these  the 
changes  were  recent.  Hence  he  thinks  that  tricuspid  endocarditis  is  generally 
recovered  from,  and  this  he  attributes  to  the  relatively  small  strain  to  which 
that  valve  is  subjected.  The  obvious  therapeutic  deduction  is  the  importance 
of  rest  in  mitral  endocarditis.] 


GENERAL   SEQUELS   AND   COMPLICATIONS   OF  VALVULAR 

DISEASE   OF  THE    HEART— SUBJECTIVE  SYMPTOMS 

—SEQUELAE   IN   THE   HEART   ITSELF 

After  having  discussed,  in  what  precedes,  the  mechanism  of  the  single 
forms  of  valvular  disease,  and  the  physical  signs  derived  from  it,  we  must  now 
describe  a  number  of  symptoms  and  sequelae  which  may  be  present  to  a  greater 


VALVULAR   DISEASE  OF  THE   lll,\l;'l  397 

or  less  degree  in  all  forms  of  valvular  disease.     With  them  we  musl  also  men- 
tion certain  peculiarities  of  the  individual  forms. 

1.  Subjective  Symptoms. —  Fully  compensated  heart  disease  may  exist,  at 
least  for  a  long  time,  without  any  subjective  symptoms.  This  is  especially  the 
case  in  aortic  insufficiency,  more  rarely  in  mitral  insufficiency.  Stenosis  of  the 
mitral  or  of  the  aortic  valves  almost  always  causes  subjective  symptoms. 
These  symptoms  often  do  not  exist  so  long  as  the  patienl  keeps  perfectly  quiel 
physically  and  mentally,  but  they  develop  under  appropriate  circumstances, 
especially  upon  bodily  exertion. 

The  existing  subjective  symptoms  in  heart  disease  are  by  no  means  always 
referred,  in  the  first  place,  to  the  heart  itself.  It  sometime.--  happens  thai  the 
patient  comes  to  the  physician  complaining  of  various  digestive  disturban 
or  in  other  cases  of  headache,  vertigo,  etc.  The  physical  examination  alone 
leads  us  to  recognize  the  heart  disease.  As  a  rule,  the  patient's  first  and  chief 
complaint  is  directed  toward  his  difficulty  in  breathing.  The  shortness  of 
breath,  which  increases  on  any  physical  exertion,  comes  on  quite  early  in  many 
cases.  In  the  later  stages  it  is  almost  always  the  mosl  distressing  symptom. 
The  causes  of  dyspnoea  in  heart  disease  are  manifold.  In  the  first  place 
dyspnoea  results  from  congestion  of  the  pulmonary  circuit,  with  consequent 
slowing  of  the  circulation  in  the  lungs,  and  limitation  of  the  exchange  of  gases 
in  those  organs.  In  later  stages  the  anatomical  changes  in  the  lungs  contribute 
also  to  an  increase  of  the  dyspnoea  (vide  supra,  the  chapter  on  Brown  Indura- 
tion of  the  Lungs).  Basch  ascribes  special  importance  to  the  fact  that  the 
distended  capillaries  encroach  upon  the  alveoli  as  a  result  of  the  passive  con- 
gestion. This  broadens  the  alveoli  ("swelling  of  the  lungs"),  but  at  the 
same  time  impairs  the  mobility  of  the  lungs  ("rigidity  of  the  lungs"),  and 
thus  embarrasses  the  exchange  of  gases  in  the  lungs,  just  as  in  emphysema. 
The  occurrence  of  the  "  rigidity  of  the  lungs  "  is  to  be  admitted ;  but  I  cannot 
admit  a  "  swelling  of  the  lungs  "  according  to  Basch' s  ideas.  In  microscopic 
preparations  of  lungs  affected  by  passive  congestion  I  find  the  alveolar  spaces 
diminished  rather  than  enlarged. 

The  secondary  bronchitis  of  heart  disease  is  a  very  great  factor  in  the  dysp- 
noea. This  bronchitis  is  a  frequent  result  of  the  pulmonary  stasis.  Often  the 
respiratory  distress  increases  and  decreases  simultaneously  with  corresponding 
variations  in  the  bronchitis.  A  purely  mechanical  cause  of  dyspnoea  is  the 
compression  of  the  lower  portion  of  the  left  lung  by  great  cardiac  hypertrophy. 
The  highest  grade  of  dyspnoea  is  reached  when  finally  hydrothorax,  hydroperi- 
cardium,  and  pulmonary  oedema  are  developed.  From  what  has  already  been 
stated,  it  is  easy  to  see  why  lesions  of  the  mitral  valve  which  directly  impair  the 
pulmonary  circulation  lead  sooner  to  shortness  of  breath  than  do  lesions  of  the 
aortic  valves.  Finally,  it  is  self-evident  that  the  condition  of  the  heart  has 
the  greatest  influence  upon  the  degree  of  dyspnoea  present,  for  all  the  phenom- 
ena of  pulmonary  congestion  must  increase  or  diminish,  according  to  the  func- 
tional integrity  of  the  heart,  and  particularly  of  the  left  ventricle.  If  the 
contractile  power  of  the  left  ventricle  grows  less,  dyspnoea  must  at  once  in- 
crease. Not  infrequently  conditions  of  cardiac  weakness  develop  with  consid- 
erable suddenness,  and  occasion  attacks  of  dyspnoea  which  are  termed  cardiac 
asthma.  At  the  same  time  the  enfeeblement  of  the  left  ventricle  often  leads 
to  a  transient  stasis  of  the  pulmonary  vessels,  and,  as  a  consequence  thereof, 


398  DISEASES   OF  THE   CIRCULATORY   ORGANS 

to  a  congestive  transudation  into  the  bronchi.  The  patients  feel  impelled  to 
cough  and  expectorate  small  or  even  large  quantities  of  a  serous  or  sero- 
sanguineous  sputum. 

Palpitation  is  the  first  subjective  symptom  to  be  mentioned  of  those  which 
are  referred  directly  to  the  heart.  It  is  not  yet  accurately  determined  under 
what  circumstances  the  action  of  the  heart  is  perceived  by  the  patient  himself. 
We  sometimes  see  an  uncommonly  strong  action  of  the  heart,  as  in  aortic 
insufficiency,  which  is  not  perceived  at  all  subjectively.  In  other  cases,  where 
objectively  the  heart  is  not  especially  active,  palpitation  forms  the  patient's 
chief  complaint.  It  usually  first  appears  when  the  heart  disease  ceases  to  be 
fully  compensated.  It  is  increased  or  first  excited  by  physical  exertion  or  men- 
tal excitement.  In  many  patients  attacks  of  palpitation  occur  without  any  dis- 
coverable external  cause,  due  apparently  to  nervous  disturbance.  They  are 
sometimes  associated  with  a  striking  acceleration  of  the  pulse,  the  so-called 
tachycardia. 

Pain  in  the  cardiac  region  is  only  rarely  present  in  heart  disease.  The 
patients  more  frequently  complain  of  an  indefinite  feeling  of  pressure  and 
oppression  in  the  chest,  but  still  there  do  occur,  particularly  in  aortic  insuffi- 
ciency, attacks  of  violent  pain  in  the  front  part  of  the  chest  and  the  region 
of  the  heart,  radiating  to  the  shoulders  and  arms,  and  associated  with  a  general 
feeling  of  extreme  anxiety  and  weakness.  Such  conditions  are  termed  angina 
pectoris,  or  attacks  of  stenocardia.  They  are  probably  generally  dependent 
upon  the  coexisting  aortic  sclerosis  (vide  infra).  Pains  in  the  epigastrium 
and  abdomen,  which  sometimes  form  the  chief  annoyance  of  the  patient,  usu- 
ally depend  upon  passive  congestion  of  the  liver  (vide  infra),  or  upon  the 
tension  of  the  abdominal  walls  from  ascites,  oedema,  etc. 

We  must  finally  mention  here  the  rheumatoid  pains  in  the  joints  and  mus- 
cles, from  which  many  patients  with  heart  disease  suffer. 

The  greatest  subjective  distress  occurs  in  the  last  stages  of  heart  disease, 
when  general  dropsy  develops.  The  patient's  helplessness  then  usually  culmi- 
nates. All  motions  of  the  body  are  difficult,  the  dyspnoea  and  oppression  in 
the  chest  constantly  increase,  until  death  finally  releases  the  patient  from  his 
mournful  condition. 

2.  Sequelae  in  the  Heart  Itself. — We  have  already  discussed  the  most  impor- 
tant sequela?  of  valvular  disease  in  the  heart  itself,  its  hypertrophies  and  dilata- 
tions. It  remains  for  us  to  describe  the  influence  of  the  cardiac  disease  on  the 
frequency  and  regularity  of  the  lieart's  action,  and  also  to  discuss  some  sec- 
ondary diseases  of  the  cardiac  muscle  and  of  the  pericardium. 

In  every  well-compensated  heart  disease  the  heart's  action  may  for  a  long 
time  be  of  approximately  normal  frequency  and  regularity.  We  often  find  a 
constant  and  moderate  acceleration  of  the  pulse,  which  is  easily  increased 
from  temporary  causes.  Diminution  of  the  pulse  rate  (bradycardia)  is  ex- 
ceptional in  valvular  heart  disease,  except  when  it  is  artificially  caused  by 
large  doses  of  digitalis.  It  is  most  frequent  in  aortic  stenosis.  Marked 
changes  in  the  rate  of  the  pulse  are  due  to  severe  disturbances  of  the  nervous 
apparatus  of  the  heart,  and  hence  they  are  often  associated  with  arrhythmia. 
Under  such  circumstances,  the  pulse  rate  may  be  as  high  as  120  to  140  beats 
per  minute.  A  rare  but  interesting  symptom  is  the  sudden  onset  of  attacks 
of  enormous  rapidity  of  the  pulse,  up  to  160  to  200  beats  and  more  (tachy- 


VALVULAR   DISEASE  OF  THE   HEART 

cardia).  This  is  especially  connecter]  with  mitral  lesions.  In  the  inlervalfi  the 
action  of  the  heart  is  quiet,  with  approximately  complete  compensation  of  the 
cardiac  lesion.  The  acceleration  of  the  pulse  occurs  rather  suddenly,  and  if 
usually  associated  with  a  subjective  sensation  of  palpitation  and  distress.  It 
may  last  several  hours  and  then  vanish,  usually  with  the  same  suddenness.  The 
exact  cause  of  these  attacks  is  unknown.  They  suggesl  a  temporary  paralysis  of 
the  inhibitory  apparatus  of  the  heart.  Sometimes  a  well-marked  acute  dilata- 
tion may  he  demonstrated  by  percussion  during  the  attack  of  tachycardia. 

Arrhythmia  of  the  heart  is  of  still  greater  importance  than  anomalies  of  (he 
pulse  frequency.  It  always  points  to  a  severe  disturbance  of  the  heart  muscle 
(vide  infra),  and  perhaps,  too,  of  the  nervous  apparatus  of  the  heart.  In 
many  cases  the  arrhythmia  is  the  direct  result  of  a  simultaneous  chronic  myo- 
carditis. But  in  addition  to  this,  the  general  disturbance  of  the  circulation 
in  consequence  of  the  valvular  defect  must,  of  course,  make  itself  evident  in 
the  heart  itself,  and  the  musculature  as  well  as  the  nerves  and  ganglia  of  the 
heart  cannot  remain  unaffected  by  these  circulatory  disturbances.  Hence  we 
generally  see  marked  variations  in  the  frequency  and  rhythm  of  the  heart's 
action  along  with  the  other  signs  of  beginning  disturbance  of  compensation  ; 
but  daily  clinical  experience  teaches  us  that  there  is  not  a  perfect  parallelism 
between  the  two  symptoms.  We  find  often  enough  in  heart  disease  a  consid- 
erable irregularity  of  the  pulse  without  any  of  the  other  signs  of  marked  dis- 
turbance of  compensation,  and,  on  the  other  hand,  we  see  in  many  patients 
an  almost  perfect  regularity  of  the  pulse  up  to  death.  In  mitral  disease, 
especially  in  mitral  stenosis,  arrhythmia  of  the  heart  is  much  more  frequent 
than  in  aortic  disease. 

Recent  experimental  investigations  have  resulted  in  interesting  disclo- 
sures relative  to  the  causes  of  irregularities  in  the  action  of  the  heart.  Every 
contraction  of  the  heart  begins  at  the  point  of  entrance  of  the  veins  into  the 
auricles,  and  is  then  transmitted  to  the  auricles.  From  the  auricles  the  stimu- 
lus is  transmitted  to  the  ventricles,  probably  by  means  of  a  bundle  of  muscle, 
situated  in  the  auriculo- ventricular  septum  (the  so-called  bundle  of  His). 
Now,  irregularities  in  cardiac  activity  are  often  due  to  abnormal  stimuli  origi- 
nating in  the  ventricle  itself  (and,  also,  but  more  rarely,  in  the  auricles)  that 
cause  contractions  which  are  intercalated  between  those  normally  excited 
from  the  auricle  (so-called  extra  systoles).  After  such  an  extra  systole,  the 
next  normal  ventricular  systole  is  often  miss- 
ing, for  the  auricular  stimulus  then  strikes  the 
ventricular  musculature  at  a  time  when,  by 
reason  of  the  preceding  contraction,  it  is  unre- 
sponsive (the  so-called  refractory  phase).  Thus 
long  pauses  result  (intermittency  of  the  pulse). 
If  we  now  auscultate  the  heart  and  at  the  same 
time  feel  the  pulse,  we  can,  as  a  rule,  hear  the 

muscular  tone  excited  by  the  extra  systole,  but  perceive  no  pulse  beat  at  the 
radial,  although  it  can  be  demonstrated  sphygmographically  as  a  slight  ele- 
vation. We  feel,  therefore,  but  one  pulse  beat  to  every  three  or  four  heart 
sounds  (so-called  inefficient  heart  contractions).  But  not  infrequently,  after 
the  first  greater  pulse  wave,  a  second  and  smaller  one  can  be  distinctly  felt 
(bigeminal  pulse,  vide  Fig.  64).     Occasionally,  and  more  particularly,  as  a 


400  DISEASES  OF  THE  CIRCULATORY  ORGANS 

result  of  the  action  of  digitalis,  the  entire  heart  function  may  assume  the 
bigeminal  form  for  a  protracted  period;  while,  on  the  other  hand,  there  may 
often  be  an  isolated  bigeminal  pulse  wave  at  varying  intervals  in  many  forms 
of  cardiac  irregularity.  Besides  the  occurrence  of  extra  systoles,  various  other 
disturbances  may  interrupt  the  regular  mechanism  of  the  heart  action.  The 
most  frequent  are  the  so-called  transmission  disturbances — i.  e.,  disturbances 
in  the  normal  transmission  of  the  stimulus  from  the  auricles  to  the  ventricles 
(vide  infra,  chapter  on  Myocarditis).  As  a  result  of  these,  there  is  a  com- 
plete dissociation  of  the  auricles  and  ventricles,  so  that  the  number  of  auricu- 
lar contractions  (best  observed  by  the  number  of  visible  beats  of  the  jugular 
vein)  differs  materially  from  that  of  the  ventricular  contractions.  Perhaps, 
too,  disturbances  in  the  simultaneousness,  strength,  and  number  of  the  con- 
tractions of  the  two  sides  of  the  heart  may  occur.  In  short,  we  see  how  com- 
plicated and  difficult  is  the  correct  interpretation  of  all  existing  irregularities 
in  heart  function,  and  how  each  individual  case  can  be  explained  only  by  thor- 
ough study  of  the  heart  contractions  and  the  arterial  and  venous  pulse. 

Chronic  valvular  disease  of  the  heart  is  often  combined  with  anatomical 
changes  in  the  cardiac  muscle,  and  sometimes  in  the  pericardium. 

Among  the  changes  in  the  cardiac  muscle,  cloudy  swelling,  and  especially 
fatty  degeneration  of  the  muscular  fibers,  are  the  most  frequent.  The  fatty 
degeneration  of  the  muscle  occurs  either  in  a  diffuse  form,  or  in  little  yellow- 
ish spots,  which  are  plainly  visible  on  the  papillary  muscles  and  trabecule.  The 
opinion  has  often  been  expressed  that  fatty  degeneration  of  the  muscles  is  the 
cause  of  the  disturbance  of  compensation;  that  the  cardiac  muscle  performs 
its  increased  work  until  fatty  degeneration  ensues  and  reduces  its  strength. 
This  theory  does  not  entirely  correspond  to  the  facts.  We  have  often  seen  the 
greatest  disturbance  of  compensation  in  valvular  disease  when  section  of  the 
cardiac  muscle  showed  no  fatty  degeneration;  and,  on  the  other  hand,  we 
have  seen  great  fatty  degeneration  of  the  heart,  as  in  pernicious  anaemia,  when 
there  were  no  signs  of  cardiac  weakness  during  life.  Anatomically,  with  our 
present  aids  to  research,  we  can  hardly  ever  decide  with  certainty  whether  the 
cardiac  muscle  is  still  capable  of  performing  its  normal  functions  or  not. 
The  usual  state  of  the  case  is  probably  this,  that  fatty  degeneration  of  the  car- 
diac muscle  is  a  result  of  the  disturbance  of  compensation,  and  especially  of 
incomplete  combustion  of  the  deposited  fats  because  of  the  defective  supply  of 
arterial  blood  and  the  aiminished  muscular  activity. 

There  is  as  truly  a  passive  congestion  of  the  heart  as  there  is  a  passive  con- 
gestion of  the  liver  and  kidneys.  The  circulatory  disturbance  in  the  heart 
itself  is  the  chief  cause  of  cardiac  insufficiency,  and  of  the  phenomena  of  dis- 
turbed compensation. 

A  frequent  affection  of  the  cardiac  muscle  in  valvular  disease  is  the  pres- 
ence of  cicatricial  changes  and  so-called  myocarditic  nodules  in  the  substance 
of  the  heart.  Chronic  endocarditis  may  directly  invade  the  subjacent  parts  of 
the  cardiac  muscle  and  set  up  a  chronic  inflammation  there,  but  the  cardiac  cica- 
trices usually  have  another  origin.  The  connective-tissue  thickening  beneath 
the  endocardium  is  the. result  of  a  simple  atrophy  of  the  superficial  muscular 
fibers  due  to  the  increased  internal  pressure  of  the  blood,  as  in  mitral  or  aortic 
insufficiency.  The  connective-tissue  nodules  within  the  cardiac  muscle,  how- 
ever, depend  in  part  upon  a  deficiency  in  the  local  supply  of  arterial  blood. 


VALVUI.AII  disease  of  the  heart  401 

Simple  sclerotic  thickening  of  the  coronary  arteries,  or  complete  embolism  or 
thrombosis  of  a  small  branch  of  one  of  them,  is  the  evidenl  cause  of  these  cir- 
cumscribed cicatrices.  On  the  other  hand,  it  is  also  probable  thai  disease  of 
the  myocardium  is  associated  with  the  endocarditis,  and  is  referable  to  the 
simultaneous  action  of  the  same  causes,  such  as  the  infection  of  articular 
rheumatism,  diphtheria,  and  syphilis.  On  careful  microscopic  examination 
we  find,  in  almost  all  cases  of  valvular  disease,  quite  extensive  changes  in  the 
myocardium  (Krehj),  and  in  many  cases  these  may  certainly  impair  the 
functional  powers  of  the  heart.  Still,  we  often  find  cicatrices  of  myocarditis 
without  any  signs  of  a  previous  disturbance  in  the  compensation  of  the  heart. 
A  fuller  discussion  of  this  subject  will  be  found  in  the  next  chapter. 

Pericarditis  is  not  very  rare  as  a  result  of  chronic  valvular  disease.  It  is 
always  a  dangerous  complication,  and  it  may  cause  death.  Regarding  its  ori- 
gin, we  have  found  that  almost  all  the  cases  of  heart  disease  complicated  with 
pericarditis  show  changes  in  the  aortic  valves.  Hence  it  does  not  seem  im- 
probable to  us  that  the  secondary  pericarditis  in  such  cases  is  sometimes  due 
to  a  direct  invasion  of  the  pericardium,  by  the  excitants  of  inflammation  pass- 
ing from  the  aortic  valves  through  the  walls  of  the  blood  vessel.  On  the  other 
hand,  the  pericarditis  may  be  due  to  the  introduction  of  excitants  of  inflam- 
mation via  the  blood  current. 

3.  Symptoms  of  Stasis  in  the  Different  Organs  of  the  Body. — As  has  fre- 
quently been  mentioned  in  what  precedes,  the  results  of  stasis  of  the  blood 
make  themselves  manifest  in  heart  disease  in  various  organs.  We  have 
already  spoken  of  the  important  results  of  blood  stasis  in  the  heart  itself  and 
the  lungs.  It  remains  for  us  to  discuss  the  symptoms  of  stasis  in  the  systemic- 
veins. 

As  soon  as  the  flow  of  venous  blood  into  the  right  side  of  the  heart  is  hin- 
dered, the  venous  stasis  is  shown  by  the  cyanotic  appearance  of  the  patient. 
This  cyanosis  may  exhibit  any  degree.  In  heart  disease,  which  is  still,  on  the 
whole,  well  compensated,  it  is  recognized  only  by  the  practiced  eye  of  the 
physician  as  a  slight  bluish  tinge  of  the  lips,  the  alas  of  the  nose,  the  cheeks, 
or  the  nails.  With  the  increase  of  the  disturbance  of  compensation  the  cyano- 
sis increases,  if  it  be  not  modified  by  the  coexistence  of  general  ansernia.  In 
mitral  disease,  especially  in  mitral  stenosis,  the  cyanosis  is  usually  more 
marked  than  in  aortic  disease.  The  large  veins,  also,  become  plainly  visible 
as  a  result  of  their  complete  filling,  especially  the  large  external  jugulars. 

A  further  important  symptom  which  follows  the  venous  stasis  is  the 
oedema,  the  dropsy  of  heart  disease.  As  we  know  from  general  pathology, 
venous  stasis,  if  it  reaches  a  certain  grade,  always  leads  to  a  transudation  of 
the  fluid  of  the  blood  from  the  capillaries.  If  the  lymphatics  can  no  longer 
carry  this  transudation  away,  it  collects  in  the  meshes  of  the  tissues  and  leads 
to  oedema.  The  oedema  of  heart  disease,  therefore,  does  not  appear  until  the 
venous  stasis  has  reached  a  certain  degree,  and  the  compensation  of  the  heart 
disease  has  become  impaired.  It  first  appears  in  those  parts  where  there  is  a 
particularly  loose  tissue,  as  in  the  scrotum,  or  where  mechanical  conditions 
favor  its  development.  The  legs  usually  swell  first,  especially  about  the 
ankles,  because  here  the  stasis  of  the  venous  blood  is  increased  by  gravity. 
At  first,  slight  oedema  appears  only  temporarily  and  by  day,  and  disappears 
again  while  the  patient  is  in  bed  at  night;  but,  as  the  disturbance  of  com- 


402  DISEASES   OF  THE   CIRCULATORY   ORGANS 

pensation  increases,  the  oedema  also  constantly  grows  worse,  especially  in  the 
dependent  parts  of  the  body,  until  finally  it  may  reach  the  highest  degree  of 
dropsy.  Besides  the  oedema  of  the  skin,  transudations  into  the  internal  cavities 
occur,  especially  into  the  abdomen  and  the  pleural  cavity. 

The  relation  between  the  degree  of  cutaneous  oedema  and  the  amount  of 
dropsical  transudation  is  variable;  thus,  in  particular,  we  may  have  a  large 
amount  of  ascites,  with  only  moderate  swelling  of  the  legs.  This  is  probably 
occasioned  in  most  cases  by  special  secondary  changes  in  the  liver  (vide 
infra).  In  other  cases  the  serous  exudate,  on  one  or  both  sides  of  the  pleural 
cavity  (hydrothorax),  becomes  especially  prominent.  In  short,  besides  the 
general  circulatory  disturbances,  local  factors  (especially  the  local  condition 
of  the  vascular  walls)  appear  sometimes  to  play  a  role.  How  important  a  bear- 
ing the  condition  of  the  blood  vessels  (aside  from  the  circulatory  disturbance) 
has  upon  the  appearance  of  oedema  is  best  seen  when  we  compare  the  occur- 
rence of  oedema  in  different  forms  of  heart  disease.  How  often  have  I  seen 
juvenile  cases  of  heart  trouble  with  agonizing  dyspnoea,  cyanosis,  hepatic  stasis, 
etc.,  but  with  absolutely  no  oedema  of  the  skin,  evidently  because  the  blood 
vessels  were  still  "  tight."  On  the  other  hand,  oedema  appears  very  early  and 
to  a  striking  degree  and  extent  in  older  or  otherwise  predisposed  cardiac 
patients. 

The  patient's  distress  is  decidedly  increased  by  marked  oedema,  as  has 
already  been  said.  All  the  motions  of  the  swollen  extremities  are  consider- 
ably impeded.  Hydrothorax  and  ascites  increase  the  dyspnoea,  the  former  by 
compression  of  the  lungs,  the  latter  by  upward  pressure  on  the  diaphragm. 
The  passage  of  urine  may  be  rendered  very  difficult  by  oedema  of  the  prepuce. 
Besides  that,  we  must  mention  that  the  skin,  when  very  oedematous,  is  quite 
apt  to  become  the  seat  of  furuncular  and  erysipelatous  inflammations. 

The  results  of  stasis  in  the  internal  organs  may  be  best  seen  in  the  liver, 
spleen,  and  kidneys. 

Passive  congestion  of  the  liver  is  manifested  by  quite  a  considerable  in- 
crease in  the  size  of  the  organ.  The  lower  boundary  of  the  liver  dullness 
extends  several  fingers'  breadth  beyond  the  edge  of  the  ribs,  and  the  anterior 
surface  and  lower  border  of  the  liver  may  often  be  plainly  felt.  The  liver  may 
also  be  enlarged  in  cases  in  which  there  are  no  other  marked  signs  of  passive 
congestion,  such  as  dropsy.  Quite  severe  pain  in  the  hepatic  region  sometimes 
arises  from  the  tension  of  the  capsule  of  the  liver.  In  later  stages  the  liver 
may  grow  smaller  again  through  a  partial  atrophy  of  the  liver  cells  (atrophic 
nutmeg  liver).  Indeed,  there  may  even  develop,  as  a  result  of  the  chronic 
congestion,  a  secondary  cirrhosis  of  the  liver,  with  a  distinctly  granulated 
surface.  These  are  the  cases  in  which  marked  ascites  is  especially  apt  to  occur 
(vide  supra),  sometimes  with  almost  entire  absence  of  oedema  of  the  lower 
extremities. 

Slight  jaundice  often  develops  in  heart  disease,  as  a  result  of  passive  con- 
gestion of  the  liver,  or  perhaps  sometimes  from  a  secondary  duodenal  catarrh. 
The  peculiar  mixture  of  a  cyanotic  and  slightly  jaundiced  hue  of  the  skin  is 
very  characteristic  in  many  cases,  especially  in  mitral  disease.  It  should  be 
added  that  the  yellowish  discoloration  of  the  skin  in  heart  disease  is  probably 
not  always  a  genuine  icterus,  but  it  may  be  occasioned  by  the  deposit  of  other 
pigments  in  the  skin. 


VALVULAR  DISEASE  OF  THE   HEART  103 

Passive  congestion  of  the  spleen  arises  if  the  stasis  of  the  blood  extends  to 
the  splenic  vein.  The  spleen  increases  in  size  and  becomes  firm  and  dense. 
It  is  often  hard  to  make  out  the  congestion  from  the  increase  of  the  splenic 
dullness,  because  percussion  of  ilie  spleen  is  uncertain  if  there  be  also  ascites, 
hydrothorax,  etc.  We  can  often,  however,  plainly  feel  the  enlarged  spleen 
under  the  edge  of  the  ribs  on  the  left. 

In  passive  congestion  of  the  kidneys,  the  slowness  of  the  circulation  and  the 
diminution  of  the  arterial  tension  in  these  organs  lead  to  marked  changes  in 
the  urine.  In  particular,  there  is  a  diminution  in  the  quantity,  especially  if 
the  patient  is  at  the  same  time  dropsical.  The  amount  of  urine  falls  as  low- 
as  800  to  500  c.c.  (27  to  17  ounces),  or  even  less,  in  twenty-four  hours.  If 
becomes  dark,  concentrated,  of  high  specific  gravity,  and  abnormally  acid,  and 
hence  it  usually  has  an  abundant  sediment  of  urate  of  sodium.  In  marked 
degrees  of  stasis  there  is  albumen  in  the  urine  as  a  result  of  the  damage  done 
to  the  glomerular  epithelium.  The  amount  of  albumen  is  usually  slight,  but 
it  may  equal  one  third  or  one  fourth  of  the  volume  of  urine.  Under  the 
microscope  we  find,  in  the  urine  of  simple  passive  congestion,  only  an  occa- 
sional hyaline  cast,  and  a  few  red  and  white  blood  corpuscles. 

If  renal  stasis  continues  for  a  long  time,  permanent  sequelae  develop  in  the 
kidneys;  these  may  be  termed,  "cyanotic  induration,"  or,  finally,  "congested 
contracted  kidney."  By  reason  of  the  defective  blood  supply,  the  renal  paren- 
chyma disintegrates  and  is  replaced  by  an  increased  formation  of  connective 
tissue  (compare,  e.  g.,  brown  induration  of  the  lungs) .  The  urine  in  such  cases 
constantly  contains  albumen,  and  the  chronic  disturbance  of  the  urinary 
secretion  is  not  without  influence  on  the  entire  picture  of  the  disease.  Mild 
ursemic  symptoms  may  appear,  and  the  disturbances  of  renal  function  must 
have  a  similar  influence  on  the  heart's  action  (blood  pressure,  hypertrophy  of 
the  left  ventricle)  to  that  of  primary  chronic  renal  disease. 

Careful  examination  of  the  urine  in  cases  of  severe  heart  disease  is  of  the 
greatest  practical  importance,  for  the  character  of  the  urine,  as  shown  by 
the  color,  specific  gravity,  and  amount  of  albumen,  is  an  excellent  index  of  the 
vigor  of  the  heart  and  the  condition  of  the  circulation.  Any  change  for  the 
worse  in  the  circulation  is  directly  shown  in  a  diminution  of  the  amount  of 
urine,  and  an  increase  in  its  specific  gravity,  or,  it  may  be,  in  the  appearance  of 
albuminuria.  Any  improvement  in  the  circulation,  whether  spontaneous  or 
due  to  remedies,  is  shown  first  and  best  by  an  increase  in  the  daily  excretion 
of  urine  and  a  corresponding  diminution  in  its  specific  gravity. 

We  not  infrequently  meet  with  acute  and  chronic  nephritis,  particularly 
arteriosclerotic  nephritis,  complicating  heart  disease.  It  is  often  no  easy  mat- 
ter clinically  to  form  a  correct  opinion  about  such  cases. 

We  may  in  part  refer  the  numerous  gastric  and  digestive  disturbances,  such 
as  loss  of  appetite,  vomiting,  constipation,  and  diarrhoea,  from  which  such 
patients  often  suffer,  to  the  stasis  in  the  blood  vessels  of  the  stomach  and  intes- 
tines; but  of  course  there  are  not  infrequently  diseases,  such  as  acute  and 
chronic  catarrh  of  these  organs,  which  are  to  be  regarded  as  complications. 

4.  Embolic  Processes. — The  slowing  of  the  circulation,  and  the  disturb- 
ances in  the  nutrition  of  the  walls  of  the  vessels,  which  result  from  it,  often 
give  rise  in  heart  disease  to  the  formation  of  thrombi.  These  are  situated  in 
the  heart  itself,  on  the  diseased  valves,  in  the  recesses  between  the  trabecular, 


404  DISEASES   OF  THE   CIRCULATORY   ORGANS 

in  the  auricles,  etc.,  or  else  they  form  in  the  veins,  especially  in  those  of  the 
lower  extremity.  From  these  thrombi  fibrinous  plugs  may  easily  be  set  loose 
and  enter  the  circulation  and  thus  give  rise  to  embolic  processes  in  distant 
organs.  Some  of  the  embolisms,  whose  clinical  relations  are  especially  impor- 
tant, have  been  more  fully  described  elsewhere,  and  will  be  mentioned  only 
briefly  here. 

Embolism  of  the  pulmonary  arteries,  proceeding  from  venous  thrombi  or 
from  thrombi  in  the  right  side  of  the  heart,  gives  rise  to  hemorrhagic  infarc- 
tion of  the  lungs.  Its  pathogenesis  and  symptoms  have  already  been  discussed 
in  a  previous  section  (see  page  333). 

Embolism  of  the  cerebral  arteries  is  a  common  cause  of  apoplectic  attacks, 
which  are  not  infrequent  in  heart  disease,  and  usually  lead  to  hemiplegia.  The 
anatomical  cause  of  the  hemiplegia  in  these  cases  is  the  embolic  softening  of 
the  brain  which  ensues.  The  details  of  this  are  given  in  the  section  on  cere- 
bral diseases  (Vol.  II). 

Embolism  of  the  larger  arteries  of  the  extremities,  such  as  the  femoral  and 
the  brachial,  is  much  rarer  than  the  forms  mentioned.  It  leads  to  embolic 
gangrene  of  the  extremities,  unless  an  adequate  collateral  circulation  can  be 
established.  The  skin  of  the  peripheral  parts,  the  fingers  or  toes,  first  becomes 
cool,  bluish,  and  at  last,  if  the  circulation  be  wholly  checked,  almost  black. 
The  gangrene  advances  slowly,  usually  occupying  weeks.  Ulcerations  develop 
as  the  necrotic  portions  are  thrown  off.  The  affection  is  extremely  painful. 
The  patient  soon  becomes  very  miserable  from  the  pain  and  the  septic  fever 
that  usually  attend  the  ulcerations,  and  extensive  gangrene  almost  always 
ends  fatally.  Sometimes  there  is  embolism  of  the  abdominal  aorta.  This  is 
usually  located  at  its  bifurcation,  and  occasions  a  sudden  and  almost  complete 
paraplegia,  speedy  disturbance  of  sensation,  abolition  of  the  reflexes,  and  loss 
of  electrical  excitability.  No  pulse  can  be  felt  in  the  peripheral  arteries;  the 
feet  are  pale  and  cold,  and  soon  there  are  signs  of  gangrene  in  both  legs.  The 
condition  is  probably  invariably  fatal. 

Embolism  of  the  renal  arteries,  with  consequent  ansemic  or  hemorrhagic 
infarctions  in  the  kidneys,  may  have  no  clinical  symptoms  at  all,  but  it  is 
sometimes  indicated  by  sudden  pains  in  the  region  of  the  kidneys  and  marked 
hematuria  (see  Vol.  II). 

Embolic  infarction  of  the  spleen  is  often  marked  by  swelling  of  the  spleen 
and  by  severe  perisplenitic  pain.    In  other  cases  it  is  wholly  without  symptoms. 

Embolism  of  a  mesenteric  artery  is  a  very  rare  event.  Its  sjanptoms  con- 
sist of  a  sudden  intestinal  hemorrhage,  of  severe  colicky  pains,  general  col- 
lapse, and  peritonitis. 

5.  Complications  on  the  Part  of  the  Nervous  System. — The  most  important 
complication  on  the  part  of  the  nervous  system — embolic  softening  of  the  brain 
— has  already  been  mentioned.  We  must  also  state  that  cerebral  hemorrhage 
may  occur  in  heart  disease.  It  is  especially  frequent  in  aortic  insufficiency, 
either  as  a  result  of  coexisting  atheroma  of  the  cerebral  arteries,  or  perhaps  of 
the  abnormally  high  tension  of  the  vessels  during  systole. 

Mental  disorders  have  been  repeatedly  observed  in  chronic  valvular  disease. 
They  are  the  result  of  the  disturbance  of  the  circulation  and  the  consequent 
impairment  of  nutrition  in  the  brain.  Hence  they  usually  make  their  first 
appearance  in  the  last  stages  of  heart  disease,  at  the  same  time  with  the  other 


VALVULAR   DISEASE   OF  THE   HEART  405 

disturbances  of  compensation.  The  psychoses  in  heart  disease  most  frequently 
have  the  character  of  melancholia,  but  conditions  of  confusional  insanity  and 
excitement  also  occur. 

(>.  The  Joints. — Secondary  affections  of  the  joints  arc  not  rare  in  heart 
disease.  As  acute  endocarditis  develops  in  the  course  of  acute  articular  rheu- 
matism, so,  on  the  other  hand,  rheumatic  pains  in  the  muscles  and  joints,  and 
even  acute  swelling  of  the  joints,  associated  with  fever,  appear  in  the  course 
of  chronic  heart  disease.  Sometimes  we  have  the  complete  picture  of  acute 
articular  rheumatism.  Probably  no  fresh  infection  from  without  is  requisite 
for  the  development  of  these  secondary  lesions  in  the  joints,  hut  under  certain 
circumstances  there  is  an  unusual  development  of  infectious  germs  (staphylo- 
cocci?) on  the  diseased  valves,  and  large  numbers  of  them  passing  into  the  cir- 
culation occasion  a  fresh  constitutional  infection. 

7.  Constitutional  Symptoms.  Fever. — In  congenital  and  early  acquired 
valvular  disease,  the  general  development  of  the  child  is  ordinarily  much  re- 
tarded. In  heart  disease  in  adults,  however,  we  by  no  means  always  see  an 
injurious  influence  on  the  general  nutrition.  In  many  patients  we  even  find  a 
remarkably  good  development  of  fat.  A  marked  general  disturbance  of  nutri- 
tion, such  as  great  anaemia  and  general  emaciation,  often  develops  in  the  later 
stages,  especially  in  aortic  insufficiency.  The  wasting  is,  of  course,  often 
hidden  by  the  oedema. 

In  general,  chronic  heart  disease  runs  its  course  without  fever,  but  periods 
often  occur  in  the  course  of  the  disease  when  there  is  a  moderate  and  usually 
irregular  fever.  Marked  disturbances  of  the  general  condition  may  or  may  not 
be  associated  with  it.  The  basis  of  the  fever  is  probably  an  acute  exacerbation 
of  the  endocarditis,  except,  of  course,  in  accidental  complications.  All  grada- 
tions occur,  from  a  mild  febrile  movement  without  further  symptoms  to  a 
severe  acute  recurring  endocarditis  (q.  v.).  In  other  cases  the  fever  is  con- 
nected with  secondary  swelling  of  the  joints,  or  with  embolic  processes. 

GENERAL    COURSE  AND   PROGNOSIS   OF  VALVULAR   DISEASE 

OF   THE   HEART 

The  course  of  valvular  disease  of  the  heart  is  in  most  cases  very  chronic. 
It  may  last  for  years.  So  long  as  there  is  a  complete  compensation,  the  patient 
feels  almost  perfectly  well;  sometimes  he  even  has  no  misgivings  as  to  his 
trouble.  The  slight  difficulty  in  respiration  and  the  incapacity  for  physical 
exertion  are  noticed,  but  little  attention  is  paid  to  them,  because  the  patient 
is  used  to  them.  In  other  cases  there  is  a  moderate  disturbance  for  a  long 
time,  but  it  may  be  borne  quite  easily  if  the  patient  is  rational  and  prudent 
in  his  conduct. 

We  cannot  make  any  general  statement  as  to  the  length  of  the  stage  of 
compensation,  because  cases  differ  very  greatly  in  this  respect.  It  depends  in 
part  upon  the  intensity  of  the  heart  disease,  in  part  upon  the  external  condi- 
tions under  which  the  patient  lives,  and  in  part,  certainly,  upon  the  different 
individual  capacity  for  work  and  power  of  resistance  of  the  heart.  Thus  it 
happens  that  many  cases  last  for  decades,  while  in  others  severe  sequela? 
appear  within  a  few  months.  External  injurious  agencies,  acting  on  the 
patient,  are  of  great  influence  on  the  course  of  heart  disease.  Severe  physical 
26 


406  DISEASES  OF  THE  CIRCULATORY  ORGANS 

exertion,  an  injudicious  manner  of  living,  intercurrent  febrile  disease,  mental 
disturbances,  care,  and  anxiety  are  often  followed  by  unhappy  consequences. 
For  readily  understood  reasons,  the  difficulties  of  women  afflicted  with  heart 
affections  are  augmented  during  pregnancy,  and  similarly,  also,  the  events  of 
labor  and  the  puerperal  state  not  seldom  exert  an  unfavorable  influence  upon 
the  compensation  of  an  existing  heart  disease. 

If  the  first  signs  of  disturbed  compensation  appear,  if  severe  dyspncea, 
slight  oedema  of  the  ankles,  etc.,  develop  for  the  first  time,  these  symptoms 
may  disappear  again  completely  under  proper  treatment.  Severe  disturb- 
ances of  compensation  even,  great  general  dropsy,  associated  with  very  weak 
and  irregular  action  of  the  heart,  may  abate,  after  a  few  weeks'  duration,  and 
the  patient  may  feel  quite  well  again.  Exacerbations  of  the  disease  may  come 
on  several  times  and  as  often  improve.  Finally,  of  course,  the  improvement 
is  incomplete.  Persistent  oedema  and  the  other  results  of  venous  stasis  ensue, 
the  symptoms  constantly  increase  in  severity,  especially  the  dyspncea,  until 
the  patient  dies  after  a  long  and  distressing  illness.  Immediately  before  death 
in  heart  disease,  certain  irregularities  in  the  innervation  of  the  heart  and  in 
the  respiration  sometimes  develop.  Among  these  the  so-called  Cheyne- Stokes 
phenomenon  deserves  especial  mention.  It  consists  in  a  peculiar  periodical 
variation  in  the  respiratory  movements.  There  will  be,  first,  a  complete  pause 
in  the  respiration  (apncea),  and  this  will  be  succeeded  by  feeble  breathing 
gradually  becoming  stronger,  then  gradually  abating,  and  finally  ending  in 
another  complete  cessation  of  the  respiration.  The  patient  usually  becomes 
more  comatose  during  the  cessation  of  respiration;  his  pupils  contract.  Dur- 
ing the  hard  breathing  the  patient  recovers  somewhat,  and  his  pupils  dilate 
again.  The  chief  cause  of  this  rhythmical  breathing  is  probably  to  be  sought 
in  the  decided  lowering  of  the  excitability  of  the  respiratory  center.  During 
the  apncea  a  considerable  amount  of  carbonic  acid  collects  in  the  blood  before 
the  respiratory  center  is  sufficiently  stimulated  to  resume  its  activity.  We 
have  seen  the  heart  behave  in  a  precisely  analogous  manner,  but  independently 
of  any  Cheyne- Stokes  respiration.  There  was  a  series  of  rapid  but  regular 
pulsations,  alternating  with  a  series  of  slower  contractions. 

In  regard  to  the  particular  forms  of  valvular  disease,  aortic  insufficiency 
generally  gives  the  best  prognosis,  inasmuch  as  it  may  be  very  perfectly  com- 
pensated for  many  years.  I  know  an  officer  who,  with  his  aortic  insufficiency, 
passed  through  an  entire  campaign  without  any  particular  difficulty.  But 
if  severe  disturbance  of  compensation  once  occurs  in  this  form  of  heart  dis- 
ease, it  gives  a  very  unfavorable  prognosis,  since,  as  a  rule,  we  cannot  rein- 
vigorate  the  heart.  Mitral  insufficiency  is  also  quite  a  favorable  form  of 
heart  disease,  which  may  be  compensated  for  a  long  time.  Mitral  stenosis  is 
decidedly  more  unfavorable  in  its  prognosis,  and  is  associated  with  more  dis- 
turbance, but  it  offers  the  one  advantage  that  it  is  relatively  most  readily  in- 
fluenced therapeutically,  especially  by  proper  digitalis  treatment.  Thus,  it 
may  happen  that  a  patient  with  mitral  stenosis  repeatedly  (half  a  dozen  times 
and  more)  experiences  the  most  severe  disturbance  of  compensation,  but  always 
recuperates  and  then  for  a  considerable  time  is  tolerably  well.  Aortic  stenosis 
is  also  capable  of  quite  good  condensation,  but  it  often  causes  persistent  cere- 
bral symptoms,  such  as  headache  and  vertigo,  depending  on  anaemia  of  the 
brain,  or  very  likely  upon  simultaneous  changes  in  its  blood  vessels. 


VALVULAR  DISEASE  OF  THE  HEART  407 

Whether  established  valvular  disease  of  the  heart  is  curable  is  a  question 
which  cannot  be  answered  unconditionally  in  the  negative.  Of  course  in  the 
great  majority  of  cases  it  is  in  itself  incurable;  only  its  sequelae  can  be  pre- 
vented or  removed  to  a  certain  degree.  In  children  and  young  people,  however, 
cases  sometimes  do  occur,  as  we  ourselves  have  seen,  in  which  there  are  all  the 
signs  of  a  pronounced  heart  disease,  but  alter  a  long  time  recovery  is  complete. 
Of  course  it  is  very  hard  to  decide  whether  we  really  have  to  do  with  a  valv- 
ular disease  that  has  been  cured,  because  simple  dilatation  of  the  heart,  rela- 
tive insufficiency  of  the  valves,  anaemic  cardiac  murmurs,  etc.,  may  easily  be 
confounded  with  pure  valvular  disease  of  the  heart. 

Among  the  dangerous  intercurrent  accidents  in  valvular  diseases  we  must 
make  especial  mention  of  embolic  processes,  which  may  occur  suddenly  and 
without  warning.  The  different  forms  of  embolism  have  been  mentioned  above, 
and  also  the  possibility  of  cerebral  hemorrhage  in  heart  disease.  The  peculiar, 
and  at  times  life-menacing  attacks  of  cardiac  weakness,  cardiac  asthma,  etc., 
which  may  occur  in  all  diseases  of  the  heart,  will  later  be  more  thoroughly 
discussed. 

TREATMENT   OF  VALVULAR   HEART   DISEASE 

1.  Prophylaxis. — Our  means  for  preventing  the  development  of  heart  dis- 
ease are  very  limited.  To  avert  endocarditis  in  articular  rheumatism  by  the 
present  method  of  treating  acute  rheumatism  with  salicylates  is  impossible. 
The  probability  of  the  onset  of  endocarditis  may  be  lessened  by  this  treat- 
ment only  so  far  as  the  whole  duration  of  the  disease  is  often  considerably 
shortened. 

We  can  also  do  little  in  the  way  of  prophylaxis  against  the  development  of 
heart  disease  that  is  chronic  from  the  start,  since  the  cause  of  the  disease  is  in 
many  cases  wholly  unknown  to  us.  Those  injurious  influences  deserve  the 
most  attention  which  may  favor  the  development  of  arterial  atheroma  and  its 
consequent  chronic  valvular  disease.  The  chief  factors  in  this  connection  are 
excessive  physical  exertion  and  an  improjDer  mode  of  living,  including  the  use 
of  too  much  alcohol  and  tobacco ;  but  the  role  which  these  play  in  the  develop- 
ment of  genuine  valvular  disease  is  certainly  much  less  important  than  their 
influence  upon  certain  myopathic  and  nervous  diseases  of  the  heart  (see  the 
following  chapter). 

2.  Treatment  of  Compensated  Heart  Ilisease. — If  we  have  to  treat  a  heart 
disease  which  already  exists,  but  which  is  at  the  same  time  fully  compensated, 
our  treatment  must  be  chiefly  hygienic.  The  patient  must  be  made  aware  of 
his  heart  disease  without  making  him  needlessly  anxious.  He  must  be  told 
that  his  further  good  health  depends  in  great  part  upon  his  own  conduct,  his 
discretion,  and  his  perseverance.  The  patient  must  avoid  everything  which 
makes  great  demands  upon  the  heart,  or  which  may  have  a  directly  injurious 
influence  on  it.  All  violent  bodily  exertion,  too  intense  mental  work,  and  also 
all  excesses  in  eating,  drinking,  smoking,  etc.,  must  be  avoided.  The  use  of 
all  alcoholic  beverages  must  be  greatly  restricted;  coffee  and  tea  in  moderate 
strength  and  quantity  may  be  permitted,  if  the  patient  himself  does  not  find 
them  exciting.  That  the  dietetic  directions  will  often  collide  with  the  demands 
of  the  patient's  occupation,  as  well  as  with  his  favorite  amusements  and  his 


408  DISEASES   OF  THE   CIRCULATORY   ORGANS 

habits,  should  not  deter  the  physician  from  demanding  the  fulfillment  of  his 
prescriptions,  at  least  so  far  as  possible. 

Treatment  by  drugs  is  usually  unnecessary  in  compensated  heart  disease. 
We  do  not  know  a  remedy  which  has  a  directly  favorable  action  on  heart  dis- 
ease. The  protracted  use  of  iodid  of  potassium,  Fowler's  solution,  arsenite 
of  antimony  ("granules  of  antimony"),  etc.,  has  been  recommended.  The 
efficacy  of  these  remedies  is  very  questionable.  We  can  always  try  them,  if  a 
mild  disturbance  makes  a  prescription  desirable  and  other  remedies  are  not 
especially  indicated.  Beyond  this,  the  physician  is  usually  contented  with  an 
endeavor  to  improve  the  appetite  and  nutrition  of  the  patient  by  means  of  iron, 
quinin,  and  bitters.  If  there  is  a  suspicion  that  the  heart  disease  may  be  due 
to  syphilis,  a  trial  of  iodid  of  potassium  may  be  made,  but  a  brilliant  result 
from  the  employment  of  antisyphilitic  measures  is  hardly  to  be  expected,  be- 
cause the  mechanical  imperfections  of  the  valves,  leading  to  regurgitation  and 
stenosis,  can  scarcely  be  remedied. 

The  employment  of  baths  in  heart  disease  deserves  special  consideration. 
Numerous  experiences  go  to  prove  that  they  are  not  only  well  borne  by  pa- 
tients with  heart  disease,  but  that  they  exercise  a  peculiarly  beneficial  and 
invigorating  influence  upon  the  action  of  the  heart.  In  this  regard,  the  great- 
est reputation  is  possessed  by  the  warm  saline  baths,  which  are  rich  in  carbonic 
dioxid,  particularly  those  of  Nauheim.  Even  incipient  mild  disturbance  of 
compensation  frequently  will  be  improved  by  the  use  of  these  or  similar  baths 
(e.g.,  Cudowa,  Kissingen,  Oeynhausen,  Soden,  etc.).  Patients  may  also  em- 
ploy at  home  a  course  of  baths  with  good  results.  Short,  tepid  baths  with 
cooler  douches  sometimes  act  favorably  on  the  stronger  patients.  Or  salt 
baths  ("neurogen"  baths)  may  be  ordered,  and  especially  the  artificial  car- 
bonic-acid baths,  with  which  many  hydriatic  institutes  are  nowadays  equipped, 
but  which  may  also  be  readily  prepared  in  the  patient's  home  (artificial  C02 
baths  of  Sandow,  Quaglio,  Kopp  and  Josef,  and  others).  The  duration  of  a 
C02  bath  should  at  first  be  brief  (six  to  eight  minutes),  and  the  temperature 
about  31°  to  32°  C.  (87.8°  to  89.6°  F.).  Gradually  the  duration  may  be  some- 
what prolonged.  In  recent  years  there  has  been  much  discussion  of  the  treat- 
ment of  cardiopathies  with  electric  baths  (the  alternating  current  baths,  the 
so-called  "four-cell  baths,"  and  others).  Certain  favorable  effects  are  not  to 
be  denied,  though  it  has  not  been  scientifically  demonstrated  that  a  specific 
action  on  the  heart  can  be  ascribed  to  the  electric  baths.  At  any  rate,  the 
inconsiderate  and  sensational  exploitation  of  electric  baths  is  out  of  all  pro- 
portion to  their"  real  usefulness,  and  we  must  warn  against  their  reckless 
employment.  Where  there  is  no  marked  disturbance  of  compensation,  the 
methodical  employment  of  gymnastic  exercises,  the  so-called  Swedish  move- 
ments, has  a  certain  value  in  the  treatment  of  heart  disease.  Kegular  muscular 
movements  promote  the  circulation  of  the  blood,  and  thus  lighten  the  task 
of  the  heart.  If  they  are  carried  out  cautiously  and  with  a  proper  considera- 
tion of  the  individual  case,  they  are  not  infrequently  beneficial.  Their  value 
should,  of  course,  not  be  overestimated.  The  best  measure  for  the  amount  of 
bodily  exercise  for  patients  with  heart  disease  seems,  to  the  author,  to  be  the 
subjective  sensation  of  dyspnoea.  Any  patient  who  has  no  special  signs  of  fail- 
ing compensation  may  be  allowed  to  walk  slowly  and  also  to  climb  a  little  so 
long  as  he  experiences  no  distinct  dyspnoea.    As  soon  as  this  happens  he  must 


VALVULAR   DISEASE   OF  THE   HEART  409 

stand  still  and  rest.  The  author  regards  it  as  a  great  mistake  to  encourage 
patients  to  persist  in  their  efforts  regardless  of  difficulty  in  breathing.  We 
should  not  forget  that  any  disturbance  of  the  circulation  which  Minn--  must 
involve  the  myocardium  itself  in  its  influence.  See  also  the  remarks  made  on 
the  treatment  of  idiopathic  cardiac  hypertrophy,  which  apply  to  valvular  dis- 
ease as  well.  That  a  change  of  climate  may  prove  beneficial  Is  self-evident. 
It  is  particularly  appropriate  that  patients  with  a  tendency  to  bronchitis  or 
rheumatism  should  spend  the  winter  south. 

3.  Treatment  of  Ruptured  Compensation. — As  soon  as  the  compensatory 
activity  of  the  heart,  in  a  case  of  valvular  trouble;  begins  to  be  impaired,  as 
soon  as  there  is  marked  dyspnoea,  diminution  in  the  excretion  of  urine,  and 
cedema,  we  must  promptly  lighten  the  burden  of  the  heart  by  complete  bodily 
rest.  Many  cases,  particularly  of  mitral  disease,  are  completely  restored,  even 
when  there  are  marked  symptoms  of  cardiac  embarrassment,  by  mere  rest  in 
bed  with  simple  diet  and  without  any  other  therapeutic  measures;  but  if  the 
disturbance  of  compensation  is  more  marked  and  persistent,  the  physician  must 
have  recourse  to  digitalis,  a  remedy  which  possesses  undoubted  value  when  the 
powers  of  the  heart  are  impaired.  Digitalis  has  the  properties  of  making  the 
separate  beats  more  powerful,  of  lowering  the  pulse  rate  by  lengthening  the 
diastole,  and  above  all  of  heightening  the  arterial  tension.  Digitalis  is  there- 
fore indicated  in  every  case  of  heart  disease  when  there  is  persistent  disturb- 
ance of  compensation,  and  if  the  pulse  is  small,  of  low  tension,  and,  above  all, 
frequent  and  irregular;  the  desired  effect  of  digitalis  is  to  make  the  pulse 
slower,  more  regular,  and  especially  of  higher  tension.  Under  the  influence  of 
the  increase  in  tension  thus  produced  and  of  the  acceleration  of  the  circulation, 
the  disturbances  of  compensation  often  disappear  in  a  surprising  fashion ;  there 
is  more  abundant  diuresis,  the  scanty,  dark,  concentrated  urine  of  passive  con- 
gestion disappears,  the  daily  amount  of  urine  increases,  and  the  urine  there- 
fore becomes  clear  and  of  lower  specific  gravity.  The  cedema  then  disappears, 
the  dyspnoea  ceases,  the  head  becomes  free,  the  general  condition  improves, 
and,  in  brief,  there  may  again  ensue  a  complete  compensation  of  the  heart 
disease.  This  change  is  sometimes  accomplished  in  a  comparatively  short 
time,  in  a  few  days  or  weeks. 

It  is  very  important  to  prescribe  digitalis  in  a  correct  manner  in  order  for 
it  to  be  efficient.  Much  experience  has  shown  that  it  is  best  to  give  it  at 
regular  intervals  of  three  hours,  in  doses  of  1.5  gr.  (gm.  0.1)  of  the  powdered 
leaves,  either  in  wafers  or  simply  in  water;  so  that  the  patient  receives  in 
the  course  of  a  day  some  four  or  five  powders — that  is,  6  or  8  gr.  (gm.  0.4  to 
0.5)  of  digitalis.  If  the  remedy  is  well  borne  we  may  continue  it  in  this 
manner,  but  usually  it  is  omitted  during  the  night,  to  be  resumed  in  the  same 
way  on  the  next  day.  As  a  rule,  the  distinct  specific  influence  of  digitalis  is 
evident  after  the  employment  of  ten  to  fifteen  powders  in  the  course  of  two 
or  three  days.  This  is  recognized  by  the  marked  diminution  in  pulse  rate, 
the  increasing  strength  and  regularity  of  the  pulse,  and  the  improvement  in 
the  general  symptoms.  Instead  of  the  powder  we  may  employ  an  infusion  of 
the  strength  of  1  or  2  parts  to  150  of  water.  Of  this  a  tablespoonful  must  be 
given  regularly  every  two  or  three  hours.  In  some  cases,  particularly  if  the 
patient  has  already  become  accustomed  to  the  remedy,  we  may  prescribe  still 
larger  doses,  up  to  30  or  45  gr.  (gm.  2  to  3)  and  even  more,  daily.    On  the 


410  DISEASES  OF  THE  CIRCULATORY  ORGANS 

other  hand,  we  must  at  times  seek  to  attain  the  digitalis  effect  by  continued 
smaller  doses  (thrice  daily  gr.  jss.  [gm.  0.1]  or  even  less).  But  in  every  case 
digitalis  should  be  given  in  regularly  repeated  doses,  so  as  to  obtain  by  their 
combined  action  the  full  effect  of  the  drug.  It  is  entirely  useless  to  prescribe 
digitalis  in  small  doses  at  long  intervals.  The  remedy  must  never  be  prescribed 
unless  we  can  accurately  watch  the  pulse  and  the  heart's  action,  for  only  thus 
can  we  obtain  clear  indications  as  to  the  further  employment  or  the  omission 
of  the  drug. 

Not  rarely  some  unpleasant  incidental  effects  appear  simultaneously  with 
the  beneficial  influence  upon  the  heart's  action,  or  with  too  long  continuance 
of  the  remedy.  Among  these  are  nausea,  vomiting,  and  specks  before  the  eyes. 
If  the  digitalis  is  omitted  these  symptoms  usually  cease,  while  the  beneficial 
effect  upon  the  heart  may  last  for  a  long  time.  With  regard  to  these  inci- 
dental and  disagreeable  symptoms,  different  patients  vary  greatly.  Many  bear 
digitalis  very  well,  others  very  ill.  From  a  therapeutic  point  of  view  it  is 
particularly  embarrassing  if  the  nausea,  vomiting,  and  other  disagreeable 
symptoms  appear  before  the  digitalis  has  produced  an  effect  upon  the  heart; 
but  in  such  cases  we  should  not  be  too  hasty  in  abandoning  the  drug,  especially 
if  it  is  urgently  indicated.  If  the  patient  cannot  bear  the  infusion  we  should 
administer  the  digitalis  in  powders,  or  vice  versa.  Or  the  dosage  should  be 
varied,  and  the  digitalis  given  in  smaller,  cautious  amounts.  With  sensitive 
stomachs,  the  administration  of  digitalis  in  the  so-called  keratin  capsules,  that 
do  not  dissolve  till  they  reach  the  small  intestine,  is  to  be  recommended.  If 
the  drug  absolutely  cannot  be  given  by  the  mouth,  it  should  be  injected  into 
the  rectum  in  the  form  of  an  infusion  of  the  strength  of  1  or  2  parts  to  100 
of  water.  This  should  be  warmed  to  the  temperature  of  the  body  and  given, 
after  a  cleansing  enema  has  been  employed,  once  or  twice  a  day.  Finally,  in- 
stead of  the  infusion,  one  of  the  many  other  digitalis  preparations  which  will 
be  later  discussed,  will  in  many  cases  be  resorted  to. 

•*'  Sometimes,  especially  if  the  patient  has  not  been  carefully  watched,  the 
cumulative  effect  of  digitalis  is  shown  in  severe  symptoms  of  poisoning,  such 
as  collapse,  very  frequent  pulse,  disturbance  of  vision,  and  dilated  pupils. 
Then  such  stimulants  must  be  employed  as  camphor,  ether,  wine,  and  strong 
black  coffee.  How  often  digitalis  is  to  be  used  in  the  case  of  heart  disease 
can  be  determined  by  experience  alone.  Many  patients,  particularly  cases  of 
mitral  disease,  may  undergo  treatment  with  digitalis  twenty  to  thirty  times  or 
more,  with  the  best  results.  Every  time  that  signs  of  impaired  compensation 
return,  we  must  try  digitalis  again.  It  must  be  confessed  that  it  will  often  be 
necessary  gradually  to  increase  the  dose.  As  is  the  case  with  so  many  other 
remedies,  the  patient  becomes  habituated  to  the  drug.  There  is  no  maximum 
dose,  and  we  must  find  out  by  experience  in  each  case  what  the  satisfactory 
amount  may  be.  Some  patients  become  at  last  genuine  "  digitalis  eaters,"  and 
are  unable  to  exist  without  large  doses  of  digitalis.  We  have  ourselves  seen  a 
patient  take  75  gr.  (gm.  5)  of  the  powder  daily.  In  other  cases  it  is  advisable 
to  continue  with  smaller  closes  (about  gr.  j  [gm.  0.05]  thrice  daily)  for  some 
time  after  the  successful  administration  of  the  drug  in  larger  amounts.  And 
in  other  cases,  too,  cardiac  patients  with  moderate  disturbance  may  occasion- 
ally take  small  doses  continuously  for  a  long  time  (months)  with  visible 
benefit.    In  very  many  cases,  however,  the  beneficial  effect  of  digitalis  even  in 


VALVULAR   DISEASE  OF  THE   HEART  411 

the  larger  closes  fails  at  last  to  appear.    The  remedy  is  no  longer  borne  and 
it  must  he  abandoned.     This  usually  marks  the  I ;i - 1  stage  of  the  disease. 

Not  infrequently  we  see  patients  with  distinct  symptoms  of  passive  coi 
tion,  in  whom  the  character  of  the  pulse  seems  at  firsl  to  contraindicate  the 
administration  of  digitalis:  the  pulse  is  perhaps  frequent,  bul  regular  and 
strong;  in  other  cases  it  is  not  rapid  at  all,  but  yei  somewhal  irregular;  or  it 
may  be  even  infrequent  and  regular.  Particularly  in  cases  of  aortic  insuffi- 
ciency is  it  often  very  difficult  to  determine  whether  we  should  give  digitalis 
or  not.  With  all  patients  of  this  sort  it  is,  in  general,  worth  while  to  make  a 
trial  of  digitalis,  since  it  may  often  be  beneficial,  and  yet  we  should  exercise 
especial  caution  and  vigilance  with  regard  to  its  effects. 

[Digitalis  is  used  more  commonly  in  this  country  in  the  form  of  the  tinc- 
ture. The  urine  affords  a  good  guide  as  to  the  safety  of  the  continuance  of  the 
drug;  as  long  as  the  renal  secretion  is  sufficient  in  quantity,  and  increasing 
rather  than  diminishing,  there  is  no  danger  of  the  toxic  effects.  It  is,  conse- 
quently, a  good  plan  to  follow  carefully  the  twenty-four-hour  quantity  of 
urine  when  this  can  be  done. 

In  mitral  cases,  with  or  without  secondary  tricuspid  regurgitation,  where 
the  cyanosis  and  other  symptoms  show  that  the  right  heart  is  engorged  with 
blood  which  it  cannot  propel  onward,  the  relief  afforded  by  venesection,  or  by 
a  dozen  leeches  in  the  hepatic  region,  may  be  very  great.  Until  the  veins  are 
relieved  either  in  this  way  or  by  free  purgation,  digitalis  and  stimulants  are 
useless,  and  a  resort  to  them  results  merely  in  a  loss  of  time,  and  perhaps  in 
the  loss  of  a  life  which  might  be  saved.] 

Within  recent  times  many  attempts  have  been  made  to  prepare  the  active 
ingredients  in  a  pure  form  for  the  purpose  of  replacing  the  digitalis  leaves. 
We  would  mention  first  the  dialyzed  preparations  (didlysatum  digitalis,  Golaz, 
and  digitalysatam,  Buerger)  of  which  about  10  to  15  minims  each  are  given 
thrice  daily,  generally  well  borne.  Of  the  active  constituents  of  digitalis,  digi- 
toxin  is  most  frequently  used  in  doses  of  -^q  gr-  (gm-  0.00025),  in  pastille 
form  every  two  or  three  hours.  This  is  now  oftenest  employed  in  the  form 
of  digalen  {digitoxin  solub.,  Cloetta),  which  contains  mgm.  0.3  (m  gr.) 
digitoxin  j3er  cubic  centimeter. 

Generally  0.5  to  1  c.c.  (TTL  viij  to  xv)  of  the  solution  is  ordered  t.i.d.  The 
effect  is  often  an  excellent  one.  Digalen  may  also  be  used  for  intramuscular 
and  intravenous  injections,  especially  in  cases  of  marked  compensatory  disturb- 
ances, where  all  internal  medication  is  futile.  The  older  digitalis  prepara- 
tions (tr.  digitalis  and  vinegar  of  digitalis)  are  superfluous  and  not  to  be 
recommended.  In  general,  I  am  under  the  impression  that  digitalis  leaves  are 
still  the  best  and  most  effective  preparation,  and  should  be  tried  first  when- 
ever digitalis  is  indicated.  In  those  rather  frequent  cases  in  which  this  remedy 
fails,  the  other  digitalis  preparations,  above  all  digalen,  may  prove  very  valu- 
able.    [A  new  and  valuable  remedy  is  digipuratum.] 

When  digitalis  does  not  yield  the  desired  results,  other  cardiac  remedies 
are  resorted  to,  partly  alone  and  partly  in  conjunction  with  digitalis.  Fre- 
quently combinations  act  better  than  the  single  drugs.  Tincture  of  stro- 
pbanthus  deserves  first  mention;  its  active  principle,  strophanthin,  obtained 
from  the  seed  of  the  plant,  has  almost  the  same  pharmacological  properties 
as  digitalis.     The  tincture  is  given  thrice  daily  in  closes  of  5  to  10  minims, 


412  DISEASES   OF  THE   CIRCULATORY   ORGANS 

A.  Frankel  has  recommended  intravenous  injections  of  strophanthin  (g^-g-  gr. 
[gm.  0.0003]),  injected  into  a  vein  of  the  arm.  Upon  repeated  occasions  the 
author  has  convinced  himself  of  the  strikingly  rapid  influence  of  these  injec- 
tions on  cardiac  activity,  but  would  urge  caution,  as  also  with  intravenous 
digalen  injections,  in  employing  them  in  general  practice  (danger  of  heart- 
block).  Besides  tincture  of  strophanthus,  reference  must  be  made  to  caffein 
in  the  form  of  caffein  sodio-salicylate  and  sodio-benzoate,  given  in  powders 
of  1.5  to  4.5  gr.  (gm.  0.1  to  0.3)  several  times  daily.  Caffein  also  acts  on 
the  vasomotor  centers,  and  is  at  the  same  time  a  diuretic.  In  this  respect  theo- 
bromin  (theobrominsodio-salicylate  or  diuretin)  is  even  more  active,  and, 
especially  in  combination  with  digitalis,  is  often  a  very  valuable  remedy. 
Other  heart  remedies  which  have  been  recommended  at  times,  such  as  adonis 
vernalis,  convallaria  majalis,  spartein  sulphate,  etc.,  have  not  proved  reliable, 
and  have,  therefore,  found  little  acceptance  in  practice.  The  valerian  prepa- 
rations are  to  be  considered  only  in  cases  with  mild  subjective  symptoms. 
Camphor  is  the  best  stimulant  in  attacks  of  acute  cardiac  weakness.  The  com- 
bination of  digitalis  with  other  drugs,  usually  diuretics,  is  very  useful,  as 
already  mentioned.  A  combination  of  this  sort  is  the  following:  Infusion  of 
digitalis,  30  gr.  to  §v  of  water  (gm.  2  to  150)  ;  sodio-salicylate  of  caffein, 
30  gr.  (gm.  2)  ;  tincture  of  strophanthus,  oj  (gm.  4)  ;  liquor  potassi  acetatis, 
§ij  (gm.  60);  syrupi  aurantii,  §j  (gm.  30).  M.  S.  A  tablespoonful  every 
two  hours. 

4.  Symptomatic  Treatment. — Some  symptoms  which  often  occur  in  heart 
disease  demand  a  special  description. 

Dropsy  is  a  symptom  of  venous  stasis,  and  disappears  if  compensation  be 
restored  spontaneously  or  by  the  use  of  digitalis.  Complete  rest  in  bed  and 
elevation  of  the  swollen  parts  serve  as  the  chief  aid  in  removing  the  dropsy. 
Dropsical  patients  ought  also  to  change  their  position  in  bed  frequently,  if 
possible,  that  there  may  not  be  too  much  oedema  collected  in  the  dependent 
portions  of  the  body.  It  is  a  good  plan  to  wrap  up  the  swollen  arms  and  legs 
with  flannel  bandages  under  gentle  pressure.  Mild  passage  of  the  cedematous 
parts  may  sometimes  be  of  advantage. 

The  question  whether  the  intake  of  liquids  in  dropsical  cases  should  be 
limited  or  not  is  not  easily  answered.  Experience  teaches  that  these  patients 
often  lose  their  oedema  when  they  drink  large  amounts  of  so-called  diuretic 
teas  (equisetum,  eglantine,  species  diureticse  [P.  Gr.],  and  others).  On  the 
other  hand,  a  material  restriction  of  liquids  may  be  useful  (confer  infra,  the 
remarks  regarding  to  so-called  Karrel  milk  cure).  In  short,  general  rules 
cannot  be  laid  down,  and  we  have  to  be  guided  by  individual  experience.  Of 
internal  remedies,  besides  digitalis,  which  should  invariably  be  first  employed, 
and  drugs  of  similar  action,  the  true  diuretics  are  to  be  considered,  such  as 
acetate  of  potassium,  acetate  of  sodium,  diuretin,  the  various  diuretic  teas,  etc. 
They  are  sometimes  ordered  in  combination  with  digitalis  (above  all,  digitalis 
with  diuretin  and  digitalis  with  caffein)  and  sometimes  alone,  particularly 
when  digitalis  cannot  be  borne  or  is  not  indicated.  Calomel  sometimes  shows 
good  effects  in  cardiac  dropsy.  Its  diuretic  influence  has  lately  been  empha- 
sized by  Jendrassik  and  others.  It  is  prescribed  in  powders  of  3  gr.  (gm.  0.2) 
three  to  five  times  a  day.  Often  a  very  marked  diuresis  will  be  caused  after  one 
or  two  days,  with  rapid  abatement  of  the  dropsy.    The  administration  of  the 


VALVULAR   DISEASE  OF  THE    HEART  413 

remedy  is  stopped  as  soon  as  the  diuresis  begins.  It  is  also  omitted  if  stoma- 
titis develops. 

At  times  it  is  advantageous  to  combine  calomel  with  digitalis  (digitalis, 
1.5  gr.  [gm.  0.1];  calomel,  3  gr.  [gm.  0.2]),  five  such  powders  daily. 

In  the  last  stages  of  heart  disease  the  patient's  condition  may  be  particu- 
larly distressing  from  the  severe  general  oedema.  It  is  then  accessary  to  re- 
move the  ascites  or  hydrothorax  by  puncture,  and  also  to  try  to  relieve  the 
cedematous  condition  of  the  skin  mechanically. 

Scarification  of  the  skin  by  long  incisions  into  the  subcutaneous  cellular 
tissue  is  effective  but  dangerous,  because  erysipelatous  inflammation,  etc.,  is 
apt  to  ensue  at  the  line  of  incision.  Far  more  recommendable  are  little  silver 
capillary  trocars  (the  so-called  Southey's  trocars,  or,  still  better,  Curschmann's 
trocars),  to  which  a  thin  rubber  tube  is  attached.  Through  these  trocars, 
which  are  introduced  obliquely  into  the  subcutaneous  tissues,  frequently  many 
quarts  of  serum  flow  away,  drop  by  drop,  so  that  shapeless  swollen  limbs  be- 
come very  thin  in  one  or  two  days.  We  must  always  exercise  great  cleanliness, 
however,  and  the  utmost  disinfection  of  the  skin,  wrapping  the  parts  in  ster- 
ilized gauze.  In  patients  with  heart  disease  it  is  not,  as  a  rule,  advisable  to 
attack  the  dropsy  by  sweating,  and,  at  most,  it  is  to  be  tried  onty  with  great 
caution. 

The  dyspnoea  of  heart  disease  is  usually  the  most  distressing  symptom  of 
all.  Here,  too,  our  chief  task  is  of  course  to  restore  the  compensation;  but 
this  failing,  we  must  try  to  relieve  the  dyspnoea  symptomatically.  Morphin 
is  most  efficient  in  this  respect.  In  general,  morphin  is,  next  to  digitalis,  the 
most  indispensable  remedy  in  the  treatment  of  severe  heart  disease.  It  is 
usually  well  borne,  and  procures  great  relief,  especially  if  given  subcutaneously. 
If  we  have  to  do  with  the  last  stage  of  the  disease,  we  need  not  spare  large 
doses.  Otherwise,  of  course,  caution  is  necessary.  Besides  morphin,  dionin 
and  heroin  are  used  at  times. 

Chloral  hydrate  should  be  cautiously  employed  in  heart  disease.  It  is  often, 
however,  well  borne,  and  gives  the  patient  rest  and  comfort.  We  have  also  pre- 
scribed chloralamid  in  cardiac  cases,  with  good  results.  Where  there  is  absolute 
insomnia,  a  trial  may  be  made  of  8  to  15  gr.  (gm.  0.5  to  1)  of  veronal,  com- 
bined, perhaps,  with  ^  gr.   (gm.  0.01)  of  morphin. 

In  practice  we  must  often  prescribe  external  applications  to  the  chest,  mus- 
tard plasters,  hot  poultices,  and  also  hot  foot  baths  with  mustard,  ashes,  etc. 
In  severe  cases  their  action  is  slight.  Acetate  of  lead  in  large  doses  some- 
times seems  to  have  a  favorable  influence  in  severe  dyspnoea,  especially  with 
threatening  jmlmonary  oedema.  We  give  the  powder,  up  to  1.5  gr.  (gm.  0.1), 
every  two  or  three  hours,  and  it  is  often  a  good  plan  to  add  0.5  or  1  gr.  (gm. 
0.03  to  0.05)  of  opium.  We  can  also  frequently  obtain  decided  relief  for  the 
patient,  particularly  if  constipated,  by  a  vigorous  drastic  purge,  with  com- 
pound infusion  of  senna  or  gamboge. 

Palpitation,  constant  or  paroxysmal,  is  treated  by  applying  ice  to  the  car- 
diac region;  the  "heart  bottles,"  made  of  tin,  or  the  Leiter  heart  coils,  act 
very  well.  In  patients  with  aortic  insufficiency  and  very  excited  action  of  the 
heart,  we  may  recommend  the  protracted  use  of  ice.  Hot  poultices  also  are 
sometimes  beneficial.  The  narcotics  are  the  most  efficient  internal  remedies, 
especially  morphin,  which,  of  course,  we  should  reserve  for  severe  cases.    If  the 


414  DISEASES  OF  THE  CIRCULATORY   ORGANS 

palpitation  is  of  a  lesser  degree,  we  may  try  bromid  of  potassium,  valerianates, 
or  the  like. 

The  subcutaneous  use  of  morphin  is  again  by  far  the  most  potent  remedy 
in  the  anginous  attacks,  associated  with  pain  and  a  feeling  of  distress.  We 
may  also  use  cutaneous  irritation,  mustard  plasters,  etc.,  hot  compresses  or 
poultices,  hot  hand  and  foot  baths,  and  internally  strophanthus,  nitroglycerin, 
etc.  Compare  also  the  section  on  the  treatment  of  stenocardial  and  similar 
seizures  in  muscular  and  arteriosclerotic  cardiopathies. 

We  may  prescribe  bitter  remedies — tinctura  amara  (P.  C),  or  compound 
tincture  of  cinchona — and  muriatic  acid,  for  the  loss  of  appetite,  in  case  this 
is  not  improved  by  regulating  the  activity  of  the  heart.  In  addition,  we  must 
always  endeavor  to  get  a  regular  evacuation  of  the  bowels. 

For  the  attacks  of  faintness  and  vertigo,  occurring  especially  in  aortic 
stenosis,  as  a  result  of  cerebral  anaemia,  we  may  prescribe  a  horizontal  position, 
and  stimulants — wine,  ether,  and  Hoffmann's  anodyne. 

Especial  accidents  and  complications,  like  pulmonary  oedema,  infarctions, 
or  apoplexy,  are  to  be  treated  according  to  the  usual  rules. 


CHAPTER    III 

DISEASES   OF    THE   MYOCARDIUM 

Preliminary  Remarks. — In  valvular  disease  of  the  heart  a  disturbance  of 
the  circulation  takes  place  because  of  the  functional  impairment  of  the  valves, 
or  the  obstruction  of  the  orifices  of  the  heart ;  but  in  the  diseases  which  we  are 
now  to  consider  we  have  to  deal  with  impairment  of  the  structure  and  func- 
tional activity  of  the  cardiac  muscle  itself,  while  the  valvular  apparatus  of  the 
heart  remains  intact.  The  expression  myocardial  diseases  of  the  heart,  in  a 
strict  sense,  is  too  narrow,  inasmuch  as  we  probably  have  diseases  of  the  gan- 
glia and  nerves  of  the  heart  associated  with  the  muscular  diseases. 

As,  however,  modern  views  ascribe  great  physiological  independence  to  the 
cardiac  muscle,  and  as  our  knowledge  regarding  the  pathological  changes  in 
the  nervous  apparatus  of  the  heart  is  extremely  limited,  we  may,  in  classifying 
and  considering  these  conditions,  for  the  present  restrict  ourselves  to  the  dis- 
turbances of  heart  function  observed  during  the  life  of  the  patient,  and  to  the 
anatomical  changes  in  the  heart  muscle  found  at  autopsy.  In  this  connection 
the  changes  in  the  coronary  arteries  must  be  well  considered,  as  many  muscular 
cardiopathies  depend  on  primary  vascular  alterations.  Since  affections  of  the 
coronary  arteries  are,  as  a  rule,  connected  with  changes  in  the  aorta  and  the 
other  blood  vessels,  a  sharp  division  between  heart  disease  and  vascular  disease 
is  impossible. 

1.     INTERSTITIAL   MYOCARDITIS 

(Fibroid  regeneration  of  the  Myocardium.    Sclerosis  of  the  Coronary  Arteries) 

.ZEtiology  and  Pathological  Anatomy. — The  anatomical  changes  of  inter- 
stitial myocarditis  consist  in  irregular-shaped,  glistening  white  spots,  often 


DISEASES  OF-  THE  MYOCARDIUM  415 

very  numerous,  interspersed  through  the  cardiac  muscle  where  there  has  been 
a  partial  or  complete  destruction  of  the  muscle  fibers  and  the  substitution  i'm- 
them  of  a  firm,  fibrinous,  cicatricial  connective  tissue.  These  places,  which 
are  best  found  by  making  horizontal  sections  of  the  myocardium,  occur  par- 
ticularly in  the  left  ventricle,  and  especially  at  its  apex  and  in  its  anterior 
wall ;  hut  they  may  also  he  found  everywhere,  and  especially  in  the  papillary 
muscles. 

Besides  the  ventricles,  the  auricles  must  also  be  carefully  examined,  as  in- 
terstitial changes  sometimes  locate  themselves  there  by  preference.  Often  we 
may  observe  fibroid  changes  as  slightly  glistening  retracted  spots  on  the  endo- 
cardial or  pericardial  surface  of  the  heart.  The  microscope  alone,  naturally, 
can  give  definite  information  regarding  the  extent  of  the  disease,  and  the 
condition  of  the  muscular  tissue. 

For  the  origin  of  interstitial  myocarditis,  two  viewpoints  are  chiefly  to 
be  considered.  In  the  smaller  number  of  cases  it  is  the  sequel  to  a  genuine 
acute  localized  myocarditis,  such  as  occasionally  occurs  in  articular  rheuma- 
tism and  other  infectious  diseases  (above  all,  in  diphtheria,  but  also  in  scar- 
latina, typhoid,  influenza,  etc.). 

Here  the  history  sometimes  points  to  such  an  origin  of  the  disease.  But  in 
the  majority  of  cases  of  interstitial  myocarditis  there  is  no  inflammation  in 
the  limited  sense  of  the  term,  but  we  have  the  sequela?  of  a  preceding  endar- 
teritis (arteriosclerosis)  of  the  coronary  arteries  of  the  heart.  In  places 
where  this  change  in  the  vessel  causes  marked  diminution  of  its  lumen,  the 
corresponding  portion  of  the  myocardium  is  imperfectly  supplied  with  arterial 
blood,  and  in  consequence  the  muscular  fibers  gradually  degenerate,  lose  their 
nuclei,  and  change  into  a  friable,  cheesy  detritus.  In  place  of  the  destroyed 
muscular  fiber  there  is  a  new  growth  of  connective  tissue.  "With  ordinary 
endarteritis  these  processes  are  slow  and  gradual,  hut  under  certain  circum- 
stances there  may  be  a  somewhat  rapid  occlusion  of  the  branches  of  the  coro- 
nary arteries,  because  of  thrombosis  or  embolism  of  proximal  origin.  In  such 
cases  we  have  a  genuine  cardiac  infarction,  presenting  a  spot  of  anasmic  necro- 
sis, or  sometimes  a  rather  fresh  brownish-yellow  hemorrhagic  infiltration. 

Of  course,  this  limited  necrosis  and  interstitial  new  growth  will  not  occur 
if,  in  spite  of  the  existence  of  arteriosclerosis,  the  direct  supply  of  blood  is 
still  sufficient,  or  is  eked  out  by  the  collateral  circulation. 

If  the  formation  of  connective  tissue  is  extensive,  the  entire  heart  wall 
may  become  decidedly  thinner,  so  that  it  yields  to  the  internal  pressure 
of  the  blood.  This  sometimes  occasions  in  the  left  ventricle  the  bulging  of  a 
limited  portion  of  the  wall  of  the  heart,  so-called  cardiac  aneurism.  A  cardiac 
aneurism  of  this  sort,  and  also  an  extensive  fresh  infarction,  may  exceptionally 
result  in  rupture  of  the  heart  with  escape  of  blood  into  the  pericardium,  and 
sudden  death.  Of  still  greater  importance,  because  far  more  frequent,  is  the 
formation,  in  places  where  the  fibroid  process  reaches  to  the  endocardium,  of 
parietal  thrombi  inside  the  heart.  These  sometimes  give  rise  to  embolism  in 
distant  organs. 

As  to  further  pathologic  changes  in  the  heart  we  find  that  certain  portions 
of  the  heart  are  not  infrequently  dilated  or  hypertrophied.  The  dilatation 
may,  at  least,  in  part,  he  due  to  the  diminished  resistant  power  of  the  cardiac 
walls,  hut  in  case  of  hypertrophy  we  must  always  seek  for  special  causes,  inas- 


416  DISEASES   OF   THE   CIRCULATORY   ORGANS 

much  as  sclerosis  of  the  coronary  arteries  as  such  cannot  lead  to  hypertrophy 
of  a  portion  of  the  heart.  As  a  rule,  the  cause  is  easily  discovered,  either  in 
an  associated  arteriosclerosis,  or  in  those  factors,  such  as  dissipation,  which 
may  occasion,  simultaneously  with  arteriosclerosis,  an  idiopathic  hypertrophy 
of  the  heart.  Of  course,  we  must  also  bear  in  mind  the  possible  but  excep- 
tional presence  of  such  complicating  diseases  as  interstitial  nephritis,  or  pul- 
monary emphysema.  With  regard  to  the  right  ventricle,  the  fact  has  weight 
that  it  must  hypertrophy  as  a  result  of  congestion  in  the  pulmonary  circuit, 
when  the  left  ventricle  is  permanently  weakened. 

The  causes  of  this  by  no  means  rare  form  of  myocarditis  which  we  have 
just  described,  and  which  is  due  to  sclerosis  of  the  coronary  arteries,  are,  in 
general,  of  course,  the  same  as  those  of  chronic  endarteritis  (arteriosclerosis). 
Often  the  sclerosis  of  the  coronary  arteries  is  merely  a  part  of  a  general  arterio- 
sclerosis, but  we  sometimes  find  comparatively  marked  changes  in  the  coro- 
naries,  although  there  are  no  specially  extensive  atheromatous  changes  in  the 
other  arteries  of  the  body,  and  again,  when  there  is  well-marked  arterio- 
sclerosis elsewhere,  the  coronary  arteries  may  show  slight  symptoms  of  dis- 
ease, if  any. 

Of  the  various  active  setiological  factors,  the  most  important  are  no  doubt 
chronic  alcoholism  and  general  dissipation.  Furthermore,  excessive  smoking 
is  certainly  a  not  rare  cause,  as  I  have  had  occasion  to  satisfy  myself,  espe- 
cially in  my  present  eastern  sphere  of  activity.  In  other  cases  long-continued 
severe  physical  labor  seems  to  favor  the  development  of  arteriosclerosis,  and 
clinical  experience  shows  that  an  important  cause  of  sclerosis  of  the  coronary 
arteries,  particularly,  lies  in  great  mental  effort  and  excitement,  which  indeed 
are  not  infrequently  combined  with  the  above-mentioned  factors — for  example, 
in  the  case  of  extraordinarily  active  business  men,  speculators,  high  officials, 
physicians,  and  others.  All  these  considerations  go  to  explain  the  fact  that 
sclerosis  of  the  coronary  arteries  is  seen  far  more  often  in  the  male  than  in 
the  female  sex.  That  age  plays  an  important  part  is  universally  acknowledged. 
It  is  true  of  interstitial  myocarditis,  as  of  arteriosclerosis  in  general,  that,  as 
a  rule,  persons  attacked  in  the  second  half  of  life,  from  forty  years  of  age  on. 
Finally,  we  must  add  that  hereditary  tendencies  to  the  development  of  arterio- 
sclerosis in  general,  and  sclerosis  of  the  coronary  arteries  in  particular,  cannot 
be  denied. 

That  form  of  disease  of  the  coronary  arteries  deserves  special  mention  which 
is  of  syphilitic  origin,  and  therefore  somewhat  distinct  from  ordinary  arterio- 
sclerosis. It  is  scarcely  possible  to  doubt  the  occurrence  of  a  specific  syphilitic 
endarteritis  of  the  coronary  arteries,  usually  in  conjunction  with  a  general 
syphilitic  endarteritis  (vide  infra),  giving  rise  to  almost  exactly  the  same 
symptoms  as  ordinary  arteriosclerosis.  At  any  rate,  this  point  should  in  every 
case  be  considered,  for  therapeutic  reasons  if  for  none  other  (vide  infra). 

Secondary  chronic  myocarditis  as  a  sequel  to  chronic  endocarditis  (valvular 
disease)  is  only  exceptionally  of  any  importance  in  itself,  though  of  the  great- 
est significance  in  the  clinical  picture.  The  endocarditic  process  may  extend 
directly  to  the  neighboring  muscular  layers  of  the  heart,  or  there  may  occur, 
especially  in  association  with  aortic  endocarditis,  embolic  infarctions,  the  de- 
velopment of  which  is  the  same  as  of  the  previously  described  thrombotic  in- 
farctions of  the  heart.     Finally,  there  is  the  possibility  that  myocarditis  and 


DISEASES  OK  THE   MYOCARDIUM  417 

endocarditis  might  appear  simultaneously,  as  in  polyarllirilis  and  other  infec- 
tious diseases. 

Clinical  History. — We  must  first  mention  that  sometimes  quite  extensive 
cicatricial  formation  may  be  found  in  the  cardiac  muscle  postmortem,  without 
the  occurrence  of  any  manifest  symptoms  referable  to  the  heart  during  life. 
We  see,  then,  that  the  heart  may,  under  some  circumstances,  undergo  quite 
a  considerable  loss  in  its  contractile  substance  without  injury. 

In  many  other  cases,  however,  the  heart's  capacity  for  work  suffers  so  much 
that  the  same  symptoms  arise  as  in  valvular  disease.  The  course  of  such  cases 
may  be  very  chronic.  The  symptoms  begin  quite  gradually.  The  patient  first 
has  a  slight  dyspnoea  or  palpitation,  and  a  feeling  of  distress  and  pressure  in 
the  chest,  but  only  from  external  causes,  such  as  slight  physical  exertion. 
Sometimes  there  is  marked  general  weakness  and  languor.  The  patients  have 
an  unhealthy  sallow  look.  They  become  easily  tired,  feel  depressed,  and 
scarcely  capable  of  any  great  bodily  or  mental  exertion.  The  symptoms  grad- 
ually increase,  and  just  the  same  results  of  disturbance  of  the  circulation  appear 
as  in  all  the  other  forms  of  heart  disease.  The  difficulty  in  breathing  becomes 
more  marked,  oedema  occurs,  signs  of  stasis  in  the  liver,  intestines,  and  kidneys 
appear — in  short,  the  well-known  type  of  general  circulatory  disturbance 
develops. 

Physical  examination  of  the  heart  shows  marked  anomalies  of  the  heart's 
action  in  most  of  the  severe  cases.  The  pulse  is  often  irregular  in  regard  to 
its  rhythm  and  the  intensity  of  its  single  beats,  but  the  arrhythmia  may  also 
be  wholly  absent  in  spite  of  the  degeneration  of  the  myocardium,  as  we  have 
often  convinced  ourselves.  The  pulse  is  at  first  quite  strong  and  full,  and  often, 
because  of  the  general  arteriosclerosis,  increased  in  tension;  later  it  becomes 
weaker,  of  lower  tension,  and  at  last  sometimes  very  small.  As  a  rule,  it  is 
increased  in  frequency,  but  we  sometimes  notice  in  chronic  myocarditis  per- 
sistent slowing  of  the  pulse  to  60,  50,  or  even  less,  in  a  minute.  With  this 
slowness  of  the  pulse  there  is  also  frequently  irregularity  of  the  heart's  action, 
especially  the  appearance  of  occasional  double  beats  (pulsus  bigeminus). 

If  persistent  and  marked  slowing  of  the  pulse  exists  (30  to  40  beats),  a 
careful  observation  of  the  auricular  pulsations  (usually  observable  in  the  ve- 
nous pulsations  in  the  neck)  shows  that  their  number  is  much  greater.  Fre- 
quently it  is  just  double  that  of  the  ventricular  pulsations  (radial  pulse).  In 
isolated  and  rare  cases  a  very  extreme  slowing  of  the  cardiac  beat  occurs 
(down  to  16  to  12  beats  per  minute).  Then  occasionally  there  are  attacks 
of  unconsciousness  with  complete  cessation  of  the  pulse  and  respiration,  and 
sometimes  also  with  epileptiform  seizures  (so-called  Adams-Stokes'  disease). 
Percussion  usually  shows  an  increase  of  the  heart's  dullness,  due  to  dilatation 
or  hypertrophy  of  the  heart,  the  increase  being  either  general  or  chiefly  on  one 
side.  Auscultation  shows  the  absence  of  any  murmur,  and  hence  the  absence 
of  valvular  disease.  The  heart  sounds  are  distinctly  audible,  and  sometimes 
quite  loud  and  sharp,  but  in  the  later  stages  often  low  and  obscure.  The  pul- 
monic second  sound  is  accentuated,  when  there  is  stasis  of  the  pulmonary  cir- 
culation. Repeatedly  we  have  found  the  second  sound  for  a  long  time  very 
plainly  divided  (reduplicated).  We  must  also  mention  that  sometimes  in 
pure  myocarditis  a  systolic  murmur  is  heard  at  the  apex  which  is  due  either 
to  a  relative  insufficiency  of  the  mitral  valve,  or  to  its  incomplete  closure,  as 


418  DISEASES  OF  THE   CIRCULATORY   ORGANS 

a  result  of  defective  muscular  action  of  the  left  ventricle  (perhaps  more  par- 
ticularly the  papillary  muscle) — so-called  muscular  insufficiency  of  the  valve. 
On  the  other  hand,  slight  systolic  or  diastolic  aortic  murmurs  not  seldom 
occur  as  a  result  of  arteriosclerotic  changes. 

We  must  make  particular  mention  of  one  symptom  of  sclerosis  of  the  coro- 
nary arteries,  which,  although  it  is  not  pathognomonic,  is  by  far  most  often 
seen  in  association  with  it,  and  therefore  has  an  important  diagnostic  sig- 
nificance. We  refer  to  the  attacks  of  so-called  angina  pectoris  (stenocardia, 
heart  pang).  These  attacks  of  genuine  angina  pectoris  (compare  also  the 
following  chapter)  consist  in  the  sudden  occurrence  of  pain  in  the  region  of 
the  heart,  extending  into  the  back,  the  left  shoulder,  and  the  left  arm  even  to 
the  tips  of  the  fingers.  In  severe  cases  the  pain  is  extremely  violent.  It  is  as 
if  the  chest  were  squeezed  in  a  vise.  At  the  same  time  there  is  a  decided 
feeling  of  anxiety  and  oppression,  as  well  as  complete  loss  of  strength — a 
sense  of  impending  death.  The  patient  seeks  some  support,  he  can  scarcely 
move,  scarcely  utter  a  few  words  in  a  whisper;  the  extremities  grow  cool,  the 
brow  moist  and  cold.  The  attack  may  be  directly  fatal,  but  this  is  the  ex- 
ce|)tion.  At  a  rule,  the  symptoms  pass  away  in  fifteen  or  thirty  minutes, 
or  sometimes  only  after  one  or  two  hours,  and  the  patient  gradually  recovers. 
In  many  cases  of  sclerosis  of  the  coronary  arteries  attacks  of  this  sort  occur 
very  often,  in  varying  severity.  Not  infrequently  an  attack  may  be  due  to 
some  special  cause,  such  as  the  bodily  exertion  of  a  long  walk  or  climb,  errors 
in  diet,  or  mental  excitement.    In  such  cases  bad  news  may  cause  death. 

With  regard  to  the  true  essence  of  angina  pectoris,  we  are  confined  to 
hypothesis.  The  intense  pain  indicates  irritation  of  the  sensory  nerves.  I  am 
inclined  to  compare  these  pains  to  the  severe  pains  in  the  extremities  accom- 
panying sclerosis  of  the  arteries  of  the  lower  limbs  and  also  to  many  forms 
of  trigeminus  neuralgia,  likewise  associated  with  arteriosclerosis.  Moreover, 
angina  pectoris  is  by  no  means  alone  dependent  upon  sclerosis  of  the  coronary 
arteries,  but  also,  without  doubt,  quite  as  frequently  upon  the  aortic  sclerosis, 
which  is  usually  present  as  well  {vide  infra,  chapter  on  Aneurism  of  the 
Aorta).  The  heart's  action,  as  such,  may  be  disturbed  simultaneously  with 
the  stenocardial  attack;  then  the  pulse  is  small  and  irregular  during  the 
attack.  Occasionally,  on  the  other  hand,  as  we  have  often  convinced  our- 
selves, it  shows  no  marked  change. 

Besides  genuine  angina  pectoris,  attacks  of  cardiac  asthma  are  not  infre- 
quent in  chronic  myocarditis.  This  differs  from  angina  pectoris  in  that  the 
peculiar  pain  and  constriction  are  not  present,  while  the  distress  for  breath, 
the  paroxysmal  dyspnoea,  is  prominent.  In  most  cases  of  this  sort  we  prob- 
ably have  really  to  deal  with  sudden  weakness  of  the  left  heart. 

The  general  course  of  the  disease  varies  considerably  in  different  cases. 
Much  depends  upon  the  patient — e.  g.,  upon  his  ability  to  take  good  care  of 
himself.  Sometimes  dyspnoea,  oedema,  and  other  general  symptoms  of  passive 
congestion  are  prominent,  and  in  such  cases  the  patient  is  alternately  better  or 
worse.  Other  cases  are  characterized  by  attacks  of  angina  pectoris.  The  ter- 
mination is  invariably  unfavorable.  It  may  either  occur  gradually  with  in- 
crease in  the  circulatory  disturbance,  or  with  complete  suddenness  like  a 
stroke. 

This  important  clinical  fact  of  sudden  apoplectiform  death  ("  paralysis  of 


DISEASES  OF.  THE   MYOCARDIUM  419 

the  heart  ")  in  patients  witli  sclerosis  of  the  coronary  arteries,  demands  consid- 
eration. It  usually  happens  in  elderly  persons  in  comfortable  circumstances 
an<l  good  livers,  who  up  to  that  time  have  not  regarded  themselves  as  really 
ill;  hut  they  have  repeatedly  had  slight  attacks  of  vertigo,  of  oppression,  etc. 
Suddenly  a  sort  of  apoplectic  attack  comes  on,  often  after  some  definite  cause, 
after  a  banquet,  or  after  some  physical  exertion  or  mental  excitement.  Death 
follows  in  a  few  moments,  or  after  a  deep  coma  that  lasts  for  several  hours  or 
even  days.  The  diagnosis  often  remains  in  doubt  in  such  cases,  especially 
if  we  have  not  known  the  patient  previously.  The  autopsy  shows,  as  the  sole 
pathological  lesion,  a  sclerosis  of  the  coronary  arteries,  with  a  more  or  less 
extensive  cicatricial  formation  in  the  heart.  Apparently  in  these  cases  the 
moment  must  suddenly  arise  when  the  supply  of  blood  to  the  heart  is  insuffi- 
cient, and  thus  death  is  caused.  Experiments  upon  artificial  closure  of  the 
coronary  arteries,  by  Cohnheim  and  others,  agree  perfectly  with  the  clinical 
facts  above  mentioned.  Artificial  narrowing  &f  the  coronary  arteries  may 
also  be  well  borne  for  a  long  time,  until  suddenly  both  halves  of  the  heart 
stand  still  in  a  condition  of  diastole.  Finally,  it  should  be  mentioned  that 
sudden  death  in  sclerosis  of  the  coronary  arteries  may  also  be  caused  by 
embolism  of  the  trunk  of  the  coronary  artery,  or,  as  in  one  case  seen  by  the 
author,  by  the  bursting  of  a  focus  of  myocarditis  with  hemorrhage  into  the 
pericardial  cavity. 

Diagnosis. — The  diagnosis  of  chronic  myocarditis  is  by  no  means  always 
easy  and  certain.  We  must  first  determine  that  there  is  a  cardiac  lesion  of 
some  kind.  This  is  usually  evident  from  the  secondary  symptoms  of  stasis, 
the  condition  of  the  pulse,  the  area  of  cardiac  dullness,  etc.  Then  the  ques- 
tion arises  whether  we  have  to  do  with  a  valvular  disease  or  with  a  myopathic 
disease  of  the  heart.  Here  auscultation  must  chiefly  decide.  The  absence  of 
a  heart  murmur,  in  spite  of  other  definite  signs  of  heart  disease,  speaks  against 
valvular  disease  but  not  with  complete  certainty.  All  murmurs  may  be  absent 
in  the  last  stages,  especially  with  a  high  degree  of  mitral  stenosis,  and  hence 
we  may  easily  confuse  mitral  stenosis  with  myocarditis,  particularly  when  there 
is  marked  arrhythmia  of  the  heart.  On  the  other  hand  we  have  already  stated 
that  in  pure  myocarditis,  with  the  valves  intact,  functional  murmurs  may  be 
present,  which  may  lead  to  an  erroneous  opinion  as  to  valvular  disease. 
Chronic  pericardial  adhesions  may  likewise  be  confused  with  a  myocarditis. 
If  continued  study  of  the  case  has  enabled  us  to  exclude  valvular  disease  or  an 
obliteration  of  the  pericardium,  it  remains  to  distinguish  between  chronic 
myocarditis  or  sclerosis  of  the  coronary  arteries  on  the  one  hand,  and  the  other 
diseases  of  the  myocardium  (vide  infra)  on  the  other.  To  make  this  distinc- 
tion with  absolute  certainty  is  not  always  possible.  All  the  diseases  named 
present  the  same  clinical  picture  of  cardiac  insufficiency,  but  what  the  anatom- 
ical conditions  may  be  which  occasion  this  cardiac  insufficiency  we  can  at 
present  only  conjecture  with  more  or  less  probability,  during  life.  If  all  the 
signs  of  a  marked  general  arteriosclerosis  (q.  v.)  are  present,  we  will  gener- 
ally not  be  far  wrong  in  also  assuming  a  sclerosis  of  the  coronary  arteries.  Of 
the  special  heart  symptoms,  the  most  characteristic  of  coronary  sclerosis  are 
persistent  bradycardia,  particularly  if  associated  with  arrhythmia  and  attacks 
of  true  angina  pectoris.  Persistent  rapidity  and  arrhythmia  of  the  pulse  occur 
in  interstitial  myocarditis,  just  as  in  other  myopathic  diseases  of  the  heart; 


420  DISEASES   OF  THE   CIRCULATORY   ORGANS 

but  arrhythmia  is,  in  general,  far  more  common  when  there  is  actual  myo- 
carditis than  when  there  is  simple  muscular  weakness  of  the  heart.  There 
is  self-evident  difficulty  in  the  diagnosis  of  cases  with  sudden  apoplectiform 
paralysis  of  the  heart,  and  in  distinguishing  them  from  apoplexy,  embolism, 
pancreatic  hemorrhage,  and  similar  causes  of  sudden  death. 

Prognosis. — The  prognosis  is  evident  from  what  has  been  already  said. 
Eecovery  is  impossible,  but  even  extensive  cicatricial  formation  in  the  heart 
may  probably  last  for  years  without  causing  much  annoyance.  We  must 
always  be  prepared  for  disturbances  of  compensation,  and  the  manifold  sud- 
den accidents  to  which  patients  with  myocarditis  are  exposed,  but  we  cannot 
foretell  the  time  of  their  occurrence. 

Treatment. — The  treatment  of  chronic  myocarditis  must  be  directed  first  to 
the  dietetic  and  hygienic  care  of  the  patient.  This  is  of  the  greatest  impor- 
tance. For  obese  persons  accustomed  to  high  living,  a  moderate,  simple  diet 
must  be  accurately  prescribed.  Alcoholic  beverages  must  be  greatly  limited 
or  wholly  forbidden,  and  not  more  than  two  light  cigars  or  a  few  cigarettes 
allowed  per  diem.  It  is  often  best  to  omit  smoking  entirely.  Moderate  bodily 
exercise  is  beneficial  for  the  promotion  of  the  circulation  and  the  more  rapid 
diminution  of  the  obesity,  but  the  patient  must  be  earnestly  warned  against 
too  violent  exertion.  The  best  measure  of  the  bodily  exercise  to  be  allowed 
is  the  subjective  condition  of  the  patient.  He  should  cease  his  exercise  as 
soon  as  he  notices  the  slightest  sensation  of  oppression  in  the  chest.  Neither 
must  mental  effort  be  excessive.  In  summer,  a  quiet  life  in  the  country  or 
some  mountain  region  is  to  be  advised,  or,  under  suitable  circumstances,  the 
cautious  use  of  the  waters  of  Kissingen,  Marienbad,  Nauheim,  Cudowa,  etc. 
Tepid  baths,  carbonic-acid  baths,  or  saline  baths  may  be  employed  even  at 
home  with  advantage.  Of  internal  remedies  iodid  of  potassium  has  been 
specially  recommended  to  be  used  persistently,  in  the  amount  of  8  to  15  gr. 
(gm.  0.5  to  1.0)  or  more  daily.  Iodid  of  potassium  enjoys  a  reputation  for 
an  especial  specific  action  upon  arteriosclerosis  in  general,  and  has  per- 
haps, also,  a  beneficial  effect  upon  arteriosclerosis  of  the  coronary  arteries. 
We  have  ourselves  seldom  seen  very  striking  results  from  its  use,  though  we 
frequently  give  it  a  trial,  particularly  if  there  exists  the  slightest  suspicion 
of  a  previous  syphilitic  infection.  Iodid  of  sodium  is  also  used  instead  of 
iodid  of  potassium,  and,  particularly  of  late,  sajodin  has  been  frequently  sub- 
stituted. With  disturbance  of  compensation,  and  with  abnormally  frequent, 
weak,  and  irregular  action  of  the  heart,  digitalis  and  similar  remedies  are  indi- 
cated, just  as  in  valvular  disease.  In  cases  with  an  abnormally  slow  pulse,  we 
may  use  them,  provided  great  caution  is  exercised,  but  we  must  also  be  gov- 
erned by  the  other  prevailing  symptoms.  In  severe  attacks  of  angina  pec- 
toris (see  the  following  chapter)  the  subcutaneous  injection  of  morphin  is  by 
far  the  most  efficient,  and  often  an  indispensable  remedy.  Further,  I  recom- 
mend, above  all,  nitroglycerin,  which  has  been  greatly  lauded  by  many  of  my 
patients.    I  usually  prescribe : 

^  Nitroglycerin!    gr.  ts     (gm.  0.025) ; 

Tinct   Valerianae  aether.,  J       .         (25Q  ^ 

Spirit,  astheris.  nitrosi,  ) 
Dose:  15  to  20  drops. 


DISEASES   OP  THE   MYOCAKDJIM  42  i 

The  nitroglycerin  may  also  be  combined  with  morphin,  for  example: 

1£    Nitroglycerin!    gr.  \     (gm.  0.02); 

Morph.   linn- gr.  iij  (gm.  0.2)  ; 

Spirilus,         )  aa 3i.gs<    (1Q0  ccx 

Aquas    dest.,  ) 

Dose :  20  drops. 

Inhalations  of  amyl  nitrite  also  act  favorably  at  times.  For  the  milder 
stenocardial  symptoms  the  nitrite  of  sodium  is  occasionally  useful. 

T}   Nairn  nitrosi    gr.  xv  to  xxx   (gm.  1.0  to  2.0)  ; 

Aquam  dest.,  ad §iv  (120.0  c.c). 

Dose:  2  to  3  teaspoonfuls  daily. 

It  may  also  be  used  in  combination  with  nitrate  of  potassium,  as  in  the 
following : 

1^   Sodii  nitritis gr.  xv       (gm.  1.0) ; 

Potassii  nitratis    3vj  (gm.  24.0)  ; 

Elseosacchari   menthse    5j  gr.  xv  (gm.  5.0). 

Dose :  A  knife-pointful  three  times  daily.  Diuretin  has  also,  not  infre- 
quently, a  decidedly  favorable  effect  upon  the  stenocardial  attacks,  and  may 
be  given  in  combination  with  digitalis,  caffein,  etc.  In  cardiac  asthma,  stimu- 
lants are  indicated  (strophanthus,  camphor),  but  often  narcotics  as  well.  Mus- 
tard plasters,  the  application  of  cold  and  of  heat,  hot  foot  baths,  etc.,  are  also 
employed. 

2.     SO-CALLED    IDIOPATHIC    HYPERTROPHY    OF    THE    HEART 

(Functional  Strain  of  the  Heart.     [Heart  Overstrain.     Soldier's  Heart.]) 

iEtiology  and  General  Pathology. — Not  infrequently  cases  during  life  pre- 
sent all  the  symptoms  of  an  uncompensated  cardiac  lesion  and  yet  the  autopsy 
discloses  merely  hypertroplry  of  the  heart  with  a  greater  or  less  degree  of 
accompanying  dilatation.  There  is  no  lesion  of  valves,  coronary  arteries,  or 
myocardium.  The  cardiac  hypertrophy,  which  involves  the  left  ventricle 
chiefly,  but  often  both  ventricles,  cannot  be  regarded  as  secondary  in  the 
ordinary  sense  of  the  word,  for  in  the  heart  itself  and  in  the  other  organs  we 
find  nothing  which  can  call  forth  a  secondary  hypertrophy  of  the  cardiac 
muscle — no  valvular  disease,  no  chronic  nephritis,  no  general  arteriosclerosis, 
and  no  pulmonary  emphysema.  Hence  we  term  these  cases  "  primary  idio- 
pathic "  cardiac  hypertrophy,  in  the  sense  that  we  cannot  discover  any  other 
primary  disease. 

Notwithstanding,  we  must  in  these  cases  also  seek  the  cause  of  the  cardiac 
hypertrophy  in  some  excessive  demand  upon  the  cardiac  muscle,  and  as  there 
are  no  macroscopic  anatomical  or  mechanical  changes  involving  an  increase  in 
the  cardiac  activity,  we  must  assume  a  functional  overstrain  of  the  heart. 

As  a  matter  of  fact,  a  careful  anamnesis  often  gives  us  definite  grounds 
for  the  assumption  that  there  has  been  functional  damage  of  the  heart  muscle. 
27 


422  DISEASES  OP  THE  CIRCULATORY  ORGANS 

Among  the  most  frequent  causes  is  habitual  embarrassment  of  the  circula- 
tion by  excess  in  eating  and  drinking.  There  can  be  no  doubt  that  every  time 
food  is  taken  in  large  amount  there  is  a  temporary  increase  in  the  activity  of 
the  heart,  the  frequency  of  the  pulse,  and  the  tension  in  the  arteries.  This  is  in 
part  because  the  specific  gravity  of  the  blood  is  temporarily  increased  by  the 
material  taken  into  it,  and  in  part  because  the  products  of  metabolism  in  the 
blood  have  a  direct  stimulating  action  upon  the  heart  or  the  blood  vessels, 
and  finally,  because  an  excessive  ingestion  of  liquids  temporarily  increases 
the  total  amount  of  blood.  In  brief,  there  are  numerous  persons  of  the  more 
favored  classes  who  indulge  too  freely  in  eating  and  drinking,  and  for  years 
go  to  excess  in  the  pleasures  of  the  table ;  and  in  the  case  of  such  persons  there 
is,  during  a  great  part  of  their  life,  although  not  all  the  time,  that  condition 
which  the  older  physicians  termed  plethora.  All  these  circumstances  which 
we  have  mentioned  occasion  an  increase  in  the  demands  upon  the  heart,  espe- 
cially its  left  ventricle.  The  heart  performs  this  extra  work  laid  upon  it,  and 
consequently  becomes  gradually  hypertrophied.  From  what  has  been  said, 
it  is  easy  to  understand  why  this  form  of  cardiac  hypertrophy  is  especially  fre- 
quent in  the  obese,  and  particularly  in  men  from  forty  to  fifty  years  old, 
though  sometimes  much  younger.  We  have  seen  by  far  the  most  frequent 
examples  of  it  in  great  beer  drinkers,  and  so  in  persons  whose  business  tempts 
them  to  excessive  indulgence  in  beer,  such  as  landlords,  brewers,  hop  dealers, 
butchers,  and  many  others.  Persons  of  this  sort  often  drink  for  years,  almost 
daily,  four  or  five,  or  even  eight  or  ten,  liters  (quarts)  of  beer.  Let  the 
reader  consider  what  an  amount  of  liquid,  and  at  the  same  time  of  nourish- 
ment (for  one  liter  of  beer  contains  about  50  or  60  gm.  [2  ounces]  of  carbo- 
hydrates), is  in  this  way  alone  introduced  into  the  blood.  This  explains  the 
great  frequency  of  cardiac  hypertrophy  which  Bollinger  has  shown  to  exist  at 
Munich ;  but  the  "  Munich  beer-heart "  is  seen  with  unfortunate  frequency  in 
other  towns  than  Munich.  The  alcohol  is  probably  not  a  factor  in  the  devel- 
opment of  the  hypertrophy  of  the  heart,  but  we  may  well  suppose  that  it 
promotes,  or  at  least  hastens,  the  degenerative  changes  in  the  cardiac  muscle, 
and  particularly  in  the  cardiac  nerves,  which  at  last  render  the  heart's  action 
inadequate  and  the  circulation  imperfect.  For  the  development  of  cardiac 
hypertrophy  in  itself  is  a  circumstance  which  does  not  impair  the  health, 
but  rather  preserves  it;  only,  experience  teaches  us  that  no  heart  can  unin- 
terruptedly perform  an  amount  of  work  which  is  physiologically  excessive, 
and  escape  final  exhaustion — the  point  of  time  depending  upon  the  individ- 
ual vigor  and  other  associated  factors. 

A  second  cause  of  idiopathic  hypertrophy  is  persistent  muscular  strain. 
Muscular  exertion  always  increases  the  demands  upon  the  cardiac  activity. 
There  is  an  increase  in  the  frequency  of  the  pulse  and  in  the  amount  of  blood 
passing  through  the  heart.  If  excessive  bodily  exertion  is  habitual  for  a  con- 
siderable period  of  time,  there  finally  develops  hypertrophy  of  the  heart, 
usually  affecting  both  ventricles,  but  especially  the  left.  Thus  is  explained 
the  hypertrophy  sometimes  seen  in  blacksmiths,  locksmiths,  baggage  carriers, 
laborers  in  vineyards  ("Tubingen  heart"),  soldiers  after  severe  campaigns, 
athletes,  and  others.  Why  this  hypertrophy  should  sometimes  occur  and 
sometimes  be  absent,  under  apparently  similar  conditions,  must  be  explained 
by  the  difference  in  the  physiological  capacity  of  the  individual.     Here,  too, 


DISEASES   OF  THE   MYOCARDIUM  423 

the  ;il (normality  of  the  condition  does  not  become  evident  till  the  functional 
ability  of  the  heart  begins  to  fail  ("heart  overstrain,"  "irritable  heart  "). 
In  the  third  place,  we  must  assume  that  in  some  few  cases  of  idiopathic 

hypertrophy  of  the  heart,  in  which  none  of  tbe  causes  yet  named  are  operative, 
an  abnormal  nervous  irritation  of  the  heart  exists  which  increases  its  activity 
(force  and  rapidity),  and  hence,  finally  leads  to  its  hypertrophy.  This  is 
perhaps  the  explanation  of  many  cases  of  cardiac  hypertrophy  in  persons  who 
have  long  been  exposed  to  many  sorts  of  psychical  excitement.  The  cardiac 
hypertrophy  of  exophthalmic  goiter,  and  the  related  cardiac  hypertrophy 
often  seen  in  goiter  without  other  symptoms  of  Basedow's  disease  (the  so- 
called  goiter  heart),  may  also  be  put  in  this  category.  These  cases  suggest 
also  that  perhaps  other  abnormal  products  in  the  body,  whose  origin  may  be 
unknown,  might  stimulate  or  harm  the  heart,  and  thus  finally  lead  to  myo- 
pathic heart  affections.  Especially  in  women,  particularly  during  the  climac- 
teric period,  do  muscular  disturbances  of  the  heart  occur.  Absolutely  no 
external  causes  can  be  demonstrated  for  these  cases,  and  therefore  the 
hypothesis  of  some  kind  of  disturbance  of  "  internal  secretion  "  with  abnor- 
mal effect  upon  the  heart's  action  suggests  itself.  To  be  sure,  nothing  definite 
is  known  on  this  subject  (cf.  infra  chapter  on  the  Nervous  Affections  of  the 
Heart). 

Not  infrequently  we  may  assume  that  several  of  the  above-mentioned 
causes  of  cardiac  hypertrophy  have  been  operative  at  the  same  time.  Thus, 
idiopathic  hypertrophy  of  the  heart  is  seen  particularly  often  in  individuals 
who  have  to  undergo  great  mental  strain  and  excitement,  and  at  the  same 
time  are  heavy  drinkers,  or  in  those  who  drink  beer  to  excess  and  are  also 
at  the  same  time  compelled  to  labor  strenuously  (brewery  laborers,  etc.).  It 
is  likewise  comprehensible  that  the  same  injurious  factors  (mode  of  living, 
alcohol,  tobacco,  etc.)  may  often  produce  simultaneously  a  variety  of  effects. 
Thus  we  frequently  find  muscular  disease  of  the  heart  combined  with  other 
related  diseases  (arteriosclerosis,  chronic  nephritis,  gout,  diabetes,  affections 
of  the  liver,  etc.). 

There  is  usually  associated  with  the  hypertrophy  a  dilatation,  referable  to 
the  persistent  overdistention  of  the  ventricles  during  diastole.  The  majority 
of  cases  of  functional  cardiac  hypertrophy  belong,  therefore,  to  the  type  of 
"  eccentric  hypertrophy."  The  weaker  and  more  yielding  the  myocardium 
becomes  with  the  course  of  time,  and  the  more  passive  congestion  affects  the 
heart  itself  (particularly  the  auricles  and  right  ventricle),  the  more  the  dila- 
tation increases  (secondary  congestive  dilatation)  ;  and  with  it  comes  degen- 
eration of  the  cardiac  muscle,  or,  at  any  rate,  functional  weakness  of  the 
same,  giving  rise  to  symptoms  of  cardiac  insufficiency. 

Clinical  History. — Idiopathic  hypertrophy  of  the  heart  may  certainly  exist 
for  a  long  time  without  causing  the  patient  any  subjective  disturbance.  We 
have  already  emphasized  the  fact  that  it  is  precisely  the  cardiac  hypertrophy 
which  protects  the  patient  for  a  time  from  the  onset  of  marked  symptoms. 
Prodromata  may  occur  for  a  long  time  before  severe  disturbance  sets  in. 
Among  these  are  palpitation,  a  certain  sense  of  discomfort  in  the  cardiac 
region,  and  slight  dyspnoea.  The  symptoms  begin  when  the  heart  can  no 
longer  respond  to  the  demands  made  upon  it,  and  when  it  begins  to  fail. 
Then  all  the  symptoms  of  cardiac  insufficiency  arise,  in  just  the  same  way  as 


424  DISEASES   OF  THE   CIRCULATORY  ORGANS 

in  valvular  disease  and  in  chronic  myocarditis.  Hence  we  need  not  go  into 
the  details  of  the  disturbances  of  compensation  again.  The  whole  series  of 
symptoms  of  stasis,  as  well  as  the  attacks  of  angina  pectoris  and  cardiac 
asthma,  described  in  the  preceding  chapter,  also  occur  in  idiopathic  hyper- 
trophies and  dilatations  of  the  heart. 

Another  subjective  disturbance  is  the  peculiar  and  often  very  annoying 
feeling  of  "  fluttering  "  of  the  heart — that  is,  a  momentary  feeling  of  flutter- 
ing contraction  of  the  heart.  This  symptom  indicates,  probably,  abnormal 
conditions  of  contraction,  and  must  by  no  means  be  confounded  with  the 
numerous  sensations  which  hypochondriacal  and  neurasthenic  patients  refer 
to  the  heart.  If  the  action  of  the  heart  is  irregular,  and  especially  if  there 
is  a  tendency  to  bigeminal  pulsation,  many  patients  feel  every  bigeminal  con- 
traction as  a  jolt  or  stopping  of  the  heart  ("  stumbling  of  the  heart"). 

The  general  course  of  the  disease  differs  considerably  in  individual  cases. 
Sometimes  there  is  moderate  difficulty  in  breathing  for  a  long  time,  especially 
on  any  physical  exertion.  The  patient  often  complains  of  great  languor,  or 
nervous  irritability,  and  sometimes  of  attacks  of  vertigo  and  faintness,  and 
a  tendency  to  perspiration.  The  appetite  is  poor,  and  there  is  very  apt  to  be 
constipation.  The  condition  may  become  quite  suddenly  worse  after  any 
marked  injurious  influence,  especially  after  great  physical  exertion  or  mental 
excitement.  Physical  examination  discloses  all  the  signs  of  hypertrophy  of 
the  heart.  In  the  first  place,  the  left  ventricle  is  usually  enlarged,,  correspond- 
ing to  the  direct  causes  of  the  condition.  This  enlargement  is  often  better 
appreciated  by  accurate  observation  of  the  apex  beat  than  by  percussion. 
Later  the  right  side  of  the  heart  also  becomes  hypertrophied ;  dullness  on 
percussion  then  extends  over  the  lower  part  of  the  sternum,  with  epigastric 
pulsation  and  undulator}^  movements  in  the  veins  of  the  neck.  The  heart 
sounds  are  pure,  at  first  sharp,  later  sometimes  muffled  and  feeble.  We  lay 
especial  value  on  the  characteristics  of  the  first  sound  of  the  heart.  A  dull, 
indistinct  sound  is  probably  a  sign  of  considerable  dilatation,  while  a  normal 
valvular  sound  indicates  a  vigorous  systole.  In  general,  there  is  persistent 
frequency  of  the  pulse,  at  least  in  patients  who  are  led  to  seek  the  physician 
because  of  beginning  sjonptoms.  Infrequency  of  the  pulse  probably  indicates, 
in  most  cases,  coexistent  sclerosis  of  the  coronary  arteries  (vide  supra).  The 
frequent  pulse  may  for  a  long  time  remain  regular,  but  it  is  not  always  so. 
So  long  as  the  left  ventricle  does  its  work  well  the  pulse  may  be  tense,  and 
the  second  aortic  sound  distinct ;  but  if  the  heart  becomes  insufficient  the  pulse 
grows  small,  feeble,  often  irregular;  the  heart  sounds  grow  faint,  and  not 
infrequently  that  sign  appears  which  is  known  as  bruit  de  galop  or  gallop 
rhythm,  and  consists  in  a  peculiar  reduplication  of  the  first  sound  of  the 
heart ; 1  for  each  beat  of  the  pulse  we  hear  three  sounds  over  the  heart.  At 
the  same  time  the  dyspnoea  and  oppression  in  the  chest  increase,  the  amount 


1  This  sign  is  not  infrequently  found  in  idopathic  hypertrophy  of  the  heart,  in  myocarditis, 
and  particularly  in  secondary  cardiac  hypertrophy  following  chronic  nephritis.  It  has  not  yet 
been  fully  and  definitely  explained.  Probably  we  have  to  deal  with  an  audible  muscle-sound, 
originating  in  the  auricle,  perhaps  with  peculiar  irregularities  in  the  contraction  of  the  heart. 
Not  infrequently  we  can  infer,  from  the  palpation  of  the  apex  beat,  that  a  gallop  rhythm  exists, 
for  the  reduplication  of  the  heart  beat  is  distinctly  felt.  It  is  also  possible  that  the  two  ventricles 
may  not  contract  simultaneously. 


DISEASES  OF' THE   MYOCARDIUM  425 

of  urine  diminishes,  and  oedema  appears  in  the  legs.  We  now  have  the  com- 
plete picture  of  an  uncompensated  heari  disease!  Willi  proper  treatmenl  the 
symptoms  may  disappear  again;  but,  sooner  or  later,  they  return.  Death 
finally  ensues  from  general  dropsy  or  from  some  complications  or  intercurreni 
attacks,  among  which  we  may  mention  embolic  processes. 

Cases  of  sudden  death  (paralysis  of  the  heart)  from  heart  failure  occur 
not  very  infrequently,  as  we  know  from  experience,  in  idiopathic  hypertrophy 
of  the  heart  independently  of  chronic  myocarditis. 

Diagnosis. — It  is  by  no  means  an  easy  task  for  the  physician  to  make  an 
absolute  diagnosis  of  idiopathic  hypertrophy  of  the  heart.  Sometimes,  when 
the  subjective  symptoms  suggest  an  examination  of  the  heart,  it  is  easy  to 
make  out  an  increase  in  the  cardiac  dullness  and  a  displacement  of  the  apex 
beat;  but  in  other  cases  the  presence  of  emphysema,  or  obesity,  or  even  of 
dropsy,  makes  the  plrysical  examination  very  difficult.  If  an  enlargement  of 
the  heart  has  been  demonstrated,  we  must  then  exclude  valvular  disease,  espe- 
cially mitral  stenosis,  and  also  secondary  hypertrophy,  as  a  result  of  chronic 
interstitial  nephritis,  or  other  causes.  It  may  be  difficult  to  rule  out  nephritis 
if  the  patient  is  suffering  from  passive  congestion  when  he  first  comes  under 
observation,  for  then  it  is  often  hard  to  say  whether  the  albuminuria  which 
may  be  present  is  to  be  referred  to  actual  renal  disease,  or  to  passive  con- 
gestion. Even  if  we  can  exclude  nephritis,  we  have  still  to  determine  whether 
there  is  simple  hypertrophy  of  the  heart  or  an  interstitial  ni}rocarditis.  To 
settle  this  question'  is,  as  we  have  already  said,  not  always  easy.  JEtiology 
is  always  important — for  example,  if  there  has  been  an  excess  in  beer  or  in 
muscular  exertion.  Frequent  attacks  of  angina  pectoris,  arrhythmia,  and  a 
lowering  in  the  rate  of  the  pulse,  suggest  sclerosis  of  the  coronary  arteries. 

The  X-ray  examination  gives  very  important  information.  It  permits  of 
an  almost  certain  decision,  not  only  as  to  the  size  of  the  heart,  but  above 
all  as  to  the  condition  of  the  aorta,  whether  there  is  marked  aortic  sclerosis, 
aneurismal  dilatation,  or  the  like.  Not  infrequently  diseases  of  the  myocar- 
dium are  confounded  with  chronic  obi  iterative  pericarditis.  When  we  con- 
sider this  latter  condition  we  shall  refer  again  to  the  differential  diagnosis. 

Treatment. — The  main  points  in  the  treatment  of  idiopathic  hypertrophy 
of  the  heart  are,  in  general,  exactly  the  same  as  for  valvular  disease  and 
interstitial  myocarditis.  We  may,  therefore,  refer  the  reader  for  these  to  the 
preceding  chapters.  A  few  remarks  may  be  permitted,  however,  in  regard 
to  certain  points  of  view  in  the  so-called  dietetic  and  physical  treatment  of 
patients  afflicted  with  heart  disease. 

1.  Regulation  of  the  Amount  of  Liquids  'Token. — As  is  well  known,  it  was 
Oertel  who,  a  number  of  years  ago,  aroused  interest  in  a  "  new  method  "  of 
treatment  of  insufficiency  of  the  heart  muscle.  He  lays  particular  stress  upon 
the  "  desiccation  "  of  the  body,  and  especially  of  the  blood.  He  believes  that 
he  can  diminish  the  amount  of  blood  in  the  body  by  withdrawing  liquids,  and 
thus  lighten  the  task  of  the  heart  and  restore  the  normal  circulation.  On 
this  view  rest  the  proscription  of  excessive  drinking  and  the  limitation  of 
liquid  nourishment,  such  as  soup,  etc.  But,  from  numerous  physiological 
experiments,  we  know,  however,  that  the  body  maintains  its  amount  of  blood 
with  great  tenacity  at  a  certain  constant  ratio,  for  it  is  able  in  many  ways 
(secretion  and  absorption  of  liquids)  to  make  speedy  compensation  for  varia- 


426  DISEASES   OF  THE   CIRCULATORY   ORGANS 

tions  arising  through  changes  in  the  amount  of  water  ingested.  It  is  a  priori 
scarcely  probable  that  the  total  amount  of  blood  in  patients  with  circulatory 
derangements  is  increased;  and  if  actually  there  is  a  retention  of  fluid  in  the 
body  (as  indeed  is  certainly  the  case  where  oedema  has  developed),  yet  the 
liquid  does  not  collect  in  the  vessels,  but  in  the  lymph  spaces  of  the  inter- 
stitial tissue,  or  possibly  in  the  cells  of  the  parenchyma  itself.  That  the  total 
amount  of  water  in  the  system  may  be  subjected  to  great  variations  cannot 
be  doubted.  The  assumption,  however,  that  in  circulatory  disturbances  there 
is  an  increase  in  the  amount  of  water  contained  in  the  blood  has  been  directly 
disproved  by  the  blood  count,  by  the  determination  of  the  specific  gravity 
of  the  blood,  etc.  That  there  should  be  any  increase  in  the  labor  demanded 
of  the  heart  requires  that  a  large  amount  of  fluid  should  be  added  to  the 
blood  in  a  relatively  short  space  of  time,  so  that  an  actual,  although  extremely 
temporary,  hydramiic  plethora  should  exist.  If  this  process  is  very  frequently 
repeated,  it  will  surely  result  in  a  permanent  hindrance  to  the  circulation. 
These  circumstances  are,  however,  actually  found  only  in  certain  patients, 
particularly  in  great  beer  drinkers.  In  them,  of  course,  to  forbid  the  inges- 
tion of  fluid  means  to  forbid  the  drinking  of  beer,  and  is  therefore  of  the 
greatest  benefit ;  and  we  cannot  insist  too  strongly  upon  the  necessity  of  this 
injunction  in  the  case  of  corpulent  beer  drinkers  who  are  beginning  to  have 
some  dyspnoea.  It  is  not,  however,  in  our  opinion,  permissible  to  apply  this 
rule  about  liquids,  as  is  sometimes  done,  to  every  patient  without  individual- 
izing. For  those  who  live  temperately  and  are  of  spare  figure,  the  amount 
of  fluid  ingested  needs  no  special  attention  from  the  plrysician.  The  condi- 
tions become  decidedly  more  complicated  in  heart  patients  suffering  from 
dropsy,  especially  if,  at  the  same  time,  signs  of  kidney  insufficiency  present 
themselves.  Here,  to  be  sure,  we  often  get  the  impression  that  a  decided 
reduction  in  the  amount  of  liquid  taken  assists  considerably  in  the  absorption 
and  excretion  of  the  oedema.  The  "  Karell  milk  cure,"  recently  again  recom- 
mended by  Lenhartz  and  others,  depends  upon  this  principle.  The  dropsical 
patient  receives  for  several  days  no  nourishment  and  no  liquid  except  200  c.c. 
of  milk  four  times  daily.  Under  this  diet,  at  times,  we  note  a  striking 
increase  in  the  excretion  of  urine,  and,  associated  with  this,  a  rapid  reduction 
in  the  dropsy  and  the  symptoms  dependent  upon  it.  This  method  of  treat- 
ment deserves  consideration  in  just  those  cases  of  muscular  insufficiency  of 
the  heart  that  occur  in  heavy  beer  drinkers  and  alcoholics  (hotel  keepers, 
brewery  hands,  etc.).  As  we  shall  see  later  when  we  discuss  diseases  of  the 
kidney,  the  low  salt  content  of  the  milk  probably  plays  a  role.  Moreover,  the 
dietetic  milk  cure  can  be  very  well  combined  with  the  internal  administration 
of  pharmacological  remedies  (digitalis,  etc.). 

2.  Strengthening  of  the  Cardiac  Muscle  and  Promotion  of  Compensatory 
Hypertrophy  by  Increased  Physical  Exertion. — Oertel  and  others  have  at- 
tempted to  incite  the  heart  to  more  vigorous  contractions  by  means  of  bodily 
exertion,  and  especially  by  methodical  mountain  climbing  or  methodical  gym- 
nastic exercises,  in  order  by  these  means  to  promote  as  much  as  possible  the 
development  of  cardiac  hypertrophy.  This  view  is  probably  fully  justified 
and  of  obvious  utility  in  many  cases  of  simple  muscular  cardiac  weakness 
(vide  infra).  If,  however,  we  apply  it  to  those  cases  of  circulatory  disturb- 
ance in  which  there  is  valvular  disease,  or  some  other  actual  mechanical 


DISEASES  OF  "THE   MYOCARDIUM  427 

hindrance  to  the  circulation,  or  in  which  the  heart,  originally  sound,  is  already 
suffering  from  functional  strain,  the  matter  seems  to  be  entirely  different. 
For  we  must  consider  that  we  cannot  transfer  unreservedly  to  the  cardiac 
muscle  onr  current  views  relating  to  the  voluntary  muscles  of  the  body  with 
regard  to  exercise  and  invigoration.  The  functional  activity  of  the  hearl  is 
minutely  regulated  by  means  of  an  especial  reflex  apparatus,  independently 
of  our  volition.  We  know  that  every  increased  demand  upon  the  heart's 
activity  is  in  most  cases  directly  fulfilled  by  an  increased  cardiac  effort. 
Under  proper  conditions  the  most  marked  cardiac  hypertrophy  may  develop 
in  a  completely  bedridden  patient.  We  must  therefore  consider  carefully 
whether,  in  cases  of  this  sort,  the  further  increase  of  the  demands  upon  the 
heart  is  judicious;  whether  it  may  not,  on  the  contrary,  contribute  to  a  prema- 
ture exhaustion  of  the  myocardium.  It  certainly  seems  to  us  that  the  pre- 
scription of  increased  bodily  exertion,  such  as  mountain  climbing,  should 
always  be  given  with  great  caution,  and  with  consideration  of  the  individual 
circumstances,  if  the  physician  desires  to  avoid  unhappy  consequences.  It 
may  be  admitted  that  a  certain  measure  of  bodily  exercise  is  well  borne  by 
many  patients  with  valvular  and  other  similar  cardiac  lesions,  but  we  hold 
that  the  benefit  lies  less  in  the  resultant  "invigoration  of  the  cardiac  muscle  " 
than  in  the  promotion  of  the  venous  circulation  occasioned  by  the  motion  of 
the  extremities  and  the  deeper  inspirations ;  or,  in  the  obese,  in  the  increased 
metabolism  of  fat  occasioned  by  the  increased  muscular  effort.  Nevertheless, 
the  inconsiderate  prescription  of  muscular  exertion  has  worked  much  harm. 
At  any  rate,  therefore,  all  attempts  to  treat  heart  patients  with  regular  cura- 
tive gymnastic  exercises  or  methodical  mountain  climbing  must  be  made  with 
great  care  and  a  constant  consideration  of  the  individual  circumstances. 
Whenever  there  are  actual  signs  that  an  insufficiency  of  the  heart  has  already 
developed,  complete  bodily  rest  is,  in  general,  much  more  advantageous  for 
the  patient  than  muscular  exertion.  A  carefully  directed  mechano-therapy  is 
of  use  in  compensated  heart  disease,  although  it  frequently  can  only  be  re- 
garded as  a  suggestive  remedy.  As  soon,  however,  as  the  muscular  exertion 
is  followed  by  a  sensation  of  respiratory  distress  or  oppression,  it  must  be 
absolutely  stopped.  We  need  not  enter  here  upon  the  details  of  the  kind  of 
exercises  to  be  prescribed  (passive  resistance,  etc.).  The  scientific  physician 
will  himself  be  the  best  judge  whether  to  employ  genuine  or  merely  subjective 
therapeutic  measures.  The  employment  of  massage  is  likewise  useful  to  stimu- 
late the  circulation  in  appropriate  cases,  in  which  there  are  such  symptoms 
as  slight  oedema  and  moderate  dyspnoea. 

Bath  Treatment  of  Heart  Disease. — Although  the  different  kinds  of  baths 
have  been  frequently  utilized  in  the  treatment  of  diseases  of  the  myocar- 
dium, the  definite  scientific  foundation  for  all  these  therapeutic  measures 
(C02  baths,  electric  baths,  vide  supra,  page  408)  is  still  not  very  clear.  To  be 
sure,  we  know  that  the  thermic,  chemical,  and  physical  stimuli  produced 
thereby  bring  about  certain  changes  in  the  blood  pressure  and  vascular  ten- 
sion, which,  however,  are  usually  of  short  duration.  We  nevertheless  must  not 
ignore  our  practical  experience,  which  in  many  ways  bears  favorable  testimony 
to  the  bath  treatment.  In  practice,  therefore,  the  balneologic  treatment  of 
heart  disease  deserves  extended  application,  although  we  must  avoid  being 
influenced  by  the  exaggerated  claims  of  interested  persons.     Balneotherapy 


428  DISEASES  OF  THE   CIRCULATORY   ORGANS 

may  be  applied  either  at  certain  watering  places  (above  all  in  Nauheim,  but 
also  in  Cudowa,  Kissingen,  Orb,  etc.),  at  sanatoria  for  the  treatment  of  heart 
disease,  where  the  various  electric  baths  are  particularly  used,  or  at  home.  For 
home  treatment  are  especially  to  be  recommended  the  artificial  carbonic-acid 
baths,  to  which  may  be  added  sodium  chlorid,  neurogen,  pine-needle  extract, 
etc.  The  baths  must  always  be  used  with  care,  and  under  the  strictest  super- 
vision. The  temperature  of  the  baths  should  be  between  89°  to  91°  F.  (32° 
to  33°  C).  The  bath  at  first  should  be  of  short  duration-  (five  to  six  minutes), 
and  later,  if  necessary,  gradually  lengthened.  After  each  bath  the  patient 
must  rest  about  one  hour.    Three  to  four  baths  are  given  during  the  week. 

3.     HYPERTROFHY  OF  THE  HEART,   ASSOCIATED  WITH   CON- 
GENITAL  SMALLNESS    OF   THE   SYSTEMIC   ARTERIES 

(Hypoplasia  of  the  Aorta) 

For  a  considerable  time,  physicians  have  occasionally  noticed  cases,  of  the 
sort  to  be  described,  in  which  weakness  of  the  heart  and  disturbance  of  the 
circulation  appear  at  a  comparatively  early  age.  The  patient  complains  of 
palpitation,  dyspnoea,  and  slight  oedema.  On  examination  we  usually  observe 
ansemia,  combined  with  more  or  less  cyanosis.  The  cardiac  dullness  is  extended 
toward  the  left,  and  the  apex  of  the  heart  is  displaced  in  the  same  direction. 
There  is  no  marked  dilatation  of  the  right  ventricle  till  the  later  stages  of 
the  disease.  The  heart  sounds  are  perfectly  clear,  unless  there  may  be  a 
murmur  due  to  relative  insufficiency  of  the  mitral  valve,  or  due  to  imperfect 
muscular  contraction.  The  heart's  action  is  usually  regular,  but  considerably 
accelerated;  the  pulse  small  and  the  arteries  contracted,  but  often  of  high 
tension.  We  observe  the  ordinary  symptoms  of  increasing  circulatory  disturb- 
ance, and  finally  death.  Upon  autopsy  we  find  the  heart  hypertrophied  and 
usually  dilated.  The  valves  are  normal,  but  the  entire  aorta  and,  in  most 
cases,  probably,  the  other  large  arteries,  are  hypoplastic,  though  otherwise  of 
normal  structure.  Such  cases  are  termed  congenital  hypoplasia  of  the  sys- 
temic arteries,  and  it  is  believed  that  the  hypertrophy  of  the  heart  is  due  to 
the  increased  effort  to  drive  the  blood  through  these  small  vessels. 

In  our  opinion,  this  condition  of  the  blood  vessels  deserves  full  considera- 
tion in  forming  an  opinion  about  idiopathic  hypertrophy  of  the  heart;  but, 
ordinarily,  still  other  factors  are  potent  at  the  same  time,  for  we  sometimes 
find  this  hypoplasia  at  the  autopsy  of  persons  who  showed  no  material  dis- 
turbance of  the  circulation  during  life,  and  in  whom  the  heart  is  of  normal  or 
even  less  than  normal  size.  Virchow  has  called  special  attention  to  the  fact 
that  this  sort  of  hypoplasia  of  the  aorta  and  its  branches  is  sometimes  found 
in  association  with  chlorosis,  or,  perhaps  more  correctly,  with  constitutional 
ansemia.  In  these  cases  the  smallness  of  the  reservoir  diminishes  the  volume 
of  blood  contained  in  it,  but  it  does  not  have  any  marked  influence  upon  the 
heart,  which  indeed  has  a  less  than  normal  burden  rather  than  an  excessive 
one;  so  that  we  believe  that  in  those  instances  of  congenital  hypoplasia  of  the 
aorta  in  which  there  is  severe  circulatory  disturbance  there  is  either  coincident 
smallness  and  feebleness  of  the  heart  itself  (vide  infra),  or  an  association  of 
the  hypoplasia  with  other  influences  unfavorable  to  the  heart.  There  have 
been  repeatedly  observed  cases  of  cardiac  hypertrophy  due  to  muscular  strain 


DISEASES  OF'THE   MYOCARDIUM  429 

(for  instance,  in  soldiers),  or  due  to  excessive  drinking,  in  which  congenital 
hypoplasia  of  the  aorta  and  its  branches  has  been  found  in  association  with 
the  hypertrophy  of  the  heart;  and  in  the  cases  which  we  have  ourselves  seen 
and  in  which  the  diagnosis  was  confirmed  by  autopsy,  there  have  almosl  always 
been  some  other  factors  unfavorable  to  the  heart  besides  this  congenital  abnor- 
mality of  the  blood  vessels,  [ndeed,  one  can  easily  understand  that  the  same 
injurious  influences  which,  a  norma]  circulatory  apparatus  might  endure  for 
a  considerable  time  without  much  damage,  would  occasion  premature  symp- 
toms if  the  vascular  system  were  abnormally  developed. 

The  recognition  of  hypoplasia  of  the  systemic  arteries  during  life  is  prob- 
ably in  every  case  difficult,  and  scarcely  ever  absolutely  certain.  Important 
factors  would  he  the  existence  of  anaemia  and  a  tendency  to  shortness  of  breath 
and  palpitation  from  early  youth;  and  also  the  discovery  by  palpation  that  the 
circumference  of  the  arteries  was  less  than  normal.  The  condition  of  the  heart 
is  to  he  determined  in  the  ordinary  manner. 

Prognosis  and  treatment  must  likewise  be  governed  by  the  same  principles 
as  in  other  forms  of  heart  disease. 

4.     PRIMARY   WEAKNESS    OF   THE    MYOCARDIUM 

(Congenital   Weakness   of  the  Heart;    Weakened  Heart;  Acute  Muscular  Strain  of  the  Heart; 

Toxic  Weakness  of  the  Heart) 

Where  there  is  a  myopathic  heart  disease,  and  the  heart  is  at  the  same  time 
hypertrophied,  this  indicates  that  for  a  considerable  time  the  heart  has  done 
an  unusual  amount  of  work.  In  such  cases,  therefore,  it  cannot  be  that  the 
heart  has  been  feeble  from  the  .start.  It  must  indeed  have  been  able  to  do 
more  than  is  normally  demanded  of  it.  It  is  not  until  a  later  period,  when  its 
power  is  impaired,  that  we  can  say  that  the  heart  is  relatively  or  finally  abso- 
lutely feeble.  Another  group  of  cases,  however,  are  those  in  which  the  heart 
is  originally  feeble — that  is,  its  functional  powers  are  below  normal.  This 
weakness  is  certainly,  in  many  instances,  congenital.  It  may  be  expressed  in 
the  structure  of  the  heart,  the  organ  being  unusually  small  with  thin  walls,  or 
merely  in  physiological  incapacity,  the  organ  being  apparently  of  normal  struc- 
ture. In  either  case  the  heart  cannot  satisfy  even  the  ordinary  demands  made 
upon  it.  Patients  of  this  sort  complain,  upon  the  least  exertion,  of  palpitation, 
shortness  of  breath,  and  a  sense  of  pressure  over  the  heart.  The  pulse  is 
usually  frequent  or,  at  any  rate,  very  easily  accelerated;  a  short  but  rapid 
walk  or  a  few  gymnastic  exercises  (knee  bending,  etc.)  may  raise  the  pulse 
rate  to  120  or  140  beats  per  minute. 

In  many  cases  there  are  never  any  severer  symptoms.  The  patient  remains 
through  life  feeble,  and  "  with  a  weak  heart " ;  but  if  his  mode  of  life  is  f avor- 
ahle  the  heart  manages  to  maintain  the  circulation.  In  other  cases  the  signs 
of  heart  weakness  are  noticed  only  at  certain  times.  Of  particular  practical 
importance  is  that  frequent  form  usually  called  by  myself  the  cardiopathy  of 
adolescence.  It  occurs  in  young  people  between  the  ages  of  fourteen  and 
seventeen,  when  the  more  rapid  growth  of  the  body  makes  increased  demands 
upon  the  activity  of  the  heart,  and  the  heart  apparently  does  not  keep  pace 
in  its  development  with  that  of  the  rest  of  the  body.  The  patients  suffer  from 
frequent  palpitation,  and  even  on  slight  provocation  develop  a  very  rapid  and 


430  DISEASES   OF  THE   CIRCULATORY   ORGANS 

excited  heart  action,  and  easily  become  dyspnceic.  It  is  usually  easy  to  vjrove 
by  objective  examination  that  there  is  no  organic  disease  of  the  heart.  The 
striking  symptoms  are  the  excited  and  rapid  heart  action,  and  not  infre- 
quently a  remarkable  hardness  of  the  arteries,  apparently  strongly  contracted 
in  a  state  of  tonus.  These  symptoms  often  completely  disappear  in  time; 
occasionally  a  certain  degree  of  heart  weakness  persists,  however.  The  latter 
condition  is  particularly  evident  if  increased  demands  are  made  upon  the 
heart,  as,  for  example,  in  the  course  of  military  service,  or  in  mountain  climb- 
ing, or  in  unsuitable  modes  of  life-.  Then  more  threatening  symptoms  of 
cardiac  insufficiency  appear,  either  suddenly  or  gradually,  and  express  them- 
selves objectively  in  dilatation  (or  stretching)  of  the  heart.  In  some  cases 
the  heart  is  not  able  permanently  to  satisfy  even  the  ordinary  demands  made 
upon  it.  We  observe  all  the  symptoms  of  circulatory  disturbance,  and  at  last 
upon  autopsy  find  a  heart  which  is  dilated,  but  not  much  hypertrophied. 
Cases  of  this  sort  are  not  very  frequent,  but  they  certainly  do  occur;  their 
recognition  during  life,  however,  is  not  easy,  for  it  is  difficult  to  distinguish 
simple  dilatation  from  insufficiency  which  is  subsequent  to  hypertrophy.  We 
shall  probably  be  able  to  determine  that  there  is  some  muscular  heart  disease 
because  of  the  increase  in  cardiac  dullness,  the  smallness  and  frequency  of  the 
pulse,  and  the  ordinary  tokens  of  disturbed  circulation,  such  as  dyspnoea,  pal- 
pitation, oedema,  and  the  urine  of  passive  congestion.  If  we  consider  carefully 
the  history  of  the  case  and  the  presence  or  absence  of  special  serological  fac- 
tors, we  may  be  able  while  the  patient  is  still  alive  to  make  a  probable  diagnosis 
of  simple  dilatation  of  the  heart,  as  a  result  of  muscular  weakness. 

Acquired  muscular  weakness  of  the  heart  should  be  distinguished  from  the 
congenital  (endogenous)  variety.  It  is  occasioned  by  the  action  upon  an  origi- 
nally normal  heart  of  influences  which  damage  the  myocardium  or  its  nervous 
apparatus.  We  often  see  temporary  conditions  of  muscular  weakness  of  the 
heart  in  anaemia,  or  following  severe  attacks  of  acute  disease.  Even  in  these 
cases  there  are  such  differences  as  to  indicate  a  difference  in  the  original  vigor 
of  the  heart.  The  resulting  diseased  condition  is  always  dependent  upon  the 
ratio  between  the  active  injurious  influences,  and  the  degree  of  the  indi- 
vidual resistance.  This  law  is  also  evident  in  acute  muscular  strain  of  the 
heart.  Acute  attacks  of  cardiac  weakness  are  seen  in  the  case  of  soldiers  at 
maneuvers,  or  in  laborious  mountain  climbing  and  other  athletic  exercises 
(cycling,  rowing,  football,  etc.),  such  as  have  of  late  been  so  often  undertaken 
in  an  ill-considered  manner ;  and  these  attacks  are  usually  associated  with  acute 
dilatation.  There  is  a  sudden  and  enormous  increase  in  the  demands  made 
upon  the  heart;  the  amount  of  blood  which,  in  a  given  period  of  time,  must 
pass  through  the  muscles  is  increased;  and  not  every  heart  is  equal  to  the 
task.  A  weak  heart  yields  to  the  increased  tension  and  dilates.  The  pul- 
monary circulation  becomes  congested,  the  pressure  in  the  arteries  falls,  and 
we  have  all  the  clinical  phenomena  of  cardiac  insufficiency,  including  dyspnoea, 
cardiac  asthma,  and  sometimes  angina  pectoris.  If  there  is  prompt  cessation  of 
the  effort  and  medical  assistance,  the  condition  may  be  restored  to  normal  and 
so  remain.  This,  for  example,  we  lately  saw  in  the  case  of  a  young  and  healthy 
person  who  escaped  drowning  only  by  desperate  efforts.  But  sometimes  there 
remains  behind  a  permanent  weakness  of  the  heart,  whether  because  the  single 
excessive  strain  caused  a  permanent  damage  to  the  heart,  or  because  the  heart 


DISEASES   OF  "THE   MYOCARDIUM  431 

was  already  of  less  than  normal  vigor,  and  betrayed  its  weakness  for  the  fir-t 
time  when  this  excessive  demand  was  made  upon  it. 

Certain  tonus  of  chronic  intoxication  are  among  the  causes  which  fre- 
quently lead  to  acquired  weakness  of  the  myocardium,  or  its  nerves.    The  most 

important  of  these,  from  a  clinical  standpoint,  is  chronic  alcoholism,  the  nox- 
ious influence  of  which  upon  the  heart  is  universally  recognized.  Less  fre- 
quent, but  still  of  practical  importance,  is  chronic  nicotine  poisoning,  or,  to 
speak  in  a  more  general  and  perhaps  more  correct  manner,  the  influence  of 
excessive  smoking.  This  is  especially  evident  in  persons  who  have  smoked 
many  strong  imported  Havana  cigars  or  large  quantities  of  cigarettes.  The 
symptoms  consist  of  an  unpleasant  subjective  sensation  in  the  region  of  the 
heart  (fluttering,  pressure,  or  palpitation),  of  slight  dyspnoea,  and  objectively 
of  a  frequent,  irregular,  or  intermittent  pulse.  Other  objective  cardiac  signs 
are  not  present,  at  least  at  first;  but  there  may  be  still  other  symptoms  of 
chronic  nicotine  poisoning,  such  as  specks  before  the  eyes,  disturbance  of  vision, 
and  dyspepsia.  If  smoking  is  stopped  in  due  time,  the  symptoms  may  vanish. 
Otherwise,  there  follow  severer  disturbances  of  the  heart,  although  in  most 
cases  there  are  other  serological  factors  also  present,  such  as  alcoholism  and 
mental  strain.  Finally,  any  extensive  anatomical  changes  (above  all,  arterio- 
sclerosis) which  may  have  developed  in  the  meanwhile,  must  be  taken  into 
consideration  to  explain  the  symptoms. 

With  regard  to  prognosis  and  treatment,  there  are  few  special  statements 
to  be  made.  If  there  are  signs  of  congenital  weakness  of  the  heart  we  must 
strengthen  the  constitution  in  every  way  possible,  and  we  must  seek  to  give  the 
patient,  on  the  one  hand,  the  proper  amount  of  protection,  and,  on  the  other 
hand,  cautious  and  moderate  exercise  of  the  cardiac  muscle,  by  means  of  med- 
ical gymnastics;  and  in  other  respects  regimen  and  hygienic  precautions  are 
of  first  importance,  from  a  prophylactic  and  therapeutic  point  of  view.  Car- 
bonic-acid baths,  electric  baths,  etc.,  have  a  favorable  effect.  The  treatment 
of  acute  and  chronic  weakness  of  the  heart  by  such  remedies  as  cardiac  stimu- 
lants and  digitalis  is  controlled  by  the  ordinary  rules.  Finally,  we  may  men- 
tion in  this  connection  that  obliteration  of  the  pericardial  sac  by  chronic 
pericarditis,  or  as  a  sequel  of  antecedent  acute  pericarditis  (vide  infra),  some- 
times occasions  atrophy  of  the  myocardium,  with  resultant  feebleness  and  dila- 
tation of  the  heart.  Cases  of  this  sort  may  readily  be  confused  with  primary 
cardiac  dilatation. 

5.     THE   SO-CALLED   FATTY   HEART 

.ZEtiology  and  Pathological  Anatomy. — By  the  name  of  "  fatty  heart "  we 
often  mean,  at  present,  two  quite  distinct  conditions  of  the  heart — the  one  an 
abnormal  deposit  of  fat  in  the  heart,  and  the  other  a  fatty  degeneration  of  the 
muscular  fibers  of  the  heart. 

Fatty  overgrowth  and  fatty  infiltration  of  the  heart  are  usually  merely 
symptoms  of  great  general  obesity.  At  the  autopsy  of  very  fat  people  we 
sometimes  find  the  heart  entirely  inclosed  in  a  thick  capsule  of  fat.  The  fat 
is  situated  chiefly  in  the  external  pericardium  and  beneath  the  visceral  peri- 
cardium. It  is  usually  abundant  along  the  course  of  the  larger  vessels  within 
the  grooves  of  the  heart,  but  in  marked  cases  the  fat  also  involves  the  muscular 


432  DISEASES   OF  THE   CIRCULATORY  ORGANS 

substance,  so  that  many  groups  of  fat  cells  are  interspersed  between  the  mus- 
cular fibers.  The  heart  itself  is  otherwise  quite  normal  or  somewhat  hyper- 
trophied  or  dilated.  There  are  in  some  instances  also  present  sclerosis  of  the 
coronary  arteries  and  indurations  due  to  myocarditis. 

We  have  already  mentioned  fatty  degeneration  of  the  muscular  substance  of 
the  heart  as  a  frequent  result  of  valvular  disease.  In  myocarditis  and  idio- 
pathic cardiac  hypertrophy,  and  in  the  hypertrophy  secondary  to  chronic  ne- 
phritis and  pulmonary  emphysema,  we  also  meet  with  fatty  degeneration.  We 
often  find  fatty  degeneration  of  the  heart,  as  well  as  of  other  organs,  in  severe 
acute  infectious  diseases,  in  phosphorous  poisoning,  and  in  all  marked  pri- 
mary and  secondary  anaemias.  Under  the  microscope  we  find  the  muscular 
fibrillae  studded  with  little  drops  of  fat,  which  may  be  so  numerous  that  the 
nuclei  and  the  transverse  striation  of  the  fibers  are  quite  concealed  by  them. 
In  all  severe  cases  of  fatty  degeneration  the  contractile  portion  of  the  heart 
muscle  also  suffers;  but  investigations  into  the  details  have  not  yet  been 
reported. 

If  the  fatty  degeneration  is  of  high  degree,  we  can  easily  recognize  it  with 
the  naked  eye.  Beneath  the  endocardium,  especially  on  the  trabecules  and  pap- 
illary muscles,  we  see  very  fine  and  delicate  yellow  points  and  strise.  With 
great  fatty  degeneration,  as  in  phosphorus  poisoning  and  pernicious  anaemia, 
the  whole  cardiac  muscle  is  manifestly  yellow,  and  also  soft  and  flabby.  It  is 
claimed  that  rupture  of  the  heart  may  occur  as  a  result  of  marked  fatty  de- 
generation. 

Hitherto  it  was  usually  believed  that  in  fatty  degeneration  of  the  heart 
muscle  the  fat  resulted  from  the  decomposition  of  the  albumen  in  the  muscle 
cells.  According  to  newer  investigations  it  has  become  probable  that  the  fatty 
infiltration  of  the  muscle  fibers  is  only  the  visible  expression  of  a  deficient 
fat  oxidation,  following  insufficient  muscular  activity.  Upon  this  assump- 
tion, the  fat  does  not  originate  in  the  muscle  fibers,  but  it  is  brought  to  the 
myocardium  from  the  fat  depot  of  the  body  (the  subcutaneous  cellular  tissue). 

Clinical  Symptoms. — Fatty  degeneration  of  the  heart  has  no  characteristic 
clinical  symptoms.  In  the  conditions  under  which  we  know  it  is»apt  to  occur, 
we  can  usually  suspect  it  during  the  lifetime  of  the  patient,  but  we  cannot 
diagnosticate  it.  We  must  also'  mention  that  the  frequently  expressed  opinion, 
that  fatty  degeneration  of  the  heart  invariably  occasions  general  cardiac  weak- 
ness, is  very  often  incorrect.  In  pernicious  anaemia  there  may  be  quite  a 
strong  and  a  perfectly  regular  pulse  up  to  death  in  spite  of  the  most  marked 
fatty  degeneration,  and  many  personal  observations  leads  us  earnestly  to  dis- 
pute the  view  that  fatty  degeneration  of  the  heart  is  to  be  regarded  as  the 
regular  cause  of  cardiac  insufficiency,  and  the  consequent  disturbances  of  com- 
pensation. We  have  made  microscopic  examinations  in  many  cases,  and  failed 
to  find  any  sign  of  fatty  degeneration  in  the  myocardium,  although  during 
life  the  signs  of  cardiac  insufficiency  were  well  developed.  In  general,  with 
our  present  knowledge,  it  is  impossible  to  establish  definite  relations  between 
the  histological  condition  of  the  muscular  tissue  of  the  heart  and  its  func- 
tional activity  during  life. 

We  cannot  say  much  that  is  certain  in  regard  to  the  clinical  symptoms  of  a 
deposit  of  fat  in  the  heart.  "  Fatty  degeneration  of  the  heart "  always  plays 
a  far  larger  part  in  popular  speech  than  it  does  in  reality.     It  is  certainly  a 


DISEASES   OK  THE   MYOCARDIUM  133 

fact  that  difficulty  with  the  heart  and  respiration  is  very  often  observed  in 
fat  people.  Examination  of  the  heart,  which,  however,  is  decidedly  impeded 
by  the  thick  panniculus  adiposus,  often  shows  in  such  cases  an  increase  of  the 
cardiac  dullness,  a  small  and  sometimes  irregular  pulse,  and  faint  hut  clear 
heart  sounds.  The  disturbance  may  be  very  considerable,  attacks  of  angina 
pectoris  and  cardiac  asthma  may  come  on,  and  death  may  follow  with  increas- 
ing dyspnoea  and  general  oedema. 

If  one  has  opportunity  to  make  an  autopsy  in  such  cases,  there  will  he 
found  no  single,  constant  anatomical  change  as  the  cause  of  the  cardiac  dis- 
turbance, but  usually  idiopathic  hypertrophy  (vide  supra),  or,  less  often,  myo- 
carditic  changes  with  sclerosis  of  the  coronary  arteries,  and  the  like.  Some- 
times, but  by  no  means  invariably,  there  is,  of  course,  a  marked  deposit  of  fat 
upon  the  heart  itself,  but  the  question  arises  whether  this  can  directly  and 
seriously  embarrass  the  cardiac  activity.  The  fact  is  that  we  often  have  seen 
similar  well-marked  cases  of  fatty  heart  which  during  life  presented  no  special 
cardiac  symptoms.  There  would  be  more  reason  in  ascrihing  an  unfavorable 
influence  to  the  fatty  infiltration  of  the  cardiac  muscle;  but  in  such  cases 
there  is  almost  always  a  coincident  atrophy  of  the  muscular  structure,  so  that  it 
is  questionable  whether  the  fatty  infiltration  is  to  be  regarded  as  actually  the 
primary  pathological  process.  We  ourselves  are  far  more  inclined  to  the  view 
that  there  is  primary  atrophy  of  the  myocardium,  with  this  fatty  infiltration 
as  a  secondary  phenomenon,  similar  to  the  frequent  and  well-known  occur- 
rence of  secondary  lipomatosis  of  atrophic  voluntary  muscles.  At  any  rate, 
we  are  as  yet  entirely  unable  to  recognize  cases  of  this  sort  of  fatty  heart  dur- 
ing life,  and  it  is  certain  that  they  are  much  less  frequent  than  the  other  myo- 
pathic diseases  of  the  heart. 

Therefore  we  cannot  associate  with  the  term  "  fatty  heart "  any  uniform 
anatomical  and  clinical  conception.  It  would  be  better  to  speak  of  the  "  heart 
of  obesity  "■ — that  is,  of  all  the  manifold  injuries  to  which  the  heart  of  obese 
persons  is  exposed. 

For  the  same  conditions  that  lead  to  general  obesity  (luxurious  mode  of 
life,  excessive  beer  drinking),  produce,  in  themselves,  usually  an  injurious 
effect  upon  the  heart.  Just  what  particular  form  of  heart  disease  is  present 
in  a  case  of  obesity,  must  be  carefully  considered  in  each  individual  case. 
Without  doubt,  the  most  frequent  form  is  the  simple  "  idiopathic  "  cardiac 
hypertrophy  (the  so-called  "beer  heart,"  vide  supra).  The  arteriosclerotic 
heart  disease  is  rarer.  At  any  rate,  physicians  should  have  more  regard  for 
the  facts  of  pathology,  when  they  are  inclined  to  make  an  off-hand  diagnosis 
of  fatty  heart. 

Treatment. — A  great  part  of  the  disturbance  of  respiration  in  fat  people 
depends  not  upon  the  cardiac  weakness,  but  on  the  corpulency  itself.  The 
great  bulk  of  the  body,  and  the  hindrance  to  the  activity  of  the  respiratory 
muscles,  are  very  important  factors.  Treatment  directed  against  the  respir- 
atory disturbance  must  hence  attack  the  obesity  chiefly,  and  thus  in  many 
cases  we  shall  also  assist  the  action  of  the  heart.  The  detailed  description  of 
the  hygienic  methods  of  cure  to  be  employed  here  is  to  be  found  in  the  chapter 
on  Obesity  (q.  v.). 

In  regard  to  the  special  treatment  of  the  cardiac  symptoms  in  the  obese, 
this  does  not  differ  from  the  rules  that  obtain  in  other  forms  of  heart  disease. 


434  DISEASES   OF  THE   CIRCULATORY   ORGANS 

CHAPTER    IV 

THE    CARDIAC   NEUROSES 

Oue  medical  experience  teaches  us  that  many  people  complain  of  really 
serious  cardiac  symptoms  who,  on  the  most  careful  objective  examination, 
show  no  trace  of  organic  disease  of  the  heart  (valvular  disease,  dilatation, 
hypertrophy).  Occasionally  only  purely  subjective  sensations  are  present, 
such  as  the  feeling  of  pain,  pressure,  or  distress  in  the  cardiac  region.  Fre- 
quently, however,  functional  changes  in  the  cardiac  action  are  at  the  same 
time  present,  as,  for  example,  permanent  or  temporary  frequency  of  the  pulse, 
irregularities  of  the  heart  beat,  etc.  At  the  present  time  we  are  accustomed 
to  group  all  these  cases  under  the  general  heading  of  "  cardiac  neuroses." 
In  their  development,  however,  quite  a  number  of  factors  seem  to  require 
consideration.  So  far  as  my  personal  experiences  are  concerned,  I  would 
like  particularly  to  emphasize  the  following  aspects: 

1.  Purely  Psychogenetic  Heart  Disturbances  (i.  e.,  subjective  and  objective 
disturbances  resulting  from  a  primary  groundless  fear,  of  any  origin  what- 
ever).— It  may  be  said  without  reserve  that  the  number  of  cases  of  "imag- 
inary heart  disease  "  is  decidedly  greater  than  the  number  of  cases  of  actual 
organic  disease  of  the  heart.  The  primary  factor  is  the  fear  of  a  heart  lesion 
and  its  consequences.  The  numerous  discussions  on  disease,  the  reading  of 
medical  pamphlets  and  announcements,  often  also  the  tales  of  members  of  the 
family  or  acquaintances  who  have  suffered  from  really  serious  heart  disease, 
arouse  a  lively  fear  of  becoming  victims  to  the  malady  in  many  timid  persons. 
This  primary  change  of  consciousness  produces,  first,  a  variety  of  autosug- 
gested  subjective  sensations  in  the  cardiac  region,  and  secondly,  marked  dis- 
turbances of  the  cardiac  activity,  such  as  tachycardia,  isolated  extrasystoles 
with  intermittent  pulse,  etc.  As  these  primary  groundless  fears  are  not  con- 
tinuously present  in  the  consciousness,  the  cardiac  disturbances  not  infre- 
quently appear  in  attacks.  In  many  cases  they  occur  with  preference  at  night, 
partly  because  the  mind  is  no  longer  diverted  by  the  business  of  the  day, 
and  partly,  in  all  probability,  because  they  are  sometimes  induced  by  har- 
rowing dreams.  The  patients  then  awake  suddenly  with  marked  sensations 
of  fear,  palpitation,  and  distress.  The  diagnosis  of  the  psychogenetic  dis- 
turbances of  the  heart  is  generally  not  difficult.  The  nature  of  the  complaints 
and  the  general  neurasthenic  condition  of  the  patient  soon  show  the  experi- 
enced physician  the  actual  state  of  affairs.  Notwithstanding  this,  a  careful 
objective  examination  is,  of  course,  always  necessary.  The  treatment  must 
be  primarily  a  purely  psychic  one.  The  quieting  of  the  patient,  the  sym- 
pathetic reassurance  that  no  serious  malady  is  present,  is  the  main  thing.  In 
practice,  to  be  sure,  the  suggestive  influence  of  other  remedies  (valerian 
preparations,  C02  baths,  hydrotherapy)  cannot  be  dispensed  with  Actual 
cardiac  remedies,  such  as  digitalis,  should  be  avoided.  As  the  nervous  heart 
symptoms  are  often  only  partial  phenomena  of  a  general  neurasthenia,  the 
reader  is  referred  also  to  the  chapter  on  this  subject  in  Vol.  II. 

2.  Nervous  Heart  Disturbances  from  Endogenous  Toxic  Influences. — In  all 
probability  the  influence  upon  the  heart  and  its  nerves  of  certain  endogenous 


THE  CARDIAC   NEUROSES  435 

toxins  which  develop  in  the  process  of  tissue  metaholism  is  of  greal  im- 
portance, although  this  subject  has  as  yel  been  by  no  means  exhaustively 
investigated.  The  influence  of  the  thyroid  gland  is  hest  and  longest  known. 
We  know  that  in  exophthalmic  goiter  very  decided  changes  in  the  heart's 
action  can  be  produced  by  the  abnormal  thyroid  activity.  Besides  those  met 
with  in  fully  developed  cases  of  Basedow's  disease,  there  are  also  numerous 
other  disturbances  of  the  heart  that  are  probably  dependent  upon  morbid 
changes  in  the  thyroid  (so-called  goiter  heart).  At  any  rate,  this  possibility 
must  constantly  be  considered  and  the  treatment  arranged  accordingly,  should 
an  enlargement  of  the  thyroid  be  present  (thyroidin  tablets,  Mobius's 
serum  iodin,  X-ray  treatment).  To  be  sure,  with  our  lack  of  knowledge 
of  the  actual  processes,  the  proper  determination  of  the  indications  is  very 
difficult,  and  we  are  therefore  forced  to  careful  experimentation.  Further 
details  concerning  these  important  matters  will  be  found  in  the  chapter  on 
exophthalmic  goiter.  It  appears  to  me  very  worthy  of  consideration  that 
perhaps  other  organs  besides  the  thyroid  gland  may,  when  diseased,  disturb 
the  heart's  action.  Primarily,  in  my  opinion,  we  must  consider  the  female 
genital  organs.  The  "  nervous  "  heart  symptoms  so  frequently  developing 
in  the  menopause  are  perhaps,  in  part  at  least,  to  be  interpreted  in  this  sense, 
as  are  also  the  heart  disturbances  in  cases  of  uterine  myomata,  and  those 
following  bilateral  oophorectomy.  There  is  a  particular  variety  of  muscular 
heart  disease  with  arrhythmia,  that  I  have  observed  only  in  women.  I  am 
therefore  inclined  to  associate  these  cases  with  this  type  of  disturbances  of  the 
internal  secretion.  Occasionally  in  men,  nervous  heart  disturbances  appear 
in  connection  with  diseases  of  the  prostate.  It  must  be  mentioned  that  in 
all  the  cases  apparently  belonging  to  this  group,  general  nervous  and  psychic 
disturbances  appear.  The  cases  of  exophthalmic  goiter  are  the  best  demon- 
stration of  this  fact.  Finally,  the  influence  of  abnormal  digestive  processes 
on  the  heart's  activity  is  worthy  of  notice.  In  certain  cases  abnormal  stimu- 
lation emanating  from  the  stomach  or  intestines  seems  to  affect  the  heart. 
These  cases  are  not  particularly  frequent,  and  their  interpretation  is  by  no 
means  always  perfectly  clear.  Toxic  as  well  as  reflex  influences  may  play 
a  role.  Sometimes,  perhaps,  it  is  merely  the  mechanical  pressure  upon  the 
heart  from  the  dilated  stomach  or  colon. 

3.  Nervous  Heart  Disturbances  Due  to  Exogenous  Toxic  Influences. — In 
this  class  are  to  be  included  those  cases  where  definite  external  poisons  are 
to  be  regarded  as  the  cause  of  the  existing  heart  disturbances.  Most  im- 
portant in  this  group  is  the  tobacco-heart  neuroses  of  heavy  smokers;  those 
induced  by  lead,  alcohol,  etc.,  are  less  frequent.  We  must  further  include  the 
nervous  heart  affections  subsequent  to  acute  infectious  diseases  (influenza,  diph- 
theria, typhoid,  etc. ) .  We  must,  however,  consider  that  just  in  these  cases  the 
drawing  of  the  line  of  demarcation  between  nervous  disturbances  and  organic 
heart  diseases,  such  as  myocarditis  and  arteriosclerosis,  is  often  very  difficult. 

From  what  has  just  been  said,  it  is  obvious  how  difficult  a  really  exact 
diagnosis  of  nervous  disease  of  the  heart  often  is.  Each  case  must  be  judged 
from  the  individual  circumstances.  In  the  suggestions  given  above,  the  most 
important  diagnostic  factors,  at  least,  are  indicated. 

4.  The  Nervous  "  Attacks  "  of  Patients  with  Heart  Disease. — Under  cer- 
tain conditions,  in  almost  all  the  forms  of  heart  disease,  particular  symptoms 


436  DISEASES   OF  THE   CIRCULATORY   ORGANS 

may  develop  paroxysmally.     These  attacks  form  but  a  part  of  the  general 
clinical  picture. 

Occasionally,  however,  such  attacks  may  also  develop  apparently  inde- 
pendently with  otherwise  normal  cardiac  signs.  They  then  form  a  particular 
variety  of  "  nervous  heart  disease  "  or  "  heart  neurosis."  On  account  of  their 
practical  importance,  we  take  the  liberty  of  inserting  a  few  special  remarks 
relative  to  these  attacks. 

(a)  Attacks  of  Simple  Heart  Weakness  Associated  with  Feebleness  and 
Smallness  of  the  Pulse. — The  latter  is  usually  rapid,  and  frequently  irregular 
and  diminished  in  tension.  Along  with  these  symptoms  are  sensations  of 
distress  and  dyspnoea   (cardiac  asthma). 

(&)  Attacks  of  Stenocardia,  or  Angina  Pectoris. — The  characteristic 
feature  of  attacks  of  stenocardia  is  an  oppressive,  tightening  sensation,  that 
is  felt  occasionally  in  the  heart  region,  but  usually  in  the  front  of  the  chest 
behind  the  sternum.  The  pain  may  become  very  severe.  It  often  radiates 
to  the  left  shoulder  and  arm,  down  to  the  elbow,  and  even  to  the  finger  tips. 
The  pain  may  also  radiate  to  the  right  arm,  or  simultaneously  to  both  arms, 
and  sometimes  upward  to  both  sides  of  the  neck.  Associated  with  this  pain 
is  an  unusually  marked  feeling  of  weakness,  as  if  all  strength  were  lost  ("  feel- 
ing of  impending  dissolution  ").  Sometimes  the  arms  feel  as  if  dead.  Actual 
dyspnoea  is  not  always  present,  but  there  is  often  a  sensation  of  fear  and  dis- 
tress. The  face  is  usually  pale,  not  really  cyanotic.  During  the  attack,  the 
pulse  is  sometimes  only  slightly  changed;  in  other  cases,  its  frequency  is 
increased,  less  often  diminished,  or  it  is  irregular.  The  duration  of  such  an 
attack  is  often  only  a  few  minutes,  but  sometimes  it  may  last  half  an  hour 
or  more.  Not  infrequently,  at  the  end  of  the  attack  still  other  symptoms 
appear,  such  as  belching,  vomiting,  perspiration,  and  the  excretion  of  a  pro- 
fuse, light-colored  and  dilute  urine  ("  spastic  urination  "). 

Concerning  the  actual  processes  in  an  attack  of  stenocardia,  we  know  little 
that  is  really  definite.  I  believe  that  the  symptoms  are  best  explained  by  the 
assumption  of  a  vascular  cramp,  and  that  the  pains  actually  occur  in  the 
vessels  themselves.  The  sternal  pain  is  an  aortic  pain,  and  the  radiations  of 
the  pains  into  the  arms  and  neck,  etc.,  depend  upon  the  involvement  of  the 
brachial,  carotid,  and  other  arteries  in  the  spasm.  The  variations  in  the 
symptomatology  of  the  anginal  attacks  are  explained  by  the  different  localiza- 
tions of  the  cramps. 

[For  the  very  plausible  "  viscero-sensory  reflex"  theory  of  anginose  pain, 
see  James  Mackenzie's  "  Diseases  of  the  Heart."] 

True  angina  pectoris  occurs  principally  in  sclerosis  of  the  aorta  (q.v.), 
and  in  sclerosis  of  its  branches,  the  coronary  arteries,  etc.  I  have  seen  attacks 
with  pallor  and  coldness  of  the  arm  which  could  only  be  explained  by  a  spasm 
of  the  markedly  sclerosed  artery  of  that  extremity.  The  comparison  between 
angina  pectoris  and  the  attacks  of  intermittent  claudication  (dysbasia  arterio- 
sclerotica)  is  equally  obvious.  In  certain  cases  we  must  also  think  of  a  par- 
ticipation of  the  abdominal  aorta  and  its  branches,  giving  rise  to  abdominal 
pain,  sudden  tympanites,  and  disturbances  in  the  function  of  the  intestine, 
kidney,  etc.  It  is  possible  that  true  angina  pectoris  may  also  occur  in  other 
organic  diseases  of  the  heart,  without  simultaneous  arteriosclerosis,  but  this, 
to  my  knowledge,  has  really  not  been  definitely  proved.     Nevertheless,  some 


THE  CARDIAC   NEUROSES  137 

authors  (Nothnagel)  have  assumed  the  existence  of  a  purely  nervous  or  " 
motor  form  of  angina  pectoris."  It  is  not  impossible  thai  the  anginal  atta 
of  heavy  smokers  may  be  of  nervous  origin,  but  jusl  in  these  cases  the  exist- 
ence of  an  aortic  sclerosis  can  scarcely  ever  be  excluded  with  absolute  cer- 
tainly. In  true  angina  pectoris  the  most  important  exciting  causative 
factors  are  bodily  exertion,  further,  marked  mental  excitement,  and  errors 
in  diet. 

In  general,  the  diagnosis  of  angina  pectoris  is  not  difficult  if  one  bears 
in  mind  the  symptomatology  described  above.  It  cannot  be  denied,  however, 
that  frequently  attacks  occur  in  heart  disease  that  cannot  be  definitely  classified. 
The  boundary  between  stenocardia  and  cardiac  asthma  is  often  very  obscure. 
We  must  also  guard  against  confusing  organic  disease  of  the  heart  with  I 
terical  attacks.  The  prognosis  of  true  angina  pectoris  is  always  grave,  al- 
though some  patients  suffer  from  their  attacks  for  many  years.  The  danger 
of  a  sudden  fatal  termination  is  always  present. 

In  the  treatment  of  severe  attacks  of  stenocardia  the  most  useful  remedy 
is  a  subcutaneous  injection  of  morphin.  It  often  gives  prompt  relief  from 
the  most  agonizing  symptoms.  The  internal  administration  of  morphin, 
although  less  rapid  in  its  effect,  is  also  useful.  Xext  to  morphin,  I  con- 
sider nitroglycerin  the  best  remedy.  It  is  best  given  in  drop  form,  as  in  the 
following  mixture:  Nitroglycerin,  gr.  ^  (gm.  0.02),  and  spirits  of  wine  and 
distilled  water,  of  each  oijss.  (gm.  10.0).  Of  this,  20  drops  are  to  be 
given  to  the  dose.  To  this  solution  3  gr.  (gm.  0.2)  of  morphin  hydro- 
chlorid  may  be  added.  Many  patients  obtain  relief  from  the  inhalation  of 
amyl  nitrite.  Diuretin  is  another  useful  remedy,  but  as  it  does  not  act 
promptly,  it  is  more  to  be  used  as  a  prophylactic  against  the  attacks.  Aside 
from  the  remedies  mentioned,  mustard  applications  to  the  chest,  hot  hand 
and  foot  baths,  and  hot  applications  to  the  chest,  and  the  like,  have  also 
proved  serviceable. 

(c)  Attacks  of  Fright,  Anxiety,  and  Distress  on  Going  to  Sleep. — A  very 
characteristic  symptom  in  some  serious  cases  of  heart  disease  is  the  sudden 
occurrence  of  a  severe  feeling  of  distress  when  the  patient  is  about  to  fall 
asleep.  As  a  rule,  this  depends  upon  a  kind  of  Chejue- Stokes  symptom  (vide 
supra,  page  406 — with  a  cessation  of  respiration,  so  that  the  patient  awakes 
suddenly  in  a  great  fright. 

(d)  Attacks  of  So-called  Humid  Asthma. — These  are  attacks  associated 
with  a  very  rapidly  developing  profuse  serous  or  serosanguineous  exuda- 
tion into  the  bronchi  and  a  consequent  marked  dyspnoea  with  profuse  frothy 
serous,  and  usually  somewhat  bloody  expectoration.  Sometimes  the  exuda- 
tion into  the  bronchi  is  associated  with  a  similar  process  in  the  gastrointes- 
tinal tract,  which  shows  itself  in  vomiting  and  profuse  diarrhea.  All  these 
symptoms  suggest  a  temporary  vascular  paralysis  with  osmosis  of  serum 
through  the  walls  of  the  vessels,  which  have  become  porous.  The  local  dila- 
tation produces  anaemia  of  the  brain,  and  therefore,  at  times,  the  mind  be- 
comes clouded,  or  even  complete  loss  of  consciousness  occurs.  During  the 
attack  the  pulse  becomes  very  weak  and  small.  These  attacks  occur  in  arterio- 
sclerotic and  myocarditic  heart  disease,  and,  above  all,  in  the  heart  affections 
associated  with  nephritis.  The  most  important  indication  for  treatment  is 
the  energetic  use  of  cardiac  and  vascular  stimulants,  such  as  subcutaneous 

28 


438  DISEASES  OP  THE  CIRCULATORY  ORGANS 

injections  of  camphor,  digalen,  and  caffeine;  and  also  sinapisms,  hot  'appli- 
cations, etc. 

(e)  Attacks  of  Tachycardia. —  {Vide  infra.) 

5.  Nervous  Palpitation. — By  "  palpitation  "  we  understand  the  subjective 
perception  of  the  movements  of  the  heart.  It  is  usually  excited  by  increased 
action  of  the  heart,  but  there  is  no  constant  relation  between  the  intensity 
of  the  cardiac  pulsations  and  the  subjective  feeling  of  them.  We  sometimes 
observe  that  patients  with  aortic  insufficiency  do  not  perceive  the  very  strong 
action  of  their  hypertrophied  hearts,  while  in  other  cases  a  patient  complains 
of  a  troublesome  feeling  of  palpitation,  although  the  action  of  the  heart  does 
not  appear  objectively  to  be  especially  increased. 

"We  term  cases  "  nervous  palpitation "  if  the  patient  complains  of  palpi- 
tation when  a  physical  examination  of  the  heart  shows  no  anatomical  change 
in  it.  As  a  rule,  in  these  cases  we  really  have  to  do  with  a  heart  whose  action 
is  increased  by  abnormal  nervous  influences.  In  many  cases  the  palpitation 
arises  from  slight  external  causes,  which  may  give  rise  to  little  or  no  palpita- 
tion in  a  healthy  person,  as,  for  example,  after  the  slightest  mental  excite- 
ment, after  any  slight  physical  exertion,  after  taking  food,  after  indulging 
in  certain  drinks,  such  as  tea,  coffee,  wine,  or  beer,  or  after  assuming  certain 
positions,  as  in  lying  on  the  left  side.  Here,  then,  we  have  to  do  with  an 
abnormal  sensitiveness  of  the  heart  to  external  irritation.  Usually  the  in- 
crease in  vigor  of  the  heart's  action  is  associated  with  a  decided  increase  in 
its  frequency.  We  have  often  seen  patients  with  nervous  palpitation  who  had 
a  pulse  rate  of  140  to  160  beats  a  minute  after  comparatively  slight  exertion; 
but  in  other  cases  there  is  apparently  a  sort  of  hyperesthesia  of  the  patient 
with  regard  to  the  motions  of  the  heart,  so  that  contractions  of  normal 
strength  and  rapidity  give  rise  to  disagreeable  sensations. 

The  patient  rarely  complains  of  continuous  palpitation;  it  usually  occurs 
in  more  or  less  sharply  defined  paroxysms.  Very  commonly  in  purely  nervous 
palpitation  we  have  to  do  with  persons  who,  in  general,  suffer  from  nervous, 
hysterical,  and  neurasthenic  symptoms,  or  they  are  anaemic  persons,  chlorotic 
girls,  etc. ;  but,  on  the  other  hand,  nervous  palpitation  may  occur  in  very 
full-blooded,  "  plethoric  "  subjects. 

Often  hypochondriasis  plays  an  important  part,  and  dread  of  heart  disease 
and  the  thought  of  its  possible  consequences  excite  a  palpitation  which  con- 
firms the  patient  in  his  delusion  (vide  supra,  Psychogenetic  Heart  Disturb- 
ances). 

The  diagnosis  of  nervous  palpitation  can  be  made  only  when  repeated 
careful  examination  shows  no  objective  abnormality  in  the  heart.  In  many 
cases,  as  when  there  are  anaemic  murmurs,  the  decision  may  be  quite  difficult. 
We  must  always  pay  particular  attention  to  the  whole  constitution  and  the 
general  impression  which  the  patient  makes. 

It  is  often  especially  difficult  to  distinguish  between  purely  nervous  pal- 
pitation in  a  heart  otherwise  functionally  normal,  and  conditions  of  congenital 
or  acquired  weakness  of  the  heart   (vide  supra). 

The  prognosis  is  so  far  favorable  in  that  the  disease  is  not  dangerous.  In 
many  cases  improvement  and  final  recovery  may  be  effected,  but  other  cases, 
of  course,  resist  all  therapeutic  efforts  very  obstinately. 

The  treatment  must  first  be  directed  to  improving  the  patient's  general 


THE   CARDIAC   NEUROSES  439 

constitution.     The  anaemic  are  to  be  giver   iron,  quinin,  and   strengthening 

diet.  We  put  full-blooded  persons,  however,  on  scanty  fare,  and  prescribe 
for  them  bitter  waters,  or  a  bath  cure  at  Marienbad  or  EUssingen.  WTien 
there  is  hysteria  or  neurasthenia,  ii  requires  special  treatment.  If  the  patienl 
is  hypochondriacal,  which  is  the  ease  in  the  majority  of  "cardiac  neuroses," 
of  course  the  main  thing  is  for  the  physician  to  reassure  him.  At  the  same 
time,  we  must  not  disregard  entirely  the  use  of  other  remedies,  although  they 
may  be  of  suggestive  value  only.  The  actual  heart  drugs,  however,  such  as 
digitalis,  are  best  avoided  completely.  The  tnosl  useful  remedies  are  hydro- 
therapy, C02  baths,  and  the  internal  administration  of  tincture  of  valerian, 
validol,  bromid  of  sodium,  etc. 

As  a  symptomatic  indication  during  an  attack  we  should  recommend  the 
patient  especially  to  keep  quiet.  The  use  of  cold  to  the  cardiac  region — cold 
compresses  and  ice  bags — often  acts  beneficially.  On  the  other  hand,  how- 
ever, it  is  to  be  noted  that  a  tendency  to  palpitation  associated  with  cardiac 
weakness  may  often  be  allayed  by  methodical  exercise  and  the  invigoration 
of  the  cardiac  muscle  consequent  thereupon. 

6.  Paroxysmal  Tachycardia. — A  peculiar  and  not  very  rare  neurosis  of  the 
heart,  tachycardia,  consists  of  an  enormous  frequency  of  the  pulse  (so-called 
heart  hurry),  coming  on  in  paroxysms,  up  to  160  to  200  beats  and  more  a 
minute. 

"We  have  already  mentioned  these  attacks  as  a  symptom  in  mitral  and 
aortic  valvular  disease  and  in  diseases  of  the  myocardium,  but  precisely  simi- 
lar attacks  occur  as  a  pure  neurosis  without  demonstrable  lesion  of  the  heart, 
particularly  in  anaemic,  nervous,  or  obese  individuals.  We  saw  one  very  well- 
marked  case  in  a  lady  with  extreme  neurasthenic  melancholia,  and  other  cases 
in  patients  with  the  greatest  variety  of  other  diseases,  such  as  cirrhosis  of 
the  liver,  multiple  sclerosis,  etc.  We  do  not  know  the  exact  cause  of  the 
sudden  development  of  the  increased  pulse  frequency.  Sometimes  heavy 
smoking  seems  to  be  responsible;  in  other  cases,  bodily  exertion,  mental 
excitement,  and  previous  acute  diseases  appear  to  have  an  aetiological  signifi- 
cance, Not  infrequently,  absolutely  no  cause  for  the  appearance  of  the 
tachycardia  can  be  demonstrated.  The  individual  attack  usually  begins  quite 
suddenly,  by  day  or  by  night,  sometimes  without  any  cause,  but  often  it  is 
apparently  produced  by  certain  exciting  causes,  especially  at  times  by  over- 
distention  of  the  stomach.  The  patient  feels  that  the  attack  is  coming,  he 
becomes  anxious  and  restless,  and  looks  pale;  but  there  are  not,  as  a  rule, 
any  symptoms  like  precordial  anxiety,  dyspnoea,  or  attacks  of  faintness.  The 
majority  of  patients  lie  down  quietly  during  the  attack,  others  walk  about 
slowly.  We  notice  in  the  heart  itself,  during  the  attack,  chiefly  a  great  accel- 
eration of  the  heart  sounds.  Both  heart  sounds  become  completely  similar  in 
volume  and  pitch,  and  the  period  of  repose  of  the  heart  disappears  ("  embryo- 
cardia").  We  sometimes  hear  indefinite,  functional  murmurs.  The  action 
of  the  heart  is  usually  quite  regular,  but  there  is  occasionally  manifest  arrhyth- 
mia during  the  attack.  Acute  increase  of  the  heart's  dullness  has  been 
repeatedly  observed  during  the  attack.  We  have  been  able  to  verify  a  marked 
temporary  dilatation  of  this  sort,  particularly  in  patients  with  heart  disease, 
and  also  in  one  case  of  paroxysmal  tachycardia  affecting  a  sufferer  from 
cirrhosis  of  the  liver.     In  the  majority  of  cases,  and  especially  when  the 


440  DISEASES   OF   THE   CIRCULATORY  ORGANS 

tachycardia  is  a  mere  neurosis,  no  snch  dilatation  of  the  heart  can  be  made 
out.  As  a  rule,  the  respiration  is  not  disturbed  during  the  attack.  Some- 
times the  excretion  of  urine  is  diminished,  but  occasionally  during,  and  par- 
ticularly after,  the  attack,  polyuria  may  develop.  Gastric  disturbances  are 
not  infrequently  observed  (anorexia,  nausea,  vomiting).  The  duration  of 
the  attacks  is  very  variable,  ranging  from  a  few  moments  to  several  days. 
If  frequent  opportunity  exists  to  observe  the  end  of  the  attack,  usually  a 
sudden  cessation  of  the  tachycardia  is  noticed  in  testing  the  pulse  or  auscul- 
tating the  heart.  It  is  noteworthy  that  the  frequency  of  the  pulse  usually 
sinks  to  exactly  one  half  of  the  previous  count;  for  example,  from  180  sud- 
denly to  90.  This  is  extremely  interesting  from  a  theoretical  standpoint,  as 
it  permits  us  to  regard  the  attack  itself  as  a  duplication  of  the  heart  beats. 

The  prognosis  of  tachycardia  depends  first  upon  the  nature  of  the  under- 
lying disease.  We  do  not  know  whether  a  permanent  recovery  is  possible  in 
idiopathic  cases,  but  we  can,  at  any  rate,  succeed  in  improving  the  condition. 
If  no  other  signs  of  organic  disease  are  present,  life  is  not  actually  threatened 
by  the  attack.  The  treatment  during  the  attack  consists  in  enjoining  com- 
plete bodily  rest,  and  in  applying  ice  to  the  heart.  Such  sedatives  as  bromid 
of  potassium,  water  of  bitter  almonds,  and  tincture  of  valerian  are  particu- 
larly beneficial  in  the  "  purely  nervous "  cases.  The  application  of  a  cold 
pack  is  usually  acceptable  to  the  patient.  It  is  said  that  compression  of  the 
vagi  in  the  neck  has  caused  the  tachycardia  to  disappear  in  isolated  cases. 
In  other  respects  our  treatment  is  determined  mainly  by  the  underlying 
condition,  if  known.  [If  there  is  reason  to  think  that  the  stomach  is  over- 
loaded, gentle  measures  should  be  taken  to  empty  it.]  The  main  thing  in 
all  cases  associated  with  general  neurasthenia  and  nervousness  is  a  suitable 
constitutional  treatment  (hydrotherapy,  a  sojourn  in  the  country  or  in  the 
mountains).  Precise  regulation  of  the  diet,  according  to  the  patient's  con- 
stitution and  mode  of  life,  is  likewise  necessary. 

Concerning  bradycardia,  which  likewise  occasionally  occurs  in  attacks,  see 
above,  page  417. 


SECTION   II 

Diseases  of  the  Pericardium 

CHAPTEE   I 

PERICARDITIS 

(Inflammation  of  the  Pericardium) 

AETIOLOGY 

Pericarditis  seldom  appears  as  a  primary  idiopathic  disease.  It  is  usually 
merely  a  sequel  or  a  complication  of  otber  diseases.  Thus,  it  is  observed  with 
particular  frequency  in  the  course  of  acute  articular  rheumatism,  where  it 
appears  sometimes  alone,  sometimes  in  combination  with  acute  endocarditis. 


PERICARDITIS  441 

It  is  not  impossible  that  some  few  cases  of  apparently  primary  acute  peri- 
carditis belong,  from  an  serological  standpoint,  to  acute  articular  rheuraa 
tism — that  is,  they  are  excited  by  the  same  pathogenic  factors  which  excep 
tionally  attack  the  pericardium  alone,  without  simultaneous  participation  of 
the  joints  in  the  disease.  This  supposition  is  rendered  probable  from  the  LateT 
course  of  many  such  cases.  For  instance,  arthritis  may  ensue.  Cases  of 
ondary  pericarditis,  unassociated  with  articular  rheumatism,  occur,  although 
much  less  often,  in  other  acute  infectious  diseases,  among  which  scarlet  fever, 
measles,  and  septico-pyaemic  processes,  as  well  as  scurvy  and  purpura  hemor- 
rhagica, deserve  especial  mention.  In  sepsis  and  pyaemia  the  pericarditis  is 
purulent,  and  in  purpura,  hemorrhagic.  Among  the  chronic  diseases  in  the 
course  of  which,  pericarditis  sometimes  appears  we  must  mention  especially 
chronic  nephritis.  We  have  seen  hemorrhagic  pericarditis  in  association  with 
leukaemia.  Pericarditis  sometimes  occurs  also  in  the  victims  of  carcinoma,  but 
here  it  is  probably  dependent  upon  a  secondary  septic  infection.  Finally,  it 
should  be  mentioned  that  severe  hemorrhagic  pericarditis  is  seen  comparatively 
often  in  alcoholic  subjects,  and  apparently  as  a  primary  disease.  Often  it  is 
really  tubercular,  but  by  no  means  always;  and  if  not,  the  author  is  inclined 
to  regard  it  as  a  primary  hemorrhagic  inflammation,  analogous  to  hemorrhagic 
pachymeningitis  (hematoma  of  the  dura  mater). 

A  large  number  of  cases  arise  from  an  extension  of  the  inflammation  from 
the  vicinity.  Thus  we  not  infrequently  see  pericarditis  as  a  result  of  pleurisy, 
especially  on  the  left  side,  and  in  pneumonia  complicated  with  pleurisy.  New 
growths  and  ulcerative  processes  in  the  esophagus,  in  the  vertebrae,  in  the  bron- 
chial glands,  or  in  the  lungs,  also  lead  at  times  to  perforation  into  the  peri- 
cardium and  a  consequent  inflammation.  It  is  not  settled  whether  the  peri- 
carditis which  appears  in  the  course  of  chronic  valvular  disease  is  also  to  be 
regarded  as  arising  from  extension  by  contiguity.  We  have  thought  of  this 
possibility,  because  we  have  been  struck  with  the  fact  that  secondary  peri- 
carditis is  especially  frequent  in  valvular  disease  of  the  aorta,  suggesting  a 
direct  propagation  of  the  inflammatory  germs  through  the  aortic  wall  to  the 
pericardium.  Still,  it  must,  of  course,  be  allowed  that  this  form  of  pericarditis 
may  have  an  independent  origin,  particularly  in  cases  of  mitral  disease.  Peri- 
carditis may  also  develop  as  a  result  of  myocarditis,  abscess  of  the  heart,  etc. 

Tuberculosis  plays  a  very  important  part  in  the  aetiology  of  pericarditis. 
No  small  number  of  apparently  primary  cases  of  pericarditis  turn  out  at  the 
autopsy  to  be  tuberculous.  This  seems  to  come  on  in  quite  an  isolated  way,  or 
as  one  symptom  of  a  special  localized  form  of  tuberculosis,  which  we  term 
tuberculosis  of  the  serous  membranes.  In  many  we  can  discover  the  origin 
of  a  tuberculous  pericarditis  in  the  direct  extension  of  a  tuberculous  pleurisy. 
In  apparently  primary  cases  the  occurrence  of  the  infection  may  sometimes 
be  explained  by  the  discovery  of  a  tuberculous  lymph-gland,  which  has  broken 
through  into  the  pericardium. 

Pericarditis  is  usually  a  disease  of  youth  and  middle  life,  but  it  may  also 
occur  in  advanced  age. 

PATHOLOGICAL  ANATOMY 

Ordinary  pericarditis  involves  the  internal  surface  of  the  pericardium 
in  either  a  circumscribed  or  diffuse  manner.     Inflammation  of  the  outer  sur- 


442  DISEASES  OF  THE  CIRCULATORY  ORGANS 

face  of  the  pericardial  sac  is  distinguished  as  external  pericarditis  (vide  infra). 
The  anatomical  processes  in  pericarditis  are  precisely  analogous  to  those  in  in- 
flammations of  the  serous  membranes  in  general,  especially  of  the  pleura. 

We  usually  divide  pericarditis  into  fibrinous,  serofibrinous,  hemorrhagic, 
and  purulent  (or  ichorous)  forms,  according  to  the  character  of  the  exudation. 
Tbe  fibrinous  and  serofibrinous  forms,  with  an  abundant  fluid  effusion  into  the 
pericardial  cavity,  are  the  most  frequent,  occurring  in  articular  rheumatism, 
in  valvular  disease  of  the  heart,  etc.  Both  layers  of  the  pericardium  are  cov- 
ered with  masses  of  fibrin,  which  often  show  a  reticular  or  villous  arrangement 
(cor  villosum).  Besides  this,  we  find  more  or  less  of  a  fluid  effusion  which 
distends  the  pericardium.  The  fluid  is  of  a  serous  nature,  contains  more  or 
less  numerous  flakes  of  fibrin,  and  is  turbid  from  the  admixture  of  cells — pus 
corpuscles,  and,  in  part,  desquamated  endothelium.  A  purulent  pericarditis  is 
always  the  expression  of  a  specific  infection  of  the  pericardium.  It  is  seen  in 
pysemic  diseases,  as  a  result  of  empyema,  and  in  perforation  of  abscesses,  can- 
cers of  the  oesophagus,  etc.,  into  the  pericardium.  A  hemorrhagic  effusion  is 
seen  chiefly  in  tuberculous  pericarditis.  In  this  we  find  miliary  tubercles,  and 
little  cheesy  nodules  in  the  inflammatory  new  growths,  besides  all  the  signs  of 
inflammation.  The  specific  tuberculous  changes  are  sometimes  recognizable 
with  the  naked  eye,  but  at  other  times  we  have  to  use  the  microscope  to  find 
them.  Hemorrhagic  pericarditis  also  occurs  in  general  hemorrhagic  diseases, 
such  as  scurvy,  and  in  weak  and  debilitated  persons,  especially  drunkards 
(vide  supra). 

In  long-continued  pericarditis  the  cardiac  muscle  almost  invariably  under- 
goes changes.  The  heart  is  usually  flabby  and  dilated,  and  the  muscle  often 
shows  fatty  degeneration.  After  the  pericarditis  has  lasted  a  long  time  there 
is  often  considerable  atrophy  of  the  cardiac  muscle,  which  is  partly  replaced 
by  fat  tissue.  We  have  already  mentioned  the  occurrence  of  pericarditis  in 
connection  with  valvular  disease  and  degenerations  of  the  myocardium. 

In  favorable  cases  of  pericarditis  we  may  have  a  perfect  recovery.  The  so- 
called  maculae  tendinece  sometimes  remain  in  the  pericardium  as  residua  of  a 
past  circumscribed  pericarditis.  In  some  cases  the  pericarditis  leads  to  an  ad- 
hesion of  the  two  layers  of  the  pericardium  to  each  other,  and  obliteration  of 
the  pericardial  cavity  (vide  infra).  In  many  cases  a  chronic  pericarditis 
finally  develops  from  the  acute  form,  or  the  whole  affection  takes  a  more 
chronic  course  from  the  outset.  In  this  way  chronic  adhesions  of  connective 
tissue  arise,  and  great  thickening  of  the  pericardium,  but  the  amount  of  fluid  is 
usually  small.  Sometimes  the  chronic  pericarditis  is  interrupted  by  an  acute 
exacerbation  of  the  disease. 

CLINICAL   SYMPTOMS 

1.  Subjective  Symptoms,  General  Symptoms,  and  Fever. — Mild  forms  of 
pericarditis  may  develop,  as  in  the  course  of  an  acute  articular  rheumatism, 
without  causing  any  subjective  symptoms.  They  are  discovered  only  by  a 
careful  physical  examination  of  the  heart.  In  severe  cases,  however,  the  peri- 
carditis causes  violent  subjective  symptoms,  which,  of  course,  have  in  them- 
selves little  that  is  characteristic. 

On  careful  questioning  we  often  find  that  there  is  pain  in  the  cardiac  re- 


PERICARDITIS  443 

gion,  or  not  infrequently  in  the  epigastrium.     Tins  pain  is  of  decided  diag- 
nostic importance,  but  it  does  not  always  exist. 

A  general  feeling  of  constraint  and  distress  is  almost  constant  in  all  acute 
cases  of  any  severity,  and  so  is  a  feeling  of  dyspnoea,  which  may  increase  to 
the  highest  degree  of  orthopnoea.  The  patients  often  complain  of  headache. 
In  severe  cases  they  become  stupid  and  comatose. 

It  is  easy  to  understand  that  extensive  pericarditis  must  impede  the  mo- 
tions of  the  heart.  Probably  the  most  important  way  in  which  it  does  this 
is  by  increasing  the  tension  in  the  pericardium,  and  thus  embarrassing  the 
diastole  of  the  ventricles,  so  that  the  cavities  of  the  heart  are  not  normally 
filled  and  general  disturbance  of  the  circulation  ensues.  Furthermore,  the 
pericardiac  deposits  and  adhesions,  and  such  changes  in  the  myocardium  as 
may  occur,  interfere  with  the  cardiac  systole.  Thus  are  explained  the  early 
signs  of  diminution  in  the  amount  of  blood  received  by  the  arteries,  as  shown 
by  pallor  and  cerebral  anaemia ;  the  distention  of  the  systemic  veins,  as  shown 
by  cyanosis;  and  the  disturbance  of  the  pulmonary  circulation,  causing 
dyspnoea. 

The  dyspnoea  is  also  increased  in  large  pericardial  effusions  by  the  me- 
chanical pressure  of  the  distended  pericardium  on  the  left  lung. 

Acute  pericarditis  is  usually  associated  with  fever.  This  has  no  special 
type,  and  usually  keeps  at  a  moderate  height — 102°  to  103.5°  F.  (39°  to 
39.8°  C.) — but  it  often  exhibits  considerable  variations.  In  cases  of  recovery 
the  fever  declines  by  lysis.  Chronic  pericarditis  may  run  its  whole  course 
without  fever. 

2.  Physical  Signs. — Inspection. — The  general  hue  of  a  patient  with  severe 
pericarditis  is  pale,  but  also  more  or  less  cyanotic.  He  has  an  anxious  ex- 
pression. He  lies  with  the  upper  part  of  the  body  raised,  or  he  sits  up  in  bed. 
The  breathing  is  usually  rapid,  labored,  and  somewhat  irregular.  The  veins 
in  the  neck  are  swollen  and  prominent.  We  very  often  see  marked  undulating 
or  pulsating  movements  in  the  jugular  veins,  as  a  result  of  stasis.  The  cardiac 
region  seems  unusually  prominent  in  all  cases  with  much  effusion,  and  the 
intercostal  spaces  there  are  flattened  out.  We  sometimes  detect  a  slight 
oedematous  swelling  of  the  chest  wall  itself. 

If  the  action  of  the  heart  is  powerful  and  the  exudation  small,  the  heart's 
movements  may  be  distinctly  visible.  In  other  cases  they  are  seen  only  faintly, 
and  they  may  be  noticeably  diffuse.  If  the  exudation  is  abundant,  or  if  ad- 
hesions occur  (vide  infra),  they  may  disappear  altogether. 

Palpation. — Palpation  in  the  milder  cases  shows  the  apex  beat  in  its  nor- 
mal position  and  of  about  normal  strength;  but  if  the  amount  of  the  peri- 
cardial effusion  increases,  the  heart  is  pushed  away  from  the  chest  wall  by  it, 
and  hence  the  heart  beat  grows  weaker  until  it  disappears  entirely.  In  such 
cases  it  is  sometimes  to  be  felt  again  if  the  patient  bends  forward  or  lies  on 
his  left  side.  In  the  rest  of  the  cardiac  region  we  sometimes  feel  the  move- 
ments feebly,  but  they  entirely  disappear  as  the  effusion  increases.  There  is 
diagnostic  importance  in  the  contrast  between  the  great  extent  of  cardiac 
dullness  (vide  infra)  and  the  faintly  distinguishable  motions  of  the  heart, 
with  absence  of  a  distinct  apex  beat  and  any  marked  epigastric  pulsation.  In 
some  cases,  by  laying  the  hand  flat  on  the  chest,  we  can  feel  the  rub  of  the 
rough  pericardial  surfaces  against  each  other, 


444  DISEASES   OF  THE   CIRCULATORY   ORGANS 

The  pulse  is  usually  accelerated,  and  in  severe  cases  it  becomes  irregular. 
In  every  large  effusion,  as  we  have  already  said,  the  tension  and  height  of  the 
pulse  are  diminished.  In  severe  cases  the  pulse  sometimes  becomes  very  small 
and  weak,  but,  when  the  heart  is  otherwise  normal  and  strong,  it  may  also 
remain  quite  strong — and  indeed  this  condition  of  the  pulse,  in  contrast  to 
the  great  weakening  of  the  heart  beat,  is  sometimes  of  diagnostic  significance. 
In  some  cases  with  a  large  pericardial  effusion  we  have  seen  a  manifest  pulsus 
paradoxus — that  is,  a  diminution  or  a  complete  disappearance  of  the  radial 
pulse  on  every  inspiration. 

Percussion. — Changes  in  percussion  resonance  are  evident  as  soon  as  the 
pericardial  sac  is  distended  with  exudation.  The  so-called  triangular  or  bot- 
tle shape  of  cardiac  dullness  is  regarded  as  especially  characteristic  of  large 
pericardial  exudations.  The  blunt  apex  of  the  triangle  is  found  above  in  the 
second  or  third  left  intercostal  space,  near  the  edge  of  the  sternum.  The  lat- 
eral boundaries  run  obliquely  to  the  right  and  downward  to  about  the  right 
parasternal  line,  and  to  the  left  and  downward  to  the  left  mammillary  line, 
or  beyond.  The  broad  base  of  the  triangle  which  lies  below  is  usually  not  to 
be  defined  by  percussion,  on  account  of  the  adjacent  left  lobe  of  the  liver. 
On  the  border  of  the  dullness  we  often  find  a  tympanitic  resonance  due  to 
the  retraction  of  the  adjacent  lung. 

In  general,  the  author's  personal  experience  forces  him  to  say  that  we  must 
not  be  too  dogmatic  in  the  establishment  of  special  shapes  of  cardiac  dullness, 
as  peculiar  to  pericarditis.  The  fact  of  enlargement  of  the  area  of  cardiac 
dullness,  and  the  marked  sense  of  resistance  upon  percussion,  are  important 
signs,  but  there  is  a  considerable  variety  in  the  shapes  of  the  dull  area,  al- 
though extension  of  the  dullness  upward  and  to  the  right  may  be  regarded 
as  particularly  frequent.  According  to  Ebstein's  observations,  the  first  change 
in  percussion  in  incipient  exudation  is  usually  an  extension  to  the  right  of  the 
normal  cardiac  dullness,  in  a  triangle  between  the  heart  and  the  liver. 

The  area  of  the  dullness  depends,  of  course,  in  the  first  place,  upon  the 
amount  of  the  effusion,  but  we  must  take  special  notice  that  in  regard  to  this 
the  relation  is  not  constant.  In  old  cases  of  pericarditis  especially  we  some- 
times find  the  cardiac  dullness  quite  extensive,  while  the  autopsy  detects  only 
a  little  fluid  in  the  pericardium.  This  is  explained  partly  by  a  secondary 
dilatation  of  the  heart,  and  partly  by  a  persistent  retraction  of  the  lung. 

It  is  an  often-mentioned  but  seldom  available  diagnostic  sign  of  pericar- 
ditis that  in  many  cases  the  still  perceptible  apex  beat  lies  within  the  cardiac 
dullness,  since  the  pericardial  effusion  extends  farther  to  the  left  than  the 
heart  itself.  It  is  also  worthy  of  note  that  the  dullness  in  pericarditis  often 
shows  very  great  changes  when  the  patient  changes  his  position.  The  dullness 
is  more  extensive  when  the  body  is  erect  than  when  lying  down,  and  when  the 
patient  lies  on  his  side  it  sometimes  shows  a  lateral  displacement  of  several 
centimeters.  The  same  changes,  however,  though  rarely  so  marked,  also  occur 
in  an  hypertrophied  heart. 

Auscultation. — The  characteristic  pathognomonic  auscultatory  sign  of 
pericarditis  is  the  pericardial  friction  rub.  This  arises  during  the  movements 
of  the  heart  from  the  rubbing  of  the  rough  and  inflamed  pericardial  surfaces 
against  each  other.  The  friction  rub  is  absent  in  pericarditis  if  the  rough 
surfaces  of  the  two  layers  of  the  pericardium  are  separated  from  each  other 


PERICARDITIS  445 

by  a  considerable  fluid  effusion,  or  if  they  can  no  Longer  nib  against  each 
other  from  an  adhesion  of  the  layers  of  the  pericardium.  We  usually  hear 
the  friction  rub  loudesl  in  the  neighborhood  of  the  base  of  the  heart,  but  it 
may  also  be  heard  at  other  parts  of  the  heart.  In  general  the  adventitious 
sounds  of  pericarditis  are  not  transmitted  to  any  great  distance  The  quality 
of  the  sound  is  described-  as  rubbing,  grating,  or  scratching.  The  friction 
rub  may  be  beard  chiefly  either  during  the  systole  or  during  the  diastole  of 
the  heart,  but  it  is  in  general  not  often  closely  associated  with  the  phases  of 
the  heart's  action.  We  sometimes  find  it  intermitting  frequently,  and  jerky. 
The  intensity  of  the  friction  rub  sometimes  varies  with  the  phases  of  the 
respiration.  It  is  usually  louder  on  inspiration,  but  sometimes  on  expiration. 
If  the  patient  changes  his  position,  the  intensity  of  the  sound  is  sometimes 
altered.  It  is  louder  when  sitting  up  than  lying  down,  etc.  The  friction  rub 
often  sounds  louder  if  the  stethoscope  is  pressed  firmly  against  the  chest,  since 
in  this  way  the  layers  of  the  pericardium  are  approximated  to  each  other. 

The  heart  sounds,  when  the  valves  are  intact,  may  sometimes  be  heard  as 
well  as  the  friction  rub,  or  they  may  be  completely  drowned  by  the  loud  rub, 
at  least  in  some  parts  of  the  heart.  In  general,  they  are  faint  in  every  case  of 
pericardial  effusion,  since  their  conduction  to  the  ear  is  impaired.  In  large 
effusions  where  no  friction  rub  is  to  be  heard,  we  hear  the  heart  sounds,  espe- 
cially the  first,  but  only  very  faintly  and  obscurely.  This  condition,  in  con- 
nection with  the  increase  of  the  cardiac  dullness,  is  of  diagnostic  importance. 
If  there  is  also  valvular  disease  with  the  pericarditis,  the  pericardial  and  endo- 
cardial murmurs  are  sometimes  hard  to  distinguish  from  each  other,  but  usu- 
ally the  former  greatly  preponderate. 

3.  Sequelae  of  Pericarditis. — A  large  pericardial  effusion  may  excite  special 
symptoms  from  pressure  on  the  neighboring  organs.  Thus  we  have  already 
said  that  compression  of  the  left  lung  must  increase  the  dyspnoea.  In  many 
cases  we  also  notice  a  moderate  dullness  over  the  left  lower  back,  from  com- 
pression of  the  left  lower  lobe.  Not  infrequently  there  is  a  combination  of 
pericarditis  and  left-sided  pleurisy  with  effusion.  In  rare  cases  difficulty  in 
deglutition  has  been  observed  as  a  result  of  pressure  on  the  esophagus,  and 
paralysis  of  one  vocal  cord  from  pressure  on  the  recurrent  nerve. 

In  cases  of  long-continued  pericarditis  the  same  sequelas  may  develop  as  in 
any  chronic  disease  of  the  heart.  The  amount  of  urine  diminishes  as  a  result 
of  the  low  arterial  pressure.  The  venous  stasis  finally  leads  to  general  dropsy 
and  to  symptoms  of  passive  congestion  in  the  liver,  spleen,  and  kidneys.  We 
would  also  state  that  we  have  repeatedly  met  with  large  effusions  in  the  cav- 
ities of  the  body,  especially  hydrothorax,  without  any  oedema  of  the  skin. 
All  the  symptoms  of  stasis  mentioned,  however,  are  often  due  much  less  to 
the  pericarditis  itself  than  to  the  atrophy  and  dilatation  of  the  heart  which 
frequently  follow  it  (vide  supra). 

SPECIAL   FORMS   OF   PERICARDITIS 

1.  Pericarditis  externa  and  Mediastino-pericarditis  (Pleuro-pericarditis). 
—By  pericarditis  externa  we  mean  an  inflammation  of  the  external  surface  of 
the  pericardia]  sac,  which  is  usually  combined  with  an  inflammation  of  the 
mediastinal  connective  tissue  and  the  neighboring  pleura,  especially  over  the 


446  DISEASES  OF  THE   CIRCULATORY   ORGANS 

lingula  of  the  left  lung.  This  form  of  pericarditis  may  exist  by  itself,  or  it 
may  be  combined  with  internal  pericarditis.  It  is  a  rare  disease,  and  is  most 
frequently  seen  as  a  result  of  tuberculous  pleurisy. 

The  physical  signs  must  differ  so  much,  according  to  the  localization  and 
extent  of  the  process,  that  we  can  give  few  general  data  in  regard  to  them. 
There  are  only  a  few  peculiar  signs,  which  must  be  noted  as  characteristic  of 
many  cases.  In  the  vicinity  of  the  apex  beat,  or  at  the  left  border  of  the  car- 
diac dullness,  we  sometimes  hear  a  so-called  extra-pericardial  (pleuro-peri- 
cardial)  friction  rub.  This  depends  both  upon  the  cardiac  movements  and 
upon  the  respiratory  movements.  The  friction  sound  often  becomes  louder 
during  inspiration,  or,  again,  it  may  be  audible  only  when  the  lungs  are  fully 
inflated.  On  holding  the  breath  we  hear  merely  the  sound  due  to  the  pulsa- 
tions of  the  heart,  while  on  deep  breathing  the  pleuritic  friction  sound  is  also 
to  be  heard.  In  individual  cases  there  are  many  modifications,  which  cannot 
all  be  mentioned.  Another  interesting  sign,  first  found  by  Griesinger  and 
Kussmaul  in  a  cicatricial  mediastino-pericarditis,  is  the  so-called  pulsus  para- 
doxus. This  consists  of  a  diminution  of  the  pulse  at  each  inspiration.  This 
condition  arises,  in  part  of  the  cases  at  least,  from  the  fact  that  the  bands  and 
adhesions  of  connective  tissue  at  the  origin  of  the  aorta  mechanically  nick 
into  and  contract  its  lumen  at  every  inspiratory  movement  of  the  thorax. 
This  explanation,  of  course,  does  not  suffice  for  all  cases,  since  the  pulsus 
paradoxus  also  occurs  under  other  conditions,  as  with  large  pericardial  effu- 
sions. In  some  cases  there  may  be  seen  a  marked  swelling  of  the  jugular 
veins  in  the  neck  at  each  inspiration,  at  the  same  time  with  the  pulsus  para- 
doxus, since  the  large  venous  trunks  also  undergo  a  mechanical  nicking  and 
constriction  at  each  inspiration.  We  have  ourselves  seen  a  very  pronounced 
slowing  of  the  pulse  at  every  inspiration,  in  a  complicated  case  of  extra-peri- 
cardial adhesions  (vagus  irritation?).  We  must  also  mention  that  Eiegel 
observed  a  disappearance  of  the  apex  beat  on  expiration  in  some  cases  where 
there  were  bands  of  connective  tissue  between  the  lungs  and  the  outer  surface 
of  the  heart.  At  every  expiration  the  bands  were  stretched  more  tightly,  and 
hence  checked  the  movements  of  the  heart. 

2.  Obliteration  of  the  Pericardial  Cavity  (Adhesive  Pericarditis;  Adhesions 
of  the  Layers  of  the  Pericardium;  Concretio  seu  Synechia  pericardii). — We 
may  have  a  more  or  less  complete  adhesion  of  the  two  layers  of  the  pericar- 
dium with  each  other  as  a  result  of  pericarditis.  We  can  sometimes  observe 
the  occurrence  of  this  condition  during  the  course  of  a  pericarditis.  Quite 
frequently,  however,  we  meet  with  extensive  adhesions  of  the  two  layers  of 
the  pericardium  at  autopsies,  without  being  able  to  gather  any  history  of  a 
previous  acute  pericarditis.  The  pericarditis  must  have  occurred  here  in  a 
chronic  way,  and  without  symptoms  from  the  outset. 

Even  extensive  adhesions  of  the  pericardial  surfaces  may  develop  and  re- 
main entirely  without  symptoms,  and  be  met  with  accidentally  at  the  autopsy. 
In  other  cases,  however,  the  obliteration  of  the  pericardial  sac  causes  special 
physical  signs  and  severe  clinical  sequelae.  Of  the  physical  signs,  one  of  the 
best  known  and  most  discussed  is  the  systolic  retraction  of  the  chest,  either 
limited  to  the  apex  or  involving  a  larger  area.  This  is  most  comprehensible 
if  there  is  an  adhesion  of  the  pericardium  with  the  heart,  and  also  with  the 
chest  wall  (Skoda)  ;  but  we  certainly  find  this  retraction  at  the  systole  with- 


PERICARDITIS  447 

out  coexisting  extra-pericardial  adhesions.  It  is  not,  however,  an  absolutely 
certain  sign  of  an  intra-pericardial  adhesion,  especially  if  we  have  to  do  with 
a  systolic  retraction  at  the  apex  alone,  or  limited  to  the  third  or  fourth  inter 
costal  space,  since  systolic  retractions  may  sometimes  occur  in  other  disturb- 
ances of  the  heart's  motions,  or  even  under  normal  condition-;  but  systolic 
retractions  of  the  whole  cardiac  region  are,  in  the  majority  of  cases,  a  certain 
sign  of  pericardial  adhesion.  The  amount  of  this  retraction  is  often  dependent 
upon  the  respiration,  it  being  usually  more  marked  on  inspiration. 

On  the  other  hand,  it  must  be  noted  that  very  often  there  is  no  retraction 
of  the  praecordia  during  systole  in  many  cases  of  undoubted  obi  iterative  peri- 
carditis. In  brief,  the  symptom  under  consideration  must  always  he  viewed 
with  considerable  reserve  in  forming  a  diagnosis.  Of  at  least  equal  im- 
portance, in  our  opinion,  is  the  obscurity  or  absence  of  any  cardiac  motion 
either  to  sight  or  touch.  We  can  lay  great  diagnostic  value  upon  the  absence 
of  a  cardiac  impulse  when  the  cardiac  dullness  is  increased  in  breadth  and 
upward,  although  the  heart  sounds  are  normal;  and  when  the  adjacent  bor- 
ders of  the  lung  do  not  move  with  respiration,  because  of  the  adhesions  due  to 
the  associated  pleurisy  (vide  infra)  ;  and  finally,  when  the  history  of  the  case 
and  the  general  course  of  the  illness  are  confirmatory,  for  instance,  if  there 
are  indications  of  a  previous  acute  pericarditis. 

The  other  symptoms  of  obliteration  of  the  pericardial  cavit}^  are  more 
rare  and  in  their  diagnostic  significance  still  more  uncertain.  Friedreich  ob- 
served a  sudden  collapse  of  the  jugular  veins  at  each  diastole — the  "  diastolic 
collapse  " — while  they  became  well  filled  again  at  the  next  systole.  He  ex- 
plained this  phenomenon  by  supposing  that  the  conditions  for  emptying  the 
veins  at  the  moment  of  the  diastole  of  the  ventricle  were  especially  favorable, 
since  the  chest  wall,  which  had  previously  been  drawn  in  by  the  systole,  sprung 
back  again  quickly.  But  we  have  ourselves  seen  distinct  diastolic  collapse  of  the 
veins  in  a  case  of  adhesive  pericarditis,  the  diagnosis  of  which  was  confirmed 
by  autopsy,  in  which  there  was  no  systolic  retraction  of  the  praecordia.  Eeiss 
described  some  cases  of  pericardial  adhesions  in  which  the  heart  sounds  had 
a  metallic  character  from  the  resonance  of  the  stomach,  which  had  been  drawn 
up.  All  things  considered,  we  must  say  that  although  the  diagnosis  of  peri- 
cardial adhesions  can  be  correctly  made  in  many  cases,  yet  the  signs  given 
for  it  are  more  or  less  uncertain,  since  they  may  be  absent  in  obliteration  of 
the  pericardial  sac,  and  they  may  also  be  caused  by  other  conditions  without 
such  an  obliteration.  In  a  word,  it  is  no  easy  matter  to  establish  the  diag- 
nosis of  obliterative  pericarditis,  and  in  cases  of  this  sort  the  autopsy  not  in- 
frequently brings  surprises,  as  our  own  experience  has  shown. 

The  general  constitutional  symptoms  of  obliterative  pericarditis  are  also 
subject  to  great  variations.  In  many  cases  the  affection,  as  we  have  said,  has 
no  symptoms  at  all  or  at  least  no  grave  results.  In  other  cases,  however,  there 
is  distinct  evidence  of  circulatory  disturbance.  This  disturbance  is  some- 
times due  directly  to  the  mechanical  embarrassment  of  the  heart,  but  more 
often  to  secondary  changes  in  the  myocardium.  We  fine  atrophy,  fatty  infil- 
tration, and  fatty  degeneration,  with  consequent  dilatation.  In  such  cases 
the  pulse  becomes  small  and  frequent,  and  the  ordinary  picture  of  ruptured 
compensation  is  displayed,  characterized  by  oedema,  dyspnoea,  and  conges- 
tion of  the  liver  and  kidneys.     In  these  cases  the  diagnosis  is  often  very 


448  DISEASES  OF  THE   CIRCULATORY   ORGANS 

difficult.  It  is  scarcely  possible  to  distinguish  between  this  form  of  peri- 
carditis and  chronic  myocarditis,  or  the  "  idiopathic "  enlargement  of  the 
heart. 

There  is  another  symptom-complex,  somewhat  different  from  the  above, 
which  deserves  special  mention.  We  have  been  acquainted  with  it  for  years, 
but  it  has  only  lately  received  general  attention.  Sometimes,  when  there  is 
obliteration  of  the  pericardial  sac,  there  is  developed  a  condition  so  like  that 
of  hepatic  cirrhosis  (q.  v.),  that  Friedel  Pick  has  suggested  the  name  of 
"  pericarditic  pseudo-cirrhosis  of  the  liver "  for  it.  There  are  increasing 
cbyspncea  and  great  ascites,  with  subsequent  oedema  of  the  lower  extremities, 
so  that  we  have  dropsy  of  the  lower  half  of  the  body,  while  the  upper  half 
remains  free  from  oedema  (see  Fig.  65).  The  veins  of  the  neck,  however,  are 
usually  markedly  distended,  the  face  is  cyanotic,  and  not  infrequently  a 
serous  effusion  is  demonstrable  in  one  or  both  pleural  cavities.  At  the  autopsy 
we  do  not  find  the  hepatic  cirrhosis  which  has  in  many  cases  been  supposed 
to  exist,  but  instead,  a  total  obliteration  of  the  pericardial  sac,  with  which  is 
often  associated  a  nutmeg  liver,  and  often,  also,  chronic  peritonitis  and 
chronic  pleurisy.  The  peritonitis  causes  a  marked  fibrous  thickening  of  the 
peritoneum,  apt  to  be  especially  marked  on  the  surface  of  the  liver,  in  the 
form  of  what  is  called  "  frosted  liver."  This  condition,  therefore,  in  many 
cases,  should  be  classed  as  one  of  "  chronic  inflammation  of  the  serous  mem- 
branes "  (vide  supra,  page  352).  We  may  have  a  similar  group  of  symptoms 
not  associated  with  inflammation  of  the  peritoneum,  if  the  circulatory  dis- 
turbance resulting  from  the  obliteration  of  the  pericardium  affects  chiefly  the 
portal  circulation.  We  have  also  observed  a  combination  of  obliterative  peri- 
carditis with  genuine  hepatic  cirrhosis.  In  a  word,  the  cases  are  not  all  after 
one  pattern.  The  diagnosis  can  often  be  correctly  made  when  one  is  ac- 
quainted with  the  symptom-complex,  and  pays  especial  attention  not  only  to 
the  condition  of  the  other  serous  cavities,  and  to  the  history  of  the  case,  but 
to  the  cardiac  signs,  such  as  increase  in  the  area  of  dullness,  absence  of  apex 
beat,  or  presence  of  systolic  retraction. 

3.  Tuberculous  Pericarditis. — Tuberculous  pericarditis  is  an  important  dis- 
ease clinically,  since  in  many  cases  it  is  apparently  primary.  It  may  be  either 
quite  acute  or  chronic.  The  patient  falls  ill  suddenly,  or  more  gradually, 
with  indefinite  thoracic  symptoms,  dyspnoea,  general  weakness,  moderate 
fever,  etc.  If  the  disease  is  of  long  duration,  there  is  more  or  less  oedema. 
When  we  find  on  physical  examination,  in  such  cases,  the  signs  of  pericarditis, 
the  diagnosis  of  tuberculous  pericarditis  is  probable,  if  we  discover  a  general 
"  phthisical  habit,"  hereditary  predisposition,  and  also  coexisting  disease  of 
other  serous  membranes,  especially  pleurisy,  or  more  rarely  chronic  peritonitis. 
In  the  latter  case  the  tuberculous  pericarditis  forms  one  symptom  of  the  so- 
called  tuberculosis  of  the  serous  membranes,  but,  as  has  been  said  before,  ap- 
parently isolated  primary  tuberculous  pericarditis  does  occur  (vide  supra). 
We  have  seen  such  cases  repeatedly,  especially  in  old  people.  In  these  cases 
the  disease  is  not  easy  to  diagnosticate.  The  patient  gives  one  the  impression 
of  having  heart  disease,  but  the  physical  signs  in  the  heart  are  sometimes  of 
a  very  indefinite  nature.  Friction  rubs  may  be  entirely  absent,  on  account 
of  adhesions  or  of  large  effusions.  This  leads  to  confusion  with  myocarditis 
or  mitral  stenosis.     In  other  cases,  of  course,  all  the  physical  signs  of  peri- 


PERICARDITIS 


IV.) 


carditis    mentioned    above    may    be    manifest,    and    a    correct    diagnosi 
be  made. 

DIAGNOSIS 

From  what  precedes,  it  follows  that  the  diagnosis  of  pericarditis  is  very 
easy  in  many  cases,  but  is  very  difficult  or  impossible  in  others.  The  most 
unequivocal  sign  is  the  characteristic  friction  rub.     The  practiced  ear  can 


Fig.  65. — Pseudo-hepatic  cirrhosis  due  to  pericarditis.     (Personal  observation.) 


often  distinguish  it  from  an  endocardial  sound  by  its  quality.  The  pericardial 
sound  is  a  rubbing,  grating  noise,  near  the  ear;  the  endocardial  is  blowing 
distant  from  the  ear.  The  following  features  may  serve  as  marks  of  distinc- 
tion in  doubtful  cases:  1.  We  hear  the  pericardial  sounds  at  first,  and  also 
later,  over  the  base  of  the  heart  in  the  vicinity  of  the. pulmonary  valve;  the 
endocardial  are  often  loudest  at  the  apex.     2.  The  pericardial  murmurs  are 


450  DISEASES  OF  THE   CIRCULATORY   ORGANS 

not  so  closely  associated  with  the  phases  of  the  heart's  action,  with  systole  and 
diastole,  as  the  endocardial.  3.  We  find  that  the  pericardial  sounds  are  not 
transmitted  far.  A  loud  rub  may  be  audible  at  one  spot  which  cannot  be 
heard  a  few  centimeters  away.  Loud  endocardial  murmurs,  however,  are 
audible  over  almost  the  whole  heart.  4.  Sometimes  the  peculiarity  of  the 
pericardial  murmur — that  it  becomes  louder  when  the  patient  sits  up,  on 
pressure  with  the  stethoscope,  etc. — may  be  of  diagnostic  value.  In  many 
cases  the  loud,  functional,  so-called  anasmic  murmurs  over  the  base  of  the 
heart  may  give  rise  to  confusion  with  pericarditis. 

If  no  j>ericarditic  friction  has  been  heard  during  any  part  of  the  illness, 
it  is  seldom  possible  to  make  an  absolute  diagnosis  of  pericarditis.  At  least, 
we  must  confess  that  we  have  made  many  errors  in  the  diagnosis  of  such  cases. 
Important  factors  to  be  considered  are  the  general  course  of  the  disease,  in- 
cluding the  acute  onset  and  precordial  pain,  and  also  the  shape  of  the  car- 
diac dullness  (triangular),  and  the  signs  furnished  by  the  apex  beat,  the 
pulse,  and  the  heart  sounds.  We  have  already  pointed  out  the  possibility  of 
confusion  between  pericarditis  and  myopathic  disease  of  the  heart,  and  mitral 
stenosis  if  unattended  by  murmur.  No  rules  of  universal  application  in  these 
cases  can  be  laid  down.  It  is  very  often  advisable,  and  absolutely  devoid  of 
danger,  to  make  an  exploratory  puncture  in  doubtful  cases  with  a  hypodermic 
syringe.  This  is  done  at  the  left  edge  of  the  sternum,  or  a  little  way  in  from 
the  left  limit  of  cardiac  dullness. 

COURSE  AND   PROGNOSIS 

Many  cases  of  pericarditis  in  articular  rheumatism,  pneumonia,  or  heart 
disease,  and  also  many  of  the  rare  and  apparently  primary  forms,  may  re- 
cover completely.  In  rheumatic  pericarditis  I  have  usually  seen  recovery 
even  in  apparently  the  severest  cases.  The  disease  lasts,  in  the  mild  cases, 
only  about  a  week,  in  severe  cases  much  longer. 

Many  cases  of  pericarditis,  however,  terminate  fatally.  The  unfavorable 
issue  depends  either  upon  the  severity  of  the  primary  disease,  or  upon  the  in- 
tensity of  the  pericarditis  itself.  In  extensive  croupous  pneumonia,  in  valv- 
ular disease  of  the  heart,  or  in  severe  chronic  nephritis,  an  attack  of  peri- 
carditis is  often  the  terminal  affection — the  immediate  cause  of  death.  In 
otherwise  healthy  persons,  however,  a  severe  pericarditis  with  a  large  effusion 
may  be  the  direct  cause  of  death,  as  a  result  of  the  impairment  of  the  move- 
ments of  the  heart.  Yet  one  need  not  wholly  despair,  particularly  in  rheu- 
matic pericarditis,  even  in  cases  which  seem  very  bad.  The  prognosis  of 
tubercular  pericarditis  is  always  very  unfavorable.  This  form  may,  indeed, 
run  quite  a  chronic  course,  but  it  is  hardly  ever  capable  of  definite  recovery. 
The  prognosis  of  pysemic  pericarditis  is  also  unfavorable. 

In  one  class  of  cases  pericarditis  takes  a  chronic  course  from  the  start,  or 
chronic  pericarditis  develops  from  an  acute  attack.  The  ultimate  prognosis 
of  these  cases  is  usually  unfavorable,  since  the  secondary  atrophy  and  dilata- 
tion of  the  heart  gradually  lead  to  severe  disturbances  of  the  circulation.  We 
have  spoken  above  of  the  termination  of  pericarditis  in  obliteration  of  the 
pericardial  sac. 


PERICARDITIS  451 

TREATMENT 

Since  pericarditis  is  a  severe  affection  under  all  circumstances,  we  must 
see  especially  that  the  patient  has  perfect  rest  and  care.  Extreme  caution 
must  be  enjoined  upon  him,  especially  in  the  cases  in  which  at  first  the  sub- 
jective symptoms  are  slight.  We  must  keep  the  patient  strictly  confined  to 
the  bed,  and  not  let  him  leave  it  even  temporarily. 

The  remedies  which  are  used  for  pericarditis  aim  partly  at  keeping  the 
inflammation  in  check,  and  partly  at  aiding  the  action  of  the  heart.  For  the 
first,  the  continued  application  of  ice  to  the  cardiac  region  deserves  especially 
to  be  recommended.  Local  bloodletting,  ten  or  twelve  leeches  to  the  cardiac 
region — formerly  very  often,  but  now  more  rarely  used — may,  in  otherwise 
strong  and  healthy  persons,  afford  great  relief  in  cases  with  marked  subjective 
symptoms.  Painting  with  tincture  of  iodin  and  blistering,  however,  deserve 
little  confidence.  Digitalis  is  our  chief  means  to  bring  down  an  accelerated 
pulse  and  to  strengthen  the  heart's  action.  It  is  the  drug  which  is  the  most 
efficient  and  the  most  frequently  used  in  pericarditis,  and  is  always  indicated 
when  the  pulse  is  rapid  and  of  diminished  tension.  Of  course,  the  action  of 
the  remedy  must  be  carefully  watched,  as  in  all  cases  where  digitalis  is  pre- 
scribed. Caffein  and  tincture  of  strophanthus  are  also  useful.  As  a  pallia- 
tive, morphin  often  does  indispensable  service  when  the  subjective  symptoms 
are  marked  and  the  patient  is  very  restless.  Diuretics  are  also  employed,  as 
in  pleurisy  with  effusion  (q.v.) 

If  the  symptoms  are  threatening,  the  question  arises  whether  a  large  fluid 
pericardial  effusion  is  the  cause  of  the  severe  symptoms.  In  this  case  the 
evacuation  of  the  exudation  is,  of  course,  imperatively  indicated.  The  diffi- 
culty of  forming  a  correct  opinion,  however,  is  very  great,  because  in  any  in- 
dividual case  it  is  rarely  possible  to  determine  the  amount  of  fluid  that  may 
be  present.  In  the  first  place,  we  must  consider  the  size  of  the  cardiac  dull- 
ness and  the  weakening  of  the  movements  of  the  heart,  but  both  factors  may 
give  rise  to  deception.  Hence  we  always  first  make  an  exploratory  puncture 
with  a  Pravaz's  hypodermic  syringe.  According  to  the  newer  extended  ex- 
periences of  Curschmann,  the  best  point  of  insertion  is  in  the  left  mammary 
line,  or,  if  the  exudate  is  large,  a  point  even  more  or  less  external  to  this, 
somewhat  internal  to  the  outermost  limits  of  the  area  of  dullness.  If  the 
height  of  the  diaphragm  is  normal,  the  fifth  intercostal  space  is  entered,  while 
if  this  is  low,  the  sixth  is  utilized.  The  exudate  is.  siphoned  off  with  the  aid 
of  a  Fiedler  needle  or  a  sheath-shaped  Curschmann  trocar.  Of  course,  in 
certain  cases,  other  points  of  puncture  must  be  selected.  With  regard  to  the 
details,  we  will  refer  to  the  description  of  puncture  of  the  pleura.  Puncture 
of  the  pericardium  is  always  performed  by  the  aid  of  aspiration.  It  is  less 
dangerous  than  might  be  feared.  Even  injuries  to  the  heart  during  the 
operation  have  scarcely  ever  had  grave  results.  The  temporary  relief  to  the 
patient,  in  cases  of  successful  puncture,  is  usually  very  striking,  but  the  per- 
manent results  of  pericardial  puncture  are,  of  course,  much  less  favorable 
than  those  of  puncture  of  the  pleura,  which  is  chiefly  due  to  the  character  of 
the  underlying  disease.  In  some  cases  of  purulent  pericarditis,  incision  of 
the  pericardium  has  also  been  practiced  after  the  analogy  of  the  treatment 
of  empyema.     In  other  forms  of  pericarditis  with  an  abundant  fibrino-serous 


452  DISEASES   OF   THE   CIRCULATORY   ORGANS 

exudation,  it  might  often  be  preferable  to  make  an  incision  rather  than 
to  aspirate,  but  there  has  not  yet  been  much  experience  with  tbe  former 
method. 

If  there  is  a  condition  of  cardiac  weakness,  stimulants  are  indicated — 
strong  wine,  subcutaneous  injections  of  caffein  or  camphor,  strophanthus, 
etc.  We  try  to  keep  up  the  patient's  strength  by  the  best  of  nourish- 
ment. 

The  resulting  conditions  of  disturbance  of  the  circulation,  such  as  cedema, 
in  chronic  pericarditis,  are  treated  in  the  same  way  as  in  valvular  disease 
(vide  supra).    Digitalis  and  diuretics  are  the  chief  remedies. 

In  obliteration  of  the  pericardium,  Brauer  has  recommended  a  surgical 
procedure,  the  so-called  cardiolysis — i.  e.,  the  resection  of  the  ribs  in  the  pre- 
cordial region.  His  idea  is  thereby  to  obtain  greater  freedom  and  facility 
for  the  cardiac  contractions.  The  operation  has  already  been  frequently  per- 
formed, with  a  fair  percentage  of  really  favorable  results,  especially,  as  I 
have  personally  been  able  to  observe,  in  cases  of  so-called  pericarditic  pseudo- 
cirrhosis  of  the  liver. 


CHAPTEE    II 

HYDRO-PERICARDIUM,   HEMO-PERICARDIUM,   AND  PNEUMOPERICARDIUM 

1.     HYDRO-PERICARDIUM 

(Dropsy  of  the  Pericardium) 

The  collection  of  a  serous  transudation  in  the  pericardial  sac,  without  any 
inflammatory  symptoms  in  the  serous  membrane  itself,  we  term  hydro-peri- 
cardium, or  dropsy  of  the  pericardium.  Dropsy  of  the  pericardium,  which 
formerly  played  quite  a  great  role  in  pathology,  is  never  a  disease  of  itself, 
but  is  always  a  secondary  condition.  It  may  occur  in  ansemic  and  cachectic 
persons  as  a  result  of  hydremia,  but  it  usually  depends  upon  a  local  or  gen- 
eral venous  stasis  in  the  pericardium.  In  the  latter  case  the  hydro-pericardium 
is  one  symptom  of  general  dropsy,  and  hence  is  found  chiefly  in  heart  disease, 
renal  disease,  or  pulmonary  emphysema. 

The  clinical  symptoms  of  hydro-pericardium  are  only  exceptionally  dis- 
tinct, being  obscured  by  the  underlying  affection.  Large  amounts  of  fluid 
in  the  pericardial  sac,  which  may  amount  to  a  quart  (a  liter)  or  more,  must, 
of  course,  impair  the  action  of  the  heart,  weaken  the  heart  beat  objectively, 
and  cause  an  increase  in  the  cardiac  dullness.  Nevertheless,  if  the  lungs 
are  markedly  emphysematous,  even  large  pericardial  transudates  are  oasily 
overlooked.  The  distinction  from  pericarditis  is  rendered  possible  by 
the  absence  of  a  friction  rub,  but  still  more  by  attention  to  the  exist- 
ence of  an  underlying  disease.  Notwithstanding  this,  errors  are  easily 
possible. 

The  prognosis  and  treatment  depend  wholly  upon  the  nature  of  the  under- 
lying disease.  Only  exceptionally  do  we  need  to  puncture  when  the  exudation 
is  very  large. 


HYDRO-    HEMO-,   AND   PNEUMO  PERICARDIUM  453 

2.     HEMO-PERICARDIUM 

{Blood  in  the  Pericardial  Sac) 

In  rare  cases  hemorrhages  occur  into  the  pericardia]  sac  The  source  of 
the  hemorrhage  is  most  frequently  an  aneurism  of  the  aorta,  which  perforates 
into  the  pericardium.  Other  causes  of  hemorrhage  are  the  bursting  of 
aneurisms  of  the  coronary  arteries  and  rupture  of  the  heart.  The  Latter 
lias  heen  seen  after  injuries,  and  also  as  a  result  of  cardiac  aneurism  and  the 
•cicatricial  formations  in  myocarditis  (see  myocarditis).  Finally,  direct  in- 
juries to  the  heart,  especially  bullet  wounds,  may  also  cause  hemorrhages  into 
the  pericardia]  sac. 

In  most  cases  death  occurs  in  a  few  moments  from  compression  of  the 
heart,  when  a  hemo-pericardium  comes  on.  Hence  the  amount  of  blood 
poured  out  into  the  pericardial  sac  is  usually  not  very  considerable.  Only 
in  the  cases  in  which  the  blood  oozes  out  more  slowly  can  a  great  distention 
of  the  pericardial  sac  be  reached.  The  diagnosis  is  rarely  possible.  With 
regard  to  treatment  we  can  merely  note  that,  in  some  traumatic  cases,  aspira- 
tion of  the  blood  has  been  performed  with  success. 


3.     PNEUMOPERICARDIUM, 

(Air  in  the  Pericardial  Sac) 

The  entrance  of  air  or  gas  into  the  pericardial  sac  has  been  observed  in 
rare  cases,  apart  from  external  wounds,  as  a  result  of  the  perforation  of  a 
pyo-pneumothorax,  or  of  some  other  suppurating  process  in  organs  that  con- 
tain air.  Thus,  cases  are  known  in  which  the  rupture  into  the  pericardial 
sac  comes  from  the  oesophagus,  as  in  cancer;  from  the  stomach,  in  cancer  or 
ulcer;  or  from  the  lungs,  in  tubercular  or  gangrenous  cavities.  Since  the 
agents  of  inflammation  enter  the  pericardium  along  with  the  air,  a  purulent 
pericarditis  almost  always  develops,  besides  the  pneumo-pericardium,  or  it 
may  rarely  be  simply  a  sero-fibrinous  pericarditis. 

The  most  characteristic  and  striking  sign  of  pneumo-pericardium  is  the 
presence  of  a  metallic  sound,  due  to  the  movements  of  the  heart.  Either  the 
heart  sounds  themselves,  or  some  existing  friction  rub,  may  acquire  a  metallic 
timbre  from  the  increased  resonance,  or  splashing  metallic  sounds  may  be 
produced  in  the  pericardial  sac  from  the  movements  of  the  air  and  the  fluid, 
which  may  often  be  heard  at  a  distance  from  the  patient.  In  regard  to 
■diagnosis,  however,  it  is  important  to  know  that  signs  similar  to  those  of 
metallic  resonance  in  the  heart  may  arise  from  the  stomach,  when  it  is  drawn 
or  pushed  upward. 

In  true  pneumo-pericardium  percussion  gives  a  more  or  less  complete  ab- 
sence of  the  cardiac  dullness.  On  rod  percussion  (see  page  362)  a  metallic 
sound  is  sometimes  heard,  whose  pitch  may  vary  somewhat  with  the  phase  of 
the  heart's  action.  If  fluid  is  also  present  in  the  pericardial  sac  besides  the 
air,  the  dullness  caused  by  this  will  rise  on  raising  up  the  patient. 

The  other  symptoms  of  the  disease  and  the  treatment  are  the  same  as  in 
a  severe  pericarditis.     The  prognosis,  however,  corresponding  to  the  primary 
disease,  is  wholly  unfavorable. 
29 


454  DISEASES   OF  THE   CIRCULATORY  ORGANS 

SECTION   III 

Diseases  of  the  Vessels 

CHAPTER   I 

ARTERIOSCLEROSIS 

(Endarteritis  chronica  deformans.     Atheroma  of  the  Vessels) 

iEtiology. — Arteriosclerosis,  or  so-called  atheromatous  degeneration,  is 
probably  in  most  cases  an  expression  of  the  wearing  out  of  the  arteries,  be- 
cause of  the  many  ways  in  which  the  intima  of  the  arteries  is  damaged 
during  life,  both  chemically  and  mechanically.  Atheroma  of  the  arteries  is 
then  mainly  a  change  incident  to  age,  and  as  such  is  often  regarded  as  not 
a  true  disease. 

On  the  other  hand,  if  arteriosclerosis  appears  in  earlier  life,  say  before 
the  fortieth  year,  we  must  look  for  such  circumstances  as  would  tend  to  make 
the  ordinarily  efficient  causes  unusually  active.  We  must  not  forget  that 
there  is  an  apparent  predisposition  to  the  condition,  which  often  seems  to 
be  hereditary;  but  without  doubt  there  are  more  appreciable  causes.  The 
reason  that  arteriosclerosis  is  so  common  and  occurs  comparatively  so  early 
in  hard  laborers,  is  the  great  mechanical  strain  which  the  arteries  undergo 
during  persistent,  severe,  bodily  exertion.  Again,  in  diseases  which  are  asso- 
ciated with  a  persistent  elevation  of  arterial  tension,  such  as  hypertrophy  of 
the  left  ventricle  in  interstitial  nephritis,  arteriosclerosis  develops  probably 
as  a  result  of  the  constant  high  tension.  It  must  be  confessed  that  here  a 
decision  is  often  very  difficult,  inasmuch  as  the  arterial  disease  may  be  simul- 
taneous with  the  nephritis,  or  even  the  actual  cause  of  it  (arteriosclerotic 
contracted  kidney).  Again,  excessive  chemical  irritation  must  be  considered. 
It  is  of  great  theoretical  interest  that  by  repeated  adrenalin  injections  a 
sclerosis  very  similar  to  the  arterial  disease  can  be  artificially  produced  in 
rabbits  (Jouse,  Erb,  Jr.,  etc.).  Experience  shows  that  habitual  excess  in 
eating  and  drinking,  particularly  in  the  use  of  alcohol,  is  apt  to  occasion 
arteriosclerosis,  and  in  the  same  connection  are  to  be  named  such  constitu- 
tional diseases  as  gout  and  chronic  nephritis,  and  perhaps  also  definite  poisons 
such  as  lead.  Of  late,  particular  importance  has  been  correctly  attributed  to 
continuous  excessive  smoking  (chronic  nicotin  poisoning  and  other  harmful 
factors).  Erom  personal  experience,  I  can  substantiate  the  frequent  early 
development  of  arteriosclerosis  in  heavy  smokers.  Nor  can  we  disregard  the 
possibility  that  the  disease  may  follow  persistent  mental  strain  and  excite- 
ment. All  these  circumstances  explain  why  well-marked  atheroma  is  far  more 
frequent  in  men  than  in  women.  Syphilis  plays  a  peculiar  role  in  the  aetiology 
of  arteriosclerosis.  We  know  now  that  many  cases  of  sclerosis  of  the  aorta, 
as  well  as  of  the  other  arteries,  are  actual  syphilitic  lesions. 

Pathological  Anatomy. — Atheroma  is  almost  exclusively  confined  to  the 
arteries;  only  exceptionally  do  like  processes  occur  in  the  veins.  Among  the 
arteries  the  aorta  is  almost  always  the  most  intensely  and  extensively  diseased ; 


ARTERIOSCLEROSIS  455 

we  also  find  disease  In  the  iliac  and  femoral  arteries,  the  brachial,  radial,  and 
ulnar,  the  coronary  arteries  of  the  heart,  and  the  arteries  of  the  brain.  In 
some  of  the  other  arteries,  however,  like  the  gastric  artery,  the  hepatic,  and 
the  mesenteric,  we  very  rarely  find  atheromatous  changes. 

Nevertheless,  in  the  individual  cases,  great  variety  is  found  in  regard  to 
the  principal  localization  of  the  arteriosclerosis.  Sclerosis  of  the  peripheral 
vessels  is  not  always  associated  with  marked  aortic  sclerosis,  and  vice  versa. 
Sometimes  the  sclerosis  is  especially  well  developed  in  the  cerebral  vessels. 

The  atheromatous  process  is  easy  to  recognize  macroscopically.  Instead  of 
the  normal  smooth  internal  surface,  we  find  more  or  less  numerous  irregu- 
larities and  thickenings  on  the  intima,  which  appear  either  more  or  less  ge- 
latinous and  translucent,  or  dense  and  fibrous,  or  ossified  as  a  result  of  calci- 
fication, in  which  case  they  also  feel  perfectly  hard.  In  many  cases  we  find 
the  surface  of  the  thickenings  destroyed — atheromatous  ulcers — and  covered 
with  masses  of  fibrin. 

The  wall  of  the  arteries  is  usually  increased  in  thickness,  making  the  vessel 
feel  stiff  and  hard.  Very  frequently  the  calcareous  plates  may  be  felt  by  the 
finger.  The  frequently  associated  increase  in  arterial  tension  gradually 
stretches  the  walls  of  the  arteries,  rendering  them  tortuous.  This  is  best  seen 
in  those  of  medium  size,  such  as  the  brachial  and  radial. 

Microscopic  examination  shows  that  the  chief  changes  are  situated  in  the 
intima  of  the  arteries.  This  appears  three  or  four  times  as  thick  as  normal, 
partly  from  the  swelling  of  its  elements  and  partly  from  the  new  growth  of 
connective  tissue  and  the  deposit  of  round  cells.  In  the  connective-tissue  cells 
of  the  intima,  and  in  the  endothelial  cells  of  its  surface,  we  usually  find  a 
marked  fatty  and  hyaline  degeneration,  to  which  the  yellowish,  translucent 
appearance  of  the  surface  is  due.  Finally,  in  the  deeper  layers  there  is  a  com- 
plete breaking  down  of  the  tissue  into  a  mixture  of  fat,  detritus,  and  choles- 
terin  crystals,  which  has  given  the  whole  process  the  name  of  atheroma 
[=pulp].  If  this  destruction  extends  to  the  surface,  an  atheromatous  ulcer 
is  foimed.  In  other  places,  however,  it  does  not  reach  ulceration,  but  the 
superficial  layers  of  the  intima  become  sclerosed,  and  are  finally  changed  to 
lamellae  of  bony  hardness  from  the  deposition  of  lime  salts.  The  atheromatous 
spots  on  the  intima  of  the  vessels  often  give  rise  to  the  formation  of  parietal 
thrombi. 

The  media  and  adventitia  of  the  arteries  also  show  changes,  in  the  later 
stages  of  the  process.  Here,  too,  we  may  finally  get  fatty  degeneration  and 
calcification.    In  other  cases,  however,  there  is  a  marked  atrophy  of  the  media. 

The  immediate  result  of  the  atheromatous  changes  is  a  loss  of  elasticity  in 
the  walls  of  the  vessels.  The  ability  to  resist  the  blood  pressure  is  reduced,  and 
this  is  why  diffuse  or  circumscribed  aneurismal  dilatations  of  the  vessels  so 
often  arise  as  a  result  of  arteriosclerosis  (see  the  following  chapters). 

Another  result  of  extensive  atheromatous  degeneration  of  the  vessels  is  an 
increase  of  the  resistance  of  the  blood  current  and  a  consequent  elevation  of 
the  arterial  pressure.  Furthermore,  the  loss  of  elasticity  in  the  coats  of  the 
medium-sized  and  smaller  arteries  removes  an  important  factor  for  the  pro- 
pulsion of  the  blood.  The  left  ventricle,  in  consequence  of  the  additions  to  its 
task,  becomes  almost  invariably  hypertrophied  in  cases  of  extensive  arterio- 
sclerosis, provided  the  general  nutrition  of  the  patient  is  still  well  maintained. 


456  DISEASES   OF  THE   CIRCULATORY   ORGANS 

We  see,  therefore,  how  close  the  mutual  relations  are  between  increased 
arterial  tension,  hypertrophy  of  the  left  side  of  the  heart,  and  arteriosclerosis. 

The  thickening  of  the  intima  in  the  smaller  vessels  often  causes  so  marked  a 
diminution  of  the  blood  supply  that  secondary  disturbances  of  nutrition  are  not 
wanting  in  the  various  organs.  The  lumina  of  the  vessels  may  be  still  further 
narrowed,  or  even  completely  closed,  by  the  formation  of  thrombi  on  such  por- 
tions of  the  wall  of  the  vessels  as  have  undergone  atheromatous  changes.  We 
have  already  in  part  learned  to  recognize  the  sequelae  which  necessarily  arise  in 
the  various  organs,  such  as  indurations  in  the  heart  as  a  result  of  atheroma  of 
the  coronary  arteries,  and  we  will  return  later  on  to  the  analogous  changes  in 
some  other  organs,  such  as  cerebral  softening  and  certain  forms  of  contracted 
kidney. 

Clinical  Symptoms. — In  order  to  decide  whether  an  arteriosclerosis  is  pres- 
ent in  the  living  subject,  we  are,  of  course,  restricted  exclusively  to  the  exami- 
nation of  those  peripheral  arteries  which  are  accessible  to  palpation.  We  must 
examine,  first  of  all,  the  radial,  brachial,  femoral,  and  temporal  arteries.  If 
there  is  atheroma,  we  feel  the  hard  and  partly  calcified  vascular  tube.  In 
marked  cases  we  have  a  feeling,  especially  in  the  radial,  as  if  we  had  hold  of 
a  goose's  neck.  We  sometimes  notice  a  diffuse  dilatation  of  the  femoral  arte- 
ries. In  many  cases  the  marked  spiral  form  of  the  vessels  is  very  striking, 
and  it  is,  as  we  have  said,  a  direct  result  of  the  loss  of  elasticity  of  their  walls 
and  of  the  increased  blood  pressure.  The  spiral  form  is  most  frequently  ob- 
served in  the  temporal,  brachial,  and  radial  arteries.  The  examination  of  the 
brachial  artery  is  of  the  most  practical  importance.  Its  tortuosity  and  ab- 
normally strong  and  visible  pulsation  is  to  be  accepted  as  a  certain  sign  of 
arteriosclerosis.  The  high-tension  hard  radial  pulse  resulting  from  hyper- 
trophy and  hypertonieity  of  the  muscular  coat  in  chronic  nephritis  must  not 
be  confused  with  real  arteriosclerosis.  I  would  like  to  emphasize  the  fact 
that  with  striking  frequency  I  have  found  atheromatous  changes  in  the 
brachial  and  radial  arteries  in  laborers  more  strongly  developed  on  the  right 
side  than  on  the  left.  It  appears  to  me  not  improbable  that  this  condition 
has  some  relation  to  the  greater  muscular  activity  of  the  right  arm. 

Although  we  can  often  directly  demonstrate  atheroma  in  the  vessels  men- 
tioned, we  must  always  be  cautious  in  deciding  from  this  that  there  is  also  an 
atheroma  of  the  internal  arteries,  for  the  radial  arteries  often  feel  very  rigid, 
while  the  autopsy  later  on  shows  little  or  absolutely  no  atheroma  of  the  in- 
ternal arteries.  In  other  cases,  however,  we  find  at  the  autopsy  marked 
atheromatous  changes  in  the  arteries  of  the  brain,  the  kidneys,  the  heart,  etc., 
although  the  external  arteries  during  life  felt  perfectly  normal.  We  see  from 
this  how  hard  it  is  to  make  an  absolute  diagnosis  of  general  arteriosclerosis. 

It  is  impossible  to  give  a  uniform  picture  of  arteriosclerosis,  since  its  re- 
sults appear  now  chiefly  in  this  organ  and  now  chiefly  in  that,  whereby  en- 
tirely distinct  types  of  disease  arise.  Hence  we  must  confine  ourselves  here 
only  to  mentioning  briefly  the  most  important  sequela?.  For  the  most  part, 
they  are  described  separately  in  other  portions  of  this  work. 

In  the  heart  we  find  a  hypertrophy  of  the  left  ventricle  as  a  result  of  the 
increased  resistance  to  the  arterial  circulation.  This  is  often  apparent  during 
life  from  the  strength  of  the  apex  beat  and  its  displacement  to  the  left,  and 
also  from  the  extension  of  the  area  of  cardiac  dullness  to  the  left.     On  auscul- 


ARTEttlOSCLKROSLS  457 

tation,  the  increased  tension  in  the  aortic  system  is  made  manifest  by  the 
strength  of  the  aortic  second  sound.  The  examination  of  the  heart,  howe 
is  often  rendered  difficult  by  the  presence  of  pulmonary  emphysema.  On  the 
other  hand,  we  sometimes  cannol  decide  how  far  a  manifest  hypertrophy  of 
the  left  ventricle  is  due  to  an  arteriosclerosis,  and  no1  to  other  coexisting 
processes,  such  as  contracted  kidney.  We  often  find  other  anatomical  changes 
in  the  heart  besides  hypertrophy  of  the  left  ventricle.  We  have  already  spoken 
of  the  important  and  interesting  results  of  atheroma  of  the  coronary  arteries, 
the  formation  of  the  so-called  indurations  of  myocarditis  in  the  heart  (see 
page  41-t  at  seq.).  Sometimes,  from  an  invasion  of  the  aortic  valves  by  the 
atheromatous  process,  we  get  an  insufficiency,  or  much  more  rarely  a  stenosis 
of  the  aortic  orifice.  Of  the  greatest  clinical  significance  is  the  sclerosis  of 
the  aorta,  which  generally  leads  to  a  diffuse  dilatation  of  the  aortic  tube,  and 
not  infrequently,  also,  to  circumscribed  aneurismal  pouching.  These  condi- 
tions and  their  clinical  sequelae  will  be  separately  considered  in  the  next 
chapter. 

We  have  already  described  the  character  of  the  peripheral  arteries.  The 
radial  pulse  is  hard  and  tense,  and  the  wave  is  either  quite  large,  or,  when 
the  tube  is  narrow,  small.  Since  the  wall  of  the  vessel  contracts  slowly,  in 
consequence  of  its  loss  of  elasticity,  the  radial  pulse  is  usually  sluggish — pul- 
sus tardus.  This  condition  is  also  pronounced  in  the  splrygmographic  tracing, 
which  shows  a  slow  ascent,  and  a  still  slower  descent,  of  the  pulse  curve,  and 
an  absence  of  the  elevation  in  the  descending  limb  of  the  curve,  due  to  the 
normal  elasticity.  The  frequency  of  the  pulse  is  quite  different  in  different 
cases.  Usually  there  exists  a  continuous  increased  frequency  of  the  pulse, 
between  100  to  120  heats  per  minute.  However,  a  permanent  slowing  of  the 
pulse  may  occur,  especially,  in  all  probability,  in  sclerosis  of  the  coronary 
arteries.  The  pulse  is  very  often  irregular  as  a  consequence  of  changes  in  the 
heart.  "We  sometimes  find  an  abnormal  delay  in  the  radial  pulse,  or  in  the 
pulse  in  other  arteries,  in  comparison  with  the  heart  beat,  from  the  lessened 
rapidity  of  transmission  of  the  pulse  wave. 

Besides  the  heart,  the  brain  is  the  chief  place  in  which  we  observe  definite 
results  of  arterial  sclerosis.  The  increased  tendency  to  rupture  which  the 
atheromatous  vessel  walls  show,  and  the  coexisting  heightened  blood  pressure, 
explain  the  comparatively  frequent  occurrence  of  cerebral  hemorrhages. 
Cerebral  hemorrhages  often  result  from  little  miliary  aneurisms  which  have 
formed  in  the  atheromatous  cerebral  arteries.  Atheroma  is  also  the  most 
frequent  cause  for  the  formation  of  foci  of  softening  in  the  brain,  since  the 
arterial  changes  may  give  rise  to  a  closure  of  the  cerebral  arteries  from 
thrombosis  or  embolism.  Finally,  so-called  senile  dementia,  or,  at  any  rate, 
many  cases  of  that  condition,  are  referable  to  cerebral  atrophy,  resulting  from 
the  faulty  nutrition  of  the  brain  through  the  sclerosed  arteries  (cf.  chapter 
on  the  Arteriosclerotic  Diseases  of  the  Brain). 

In  the  kidneys,  too,  atrophic  processes  often  develop  from  the  diminution 
of  the  blood  supply  owing  to  the  narrowed  lumina  of  the  vessels,  and  they 
lead  to  a  special  form  of  contracted  kidney.  The  origin  of  the  granulated 
"  senile  kidney  "  is  in  large  part  atheroma  of  the  renal  arteries. 

The  lower  extremities  display  symptoms  of  arteriosclerosis  less  often  than 
the  parts  already  mentioned,  but  if  present  the  symptoms  may  be  very  strik- 


458 


DISEASES   OF  THE   CIRCULATORY   ORGANS 


ing.  Here  belongs  a  peculiar  group  of  symptoms,  which  has  been  specially 
studied  by  Charcot,  Erb,  and  others.  It  is  termed  intermittent  claudication 
or  lameness,  or  dyspasia  intermittens  angiosclerotica  (Erb).  It  is  sometimes 
associated  with  lesions  of  one  or  both  femoral  or  iliac  arteries,  more  often  with 
obliterative  arteritis  of  the  distal  arteries  of  the  lower  leg  and  foot.  It  usu- 
ally begins  with  disagreeable  paresthesias  of  crawling,  tickling,  or  coldness 
in  the  feet  and  calves.  If  the  patient  walks  even  for  a  short  time  the  symp- 
toms increase,  the  feet  grow  cold,  pale,  and  blue,  there  is  actual  pain,  and  the 
patient  becomes  completely  incapable  of  walking  farther.  After  a  short  pause 
he  can  resume  his  walk,  but  soon  he  has  to  stop  again.  Upon  examination 
we  find  the  feet  and  legs  cold  and  bluish-red.  If  we  palpate  the  arteria  dor- 
salis  pedis,  or  the  tibialis  postica,  we  can  detect  no  pulsation  whatever.  This 
is  the  most  important  sign.  The  course  of  the  trouble  is  chronic,  but  de- 
cided improvement  may  ensue  under  correct  treatment  (vide  infra).  From  a 
prognostic  point  of  view  there  is  an  unfavorable  tendency  to  the  development 
of  gangrene  of  the  toes,  as  the  arteritis  increases.  With  regard  to  causation, 
an  important  part  in  the  development  of  intermittent  lameness  is  played  by 
syphilis,  excess  in  tobacco,  glycosuria,  damage  from  thermic  influences,  and 
other  causes.     Conditions  analogous  to  those  developing  in  arteriosclerosis  of 

the  femoral  arteries  occasionally  occur 
in  the  arms  if  marked  sclerotic  disease 
of  the  brachial  vessels  exists. 

Sometimes  gangrene  of  the  lower 
extremities  occurs  as  a  result  of  marked 
atheroma  without  an}r  previous  ap- 
pearance of  intermittent  lameness.  So- 
called  "  spontaneous  gangrene,"  senile 
gangrene,  and  diabetic  gangrene  are 
probably,  without  exception,  due  to 
primary  lesions  from  arteritis  and  con- 
sequent impairment  in  the  arterial 
«    blood  supply. 

All  this  shows  how  different  the 
symptoms  of  arteriosclerosis  may  be  in 
different  cases.  The  symptoms  in  the 
vascular  apparatus  often  predominate 
over  all  others.  The  heart,  which  is 
simply  hypertrophied,  or  which  has  un- 
dergone in  part  cicatricial  degeneration, 
is  finally  exhausted,  and  then  all  the 
symptoms  of  a  chronic  heart  disease  de- 
velop— dyspnoea,  oedema,  etc.  If  there 
is  also  albuminuria,  a  type  of  disease  is 
produced  which  resembles  that  of  con- 
tracted kidney.  In  other  cases,  how- 
ever, the  symptoms  in  the  brain  are  especially  manifest,  either  alone  or  in 
combination  with  the  other  symptoms  mentioned,  and,  finally,  in  rare  cases 
we  have  the  above-described  symptoms  relating  to  the  lower  extremities. 

It  is  worth  mentioning  that  not  only  the  sclerotic  changes  in  the  aorta, 


Fig.  66.  —  a,  Arteriosclerosis  of  the  ulnar 
artery.     (Breslau  Medical  Clinic.) 


ANEURISM  OK  THE  THORAM'  AORTA  459 

but  also  often  the  arteriosclerosis  of  the  peripheral  vessels,  appears  distinctly 
in  the  radiogram.  It  is  obvious  that  this  fad  is  of  great  diagnostic  signifi- 
cance. The  accompanying  Fig.  <J(i  shows  an  X-ray  picture  of  an  atheromatous 
ulnar  artery. 

We  must  remark,  in  conclusion,  that  all  the  results  of  arteriosclero.-i-  men- 
tioned may  he  ahsent  for  a  long  time  or  altogether.  .Many  persons  have 
practically  no  symptoms  at  all  from  their  arteriosclerosis,  and  reach  an  ad- 
vanced age,  but  we  must  always  consider  the  possibility  of  the  sudden  occur- 
rence of  severe  symptoms,  and  make  our  prognosis  accordingly. 

Treatment. — If  we  recall  the  above-mentioned  causes  of  arterial  sclerosis, 
we  see  at  once  the  possibility  and  importance  of  prophylaxis,  and  of  course 
if  the  disease  already  exists  we  must  endeavor  to  avert  these  injurious  influ- 
ences, so  as  to  limit  the  progress  of  the  disease  as  far  as  possible.  There  is 
little  direct  influence  upon  the  arteriosclerotic  process  to  be  expected  from 
drugs.  Iodic!  of  potassium  has  won  the  highest  reputation  in  this  regard, 
and  it  is  employed  extensively  in  all  cases  of  arteriosclerosis.  Probably  it  is 
most  efficient  in  those  cases  which  are  associated  with  a  syphilitic  taint.  It  is 
best  to  give  for  some  time  daily  small  doses  (7.5  to  15  gr.  =  0.5  to  1.0  gm.) 
of  sodium  iodic!  or  sajodin.  The  value  of  the  so-called  "  antisclerosin,"  a 
mixture  of  certain  inorganic  salts,  is  quite  doubtful.  The  consideration  of 
many  therapeutic  details  will  be  found  in  the  respective  chapters  on  the 
separate  localizations  of  arteriosclerosis.  In  the  symptom-complex  known  as 
intermittent  lameness,  Erb  recommends  iodid  of  potassium,  or  iodid  of 
sodium;  local  applications  of  warmth  (for  instance,  b}r  means  of  the  warm 
pack )  ;  galvanic  foot  baths ;  such  cardiac  tonics  as  stropbanthus ;  and  careful 
regulation  of  bodily  exercise.  If  gangrene  has  set  in,  prompt  amputation 
of  the  necrotic  part  is  necessary,  for  we  have  no  means  of  influencing  the 
process  itself. 


CHAPTER    II 

ANEURISM  OF  THE  THORACIC  AORTA 

(Sclerosis  of  the  Thoracic  Aorta) 

.ZEtiology  and  Pathological  Anatomy. — The  circumscribed  dilatation  of  an 
artery  is  termed  an  aneurism.  The  cause  of  its  formation  is  always  to  be 
sought  in  a  primary  disease  of  the  vessel  wall,  which  weakens  its  resistance 
to  the  blood  pressure.  As  we  have  already  said  in  the  previous  chapter,  it  is 
chiefly  arteriosclerosis  which  lies  at  the  foundation  of  aneurisms  in  most  cases. 
The  same  factors,  therefore,  which  favor  the  origin  of  arteriosclerosis  belong 
to  the  aetiology  of  aneurism  (see  page  454).  This  explains  why  the  root  of 
the  aorta,  where  arteriosclerosis  is  most  marked,  is  also  the  most  common  seat 
of  aneurism,  and  further,  why  aneurisms  are  especially  seen  in  advanced  life 
and  in  men. 

Besides  arteriosclerosis,  syphilis  is  undoubtedly  one  of  the  most  frequent 
causes  of  aneurism.  In  my  experience,  aneurisms  developing  in  early  life 
are  almost  without  exception  referable  to  a  previous  syphilis.  Finally,  severe 
traumata  of  the  thorax  must  also  be  regarded  as  astiological  factors.     A  slight 


460  DISEASES   OF   THE   CIRCULATORY   ORGANS 

rupture  of  the  vessel  wall  may  take  place,  and  at  this  point  the  aneurismal 
dilatation  gradually  .develops.  Traumatic  aneurisms,  to  be  sure,  are  quite 
rare. 

The  size  of  aneurisms  of  the  aorta  varies  very  much,  of  course,  in  different 
cases.  They  most  frequently  are  about  the  size  of  an  apple  or  the  fist;  but 
in  rare  cases  much  larger  aneurisms  are  observed.  According  to  their  shape 
we  distinguish  the  more  diffuse  or  spindle-shaped  dilatations  from  the  saccu- 
lar aneurisms  (aneurisma  diffusum  seu  cylindricum,  aneurisma  fusiforme,  et 
aneurisma  sacciforme) .  Intermediate  forms  and  combinations  of  the  different 
forms  occur  in  manifold  ways.  There  is  no  sharp  line  of  difference  between 
the  spindle-shaped  aneurisms  and  the  diffuse  dilatations  of  the  thoracic  aorta. 
Thus,  we  may  speak  of  the  clinical  picture  of  "  sclerosis  of  the  thoracic  aorta," 
whereby  it  is  only  a  secondary  consideration  whether  the  aorta  is  at  the  same 
time  markedly  dilated  or  not. 

As  we  should  expect  from  its  origin,  we  never  find  the  wall  of  the  aneurism 
formed  of  normal  vascular  tissue.  The  intima  almost  always  shows  tbe  same 
changes  that  are  characteristic  of  arteriosclerosis,  only  in  a  much  higher 
degree.  The  media,  too,  is  usually  changed,  and  its  muscular  structure  often 
shows  fatty  degeneration.  The  adventitia  is  usually  thickened  by  chronic 
inflammatory  processes.  The  media,  and  sometimes  the  intima,  are  in  many 
cases  so  much  atrophied  that  the  wall  of  the  aneurism,  at  least  in  part,  is 
formed  only  of  the  adventitia. 

In  the  cavity  of  the  aneurism  the  blood  is  only  partly  fluid.  We  usually 
And  it  more  or  less  full  of  new  and  old  masses  of  thrombi.  The  oldest 
thrombi,  which  lie  upon  the  wall  of  the  aneurism,  are  firm,  yellowish,  adher- 
ent to  the  wall,  and  sometimes  calcified.  At  other  points  the  thrombi  are 
softened  and  broken  down.  The  most  marked  coagulation  is  usually  found 
in  the  saccular  aneurisms  with  a  narrow  entrance,  because  in  this  form  of 
aneurism  the  blood  is  almost  completely  stagnant  in  the  aneurismal  sac. 

Aneurisms  of  the  aorta  usually  have  their  seat  in  the  ascending  aorta,  or 
in  the  arch.  Aneurisms  of  the  descending  thoracic  and  of  the  abdominal 
aorta  are  far  more  rare.  The  following  description  refers  principally  to 
aneurisms  at  the  beginning  of  the  aorta. 

We  do  not  give  separate  consideration  to  aneurism  of  the  ascending  aorta 
and  of  the  arch  of  the  aorta,  respectively,  for  it  is  impossible  clinically  to 
draw  a  sharp  distinction  between  them.  Other  aneurisms  will  be  considered 
farther  on. 

Clinical  Symptoms. — 1.  Subjective  Symptoms. — The  subjective  symptoms 
indicative  of  an  aneurism  or  a  sclerosis  of  the  thoracic  aorta  are  sometimes 
very  indefinite,  although  they  often  enough  point  with  sufficient  probability 
to  the  true  nature  of  the  disease.  Most  important  are  the  painful  sensations 
in  the  front  of  the  chest  behind  the  sternum  associated  with  a  certain  feeling 
of  distress  and  oppression.  The  pains  occur  especially  after  exertion.  After 
he  has  made  a  few  rapid  steps,  the  patient  must  stand  still  on  the  street. 
Sometimes  the  pains  radiate  to  the  back,  or  to  the  shoulders  and  arms,  espe- 
cially to  the  left  arm.  Occasionally,  as  a  result  of  pressure  of  the  aneurism 
upon  a  nerve  (intercostal  nerves,  brachial  plexus),  the  pains  assume  a  true 
neuralgic  character.  If  there  are  also  associated  with  these  pains  other  sus- 
picious symptoms,  such  as  palpitation,  dyspnoea,  cough,  dizziness,  headache, 


ANEURISM   OF  -THE   THORACIC    AORTA  461 

general  malaise,  dyspepsia,  etc.,  a  careful  consideration  of  the  caee  and  an 
exhaustive  objective  examination  are  urgently  demanded.  Concerning  the 
occurrence  of  true  anginose  attacks  in  sclerosis  of  the  aorta  and  the  coronary 

arteries,  see  page  418. 

2.  Physical  Signs  of  Aneurism. — We  begin  the  objective  examination  with 
inspection  and  palpation.  We  look  for  an  abnormal  pulsation.  This  cannol 
be  observed  in  many  of  the  more  deeply  seated  and  in  the  more  spindle- 
shaped  aneurisms.  In  other  cases,  however,  the  immediately  noticeable  ab- 
normal pulsation,  to  a  certain  extent,  permits  of  the  diagnosis  of  aneurism 
at  the  first  glance. 

Usually  the  pulsation  appears  in  the  second  intercostal  space,  on  the  right 
side,  in  aneurism  of  the  ascending  aorta,  and,  on  the  left  side,  in  that  of 
the  arch.  In  aneurisms  of  the  arch,  occasionally  a  pulsation  may  be  felt  in 
the  suprasternal  fossa  upon  deep  pressure  with  the  finger.  If  no  pulsation 
is  felt  with  the  patient  in  the  dorsal  position,  he  must  then  be  also  examined 
standing,  and  with  the  trunk  bent  forward.  Sometimes  a  distinctly  palpable 
thrill  is  associated  with  the  pulsation. 

In  the  rare  aneurism  of  the  descending  thoracic  aorta  the  pulsating  swell- 
ing may  make  its  appearance  in  the  back,  between  the  vertebral  column  and 
the  left  scapula.  If  the  aneurism  has  reached  a  certain  size,  the  pulsating 
part  protrudes  as  a  tumor.  The  protrusion  is  either  slight,  or  in  many  cases 
it  forms  a  large  prominent  swelling.  This  tumor  then  shows  usually  a  marked 
pulsation,  not  only  from  below  upward,  but  also  in  a  lateral  direction,  which 
is  of  diagnostic  significance.  In  large  aneurisms,  however,  the  pulsation  some- 
times is  very  weak,  and  scarcely  perceptible,  from  the  formation  of  many 
coagula. 

The  marked  prominence  of  large  aneurisms  is  possible  only  because  the 
covering  parts,  not  only  the  muscles  and  skin,  but  also  the. cartilages  and 
bones,  the  ribs  and  sternum,  are  brought  to  a  gradual  atrophy  and  wasting  by 
the  persistent  pressure.  The  skin  over  large  aneurisms  gradually  becomes 
thinner  and  thinner,  until  finally  it  may  even  become  necrotic. 

There  is  of  necessity  more  or  less  dullness  on  percussion  over  every  aneur- 
ism of  any  size,  provided  it  approaches  the  thoracic  Avail.  The  dullness  is 
usually  evident  in  the  upper  right  intercostal  spaces,  or  the  adjacent  parts  of 
the  sternum.  Frequently  it  even  precedes  the  palpable  pulsation,  although 
then  its  significance  is  usually  still  very  uncertain.  Aneurisms  of  the  arch 
occasionally  produce  dullness  in  the  first  and  second  left  intercostal  spaces. 
To  determine  the  areas  of  dullness,  the  entire  upper  anterior  chest  wall  should 
be  gone  over  from  right  to  left,  the  percussion  being  performed  upon  the 
finger  held  vertically.  Small  areas  of  tympanitic  resonance  should  be  looked 
for.  I  have  repeatedly  found  these  in  aneurism  in  the  neighborhood  of  an 
area  of  dullness,  although  they  may  be  present  even  without  the  latter.  They 
are  undoubtedly  due  to  the  retraction  of  the  part  of  the  lung  adjacent  to  the 
aneurism.  In  diffuse  dilatation  of  the  sclerotic  aorta,  the  presence  of  sternal 
dullness  can  often  be  demonstrated  by  careful  percussion. 

Auscultation  gives  varying  results.  In  some  cases  (probably  chiefly  when 
many  coagula  form)  we  hear  nothing  at  all  over  the  aneurism.  In  other 
cases  we  hear  one  or  two  sounds,  which  are  usually  the  -audible  heart  sounds 
transmitted.     Perhaps  a  systolic  sound  may  also  arise  from  vibration  of  the 


462 


DISEASES   OF   THE   CIRCULATORY   ORGANS 


wall  of  the  aneurism.  In  other  cases  we  hear  a  murmur  over  the  aneurism. 
A  dull  and  usually  not  very  loud  systolic  murmur  often  arises  from  the 
formation  of  eddies  in  the  aneurismal  sac.  If  we  also  hear  a  diastolic  mur- 
mur, it  is  almost  always  due  to  a  coexisting  insufficiency  of  the  semilunar 
valves  of  the  aorta  (vide  infra). 

In  those  rather  frequent  cases  in  which  the  physical  examination  leaves 
us  in  the  lurch,  the  radiographic  examination  of  the  chest  furnishes  an  un- 
usually reliable  means  of  gaining  definite  knowledge  of  the  condition  of  the 
aorta.    It  can  be  said  without  exaggeration  that  we  did  not  have  an  idea  of 

the  frequency  of  aneu- 
rism until  the  introduc- 
tion of  radiography.  The 
diffuse  and  spindle- 
shaped  dilatations  of  the 
aorta  especially  can  often 
be  recognized  by  this 
means  alone;  but  also 
numerous  sacculated  an- 
eurisms, that  give  no 
other  objective  signs, 
can  be  diagnosed  with 
absolute  certainty  by  the 
X-ray  examination.  The 
dilatation  is  recognized 
in  the  aortic  shadow,  and 
the  pulsation  can  be  seen 
with  the  fmoroscope. 

An  aneurism  of  the 
aorta  by  itself  probably 
never  causes  such  an  increased  resistance  to  the  blood  current  as  to  give  rise  to 
the  development  of  a  hypertrophy  of  the  left  ventricle.  Therefore,  in  many 
cases  of  aneurism,  particularly  of  the  arch,  we  find  the  heart  unchanged. 

In  the  quite  frequent  cases  in  which  hypertrophy  of  the  left  side  of  the 
heart  exists,  it  may  almost  always  be  referred  to  a  coexisting  insufficiency  of 
the  aortic  valves,  and  sometimes  to  general  atheroma  of  the  arteries.  During 
life  a  hypertrophy  of  the  heart  may  be  simulated,  because  the  heart  is  pushed 
to  the  left  by  the  aneurism. 

In  many  cases  the  signs  in  the  peripheral  arteries  are  important.  Marked 
inequality  of  the  pulse  in  symmetrical  arteries  is  often  an  especially  valuable 
diagnostic  sign.  Either  the  trunk  of  an  efferent  vessel  is  compressed  by  the 
aneurism,  or  the  lumen  of  the  exit  of  the  vessel  is  itself  involved  in  the 
aneurism,  and  hence  the  opening  of  the  vessel  is  distorted  or  contracted,  or 
partly  stopped  by  a  coagulum.  This  readily  explains  why,  in  aneurism  of  the 
ascending  aorta,  the  radial,  and  sometimes  the  carotid  pulse,  are  plainly 
weaker  on  the  right  than  on  the  left,  as  a  result  of  implication  of  the  trunk 
of  the  innominate,  while  in  aneurism  of  the  arch  or  of  the  beginning  of  the 
descending  aorta  the  opposite  condition  may  obtain.  Abnormal  differences, 
too,  in  the  intensity  of  the  pulse  in  the  upper  and  lower  halves  of  the  body 
may  arise  under  some  circumstances. 


Fig.  67. — Radiogram  of  a  case  of  aneurism  of  the  arch  of  the 
aorta.     (Breslau  Medical  Clinic.) 


ANEURISM   OF  THE   THORACIC   AORTA  463 

A  marked  delay  of  the  pulse  in  the  arteries  arising  below  the  aneurism 
is  a  symptom  that  is  occasionally  seen.  Thus,  we  see  in  aneurism  of  the  arch 
of  the  aorta  that  the  left  radial  pulse  is  later  than  the  right,  and  that  in 
aneurism  of  the  descending  aorta  the  pulse  in  the  Lower  extremities  is  Later 

than  the  radial  pulse. 

3.  Signs  of  Compression. — It  is  quite  in  accordance  with  the  anatomical 
relations  of  an  aneurism  that  numerous  neighboring  structures  are  exposed 
to  a  greater  or  lesser  degree  of  pressure  from  the  sac.  From  this  a  further 
train  of  symptoms  may  develop.  First  of  all,  the  adjacent  veins  (the  larger 
venous  trunks  in  the  thorax,  the  superior  vena  cava,  or  one  of  the  innominate 
veins)  may  be  compressed.  The  veins  swell  in  the  neck,  in  the  upper  extremi- 
ties, or  upon  the  surface  of  the  thorax,  according  to  the  seat  of  the  compres- 
sion. Local  oedema  may  also  be  produced  in  this  way  (oedema  of  the  face, 
neck,  and  arms). 

The  respiratory  organs  are  exposed  to  the  pressure  of  aortic  aneurisms  in 
many  ways.  Compression  of  the  lungs  by  large  aneurisms  actually  contributes 
toward  increasing  the  dyspnoea  in  many  cases.  This  may  be  still  more  dis- 
tressing if  the  trachea  be  compressed.  Of  the  two  main  bronchi,  the  left 
bronchus,  which  lies  beneath  the  arch  of  the  aorta,  is  more  apt  to  be  com- 
pressed. This  produces  the  symptoms  of  a  unilateral  bronchial  stenosis  (q.  v.). 
From  the  constant  compression  of  a  bronchus,  retention  of  the  secretions, 
chronic  bronchitis,  and,  finally,  atelectasis  and  fibroid  consolidation  develop 
in  the  corresponding  portion  of  the  lung.  Thus  are  explained  the  peculiar 
pulmonary  complications,  such  as  chronic  interstitial  pneumonia  with  chronic 
bronchitis  and  pleurisy.  These  are  not  infrequent,  and  we  have  personally 
seen  a  considerable  number  of  examples.  Many  a  case  of  severe  diffuse  bron- 
chitis in  an  elderly  arteriosclerotic  patient  at  the  X-ray  examination  (or  at 
autopsy!)  turns  out  to  be  an  aneurism  of  the  aorta.  If  an  aneurism  of  the 
concave  side  of  the  arch  of  the  aorta  transmits  its  pulsation  to  the  left  bron- 
chus lying  below,  in  and  thence  to  the  trachea  and  larynx,  a  systolic,  down- 
ward pull  of  the  larynx  may  be  observed — the  so-called  Oliver-Cordarellis 
sign  [tracheal  tug]. 

The  comparatively  frequent  compression  of  the  left  recurrent  laryngeal 
nerve,  producing  a  paralysis  of  one  vocal  cord,  is  of  great  diagnostic  im- 
portance. Such  a  unilateral  recurrent  paralysis  and  the  resulting  discordant, 
hoarse  voice  are  very  often  the  first  symptoms  to  arouse  suspicion  of  the  ex- 
istence of  an  aortic  aneurism.  Paralysis  of  the  right  recurrent  nerve  occurs 
in  aneurisms  of  the  innominate  artery. 

Pressure  on  the  vagus  may  occasion  changes  in  the  rate  of  the  pulse,  and 
perhajDS  sometimes  attacks  of  dyspnoea.  The  dyspnoea  in  most  cases,  however, 
takes  the  form  either  of  angina  pectoris  or  of  cardiac  asthma,  and  is  referable 
to  the  other  coincident  lesions  of  the  heart  and  the  coronary  arteries. 

A  very  characteristic  clinical  picture  presents  itself  if  the  aneurism  com- 
presses the  superior  vena  cava.  We  see,  then,  all  the  sequelae  of  a  venous 
congestion  of  the  upper  part  of  the  body,  extreme  cyanosis  of  the  neck  and 
face,  marked  prominence  of  the  veins  of  the  neck,  and  oedema  of  the  face 
and  arms.  As  a  result  of  compression  of  the  intercostal  nerves  or  branches 
of  the  brachial  plexus,  most  severe  and  distressing  neuralgias  arise  in  the 
nerve  territories  affected,  and  sometimes  we  see  motor  paresis  in  the  arm. 


484  DISEASES   OF  THE   CIRCULATORY   ORGANS 

Finally,  disturbances  of  deglutition  are  seen  in  many  cases  from  compres- 
sion of  the  oesophagus.  If  this  be  falsely  interpreted,  it  may  lead  to  a  mis- 
chievous use  of  the  oesophageal  sound,  as  perforation  of  the  aneurism  may  be 
caused.     Hence,  we  must  always  remember  this  possibility  in  practice. 

Course  and  Termination  of  the  Disease. — Aneurisms  may  remain  latent 
for  a  long  time  without  causing  any  symptoms.  In  such  cases  a  sudden 
perforation  may  lead  to  speedy  and  unexpected  death. 

In  the  cases  which  have  shown  the  above  symptoms  to  a  greater  or  less 
extent  for  a  long  time,  and  often  for  years,  sudden  death  quite  frequently 
results  from  rupture  of  the  aneurismal  sac  and  perforation  into  a  neighbor- 
ing organ.  In  perforation  into  the  pericardium  death  follows  almost  instantly 
from  cessation  of  the  heart's  action.  In  perforation  into  the  oesophagus  a 
fatal  hemorrhage  occurs.  In  perforation  of  the  aneurism  into  the  air-passages 
(the  trachea  or  bronchi)  or  into  one  pleural  cavity,  two  factors,  hemorrhage 
and  suffocation,  unite  in  causing  death.  Often  several  smaller  hemorrhages, 
which  are  frequently  not  noticed  or  incorrectly  interpreted,  precede  the  fatal 
hemorrhage. 

In  aneurisms  which  gradually  erode  the  anterior  wall  of  the  chest,  the 
perforation  is  in  rare  cases  external;  but  here  a  sudden,  immediately  fatal 
hemorrhage  seldom  ensues ;  much  more  commonly  a  slowly  increasing  anaemia 
develops  as  a  result  of  repeated  slight  hemorrhages  which  may  sometimes  go 
on  for  weeks.  Death  then  is  due  to  the  gradually  increasing  weakness,  or  to 
a  final  severe  hemorrhage.  Perforation  of  an  aneurism  into  the  right  side 
of  the  heart,  into  the  pulmonary  arteries,  or  the  vena  cava,  is  a  rare  ter- 
mination. Here  death  does  not  follow  at  once,  but  severe  general  disturbances 
of  the  circulation,  such  as  dropsy,  soon  arise.  In  many  of  these  rare  cases 
peculiar  physical  signs  also  appear — a  venous  pulse,  a  loud  systolic  murmur 
over  the  point  of  perforation,  etc. 

If,  in  patients  with  aneurism  of  the  aorta,  death  does  not  ensue  from  a 
sudden  perforation,  the  general  type  of  the  disease  takes  a  form  similar  to 
chronic  heart  disease.  The  aneurism,  as  we  have  said,  is  often  also  combined 
with  aortic  insufficiency,  or  with  sclerosis  of  the  coronary  arteries  and  sub- 
sequent interstitial  myocarditis.  The  left  ventricle  gradually  becomes  para- 
lyzed, and  the  well-known  disturbances  of  compensation  set  in — increasing 
dyspnoea,  oedema,  etc.  In  other  cases  the  patient  gradually  becomes  duller 
and  weaker  from  the  distressing  pain,  the  sleeplessness,  and  the  other  symp- 
toms, and  dies  with  the  signs  of  increasing  general  weakness. 

Recovery  from  aneurism  of  the  aorta  scarcely  ever  occurs. 

Diagnosis. — The  diagnosis  of  aneurism  of  the  aorta  can  in  many  cases  be 
made  Avith  great  ease  and  certainty,  but  in  other  cases  it  is  very  difficult  and 
even  impossible.  If  the  direct  physical  signs  are  plain,  especially  if  we  feel 
an  abnormal  pulsation,  we  shall  not  be  apt  to  commit  an  error;  but  the 
diagnosis  presents  great  difficulties  in  those  cases  in  which  the  aneurism  is 
not  accessible  at  all,  or  accessible  only  with  great  difficulty,  where  it  merely 
causes  indefinite  symptoms,  pain  in  the  chest,  occasional  oppression,  symp- 
toms of  pressure  on  neighboring  organs,  etc.  A  very  stubborn  intercostal 
neuralgia,  which  no  remedy  can  relieve,  may  for  a  long  time  be  the  only 
symptom,  often  misinterpreted,  of  a  latent  aneurism.  The  disease  is  often 
not  recognized,  however,  because  in  such  and  similar  cases  we  do  not  crenerallv 


ANEURISM   OF  THE  THORACIC   AORTA  465 

think  of  the  possibility  of  an  aneurism,  and  hence  we  negled  a  careful  exam- 
ination of  the  hearl  and  the  arteries,  and  also  the  search  for  oilier  symptoms 
of  compression,  such  as  paralysis  of  the  vocal  cords,  and  above  all  the  mosl 
significant  X-ray  examination. 

The  distinction  between  aneurism  and  other  tumors  in  and  about  the 
thorax  sometimes  presents  difficulties  in  diagnosis.  Mediastinal  sarcomata 
and  abscesses,  circumscribed  empyemas,  tumors  arising  from  the  sternum,  or 
new  growths  in  the  lungs  and  bronchial  glands,  may  all  give  rise  to  confu- 
sion. We  can  scarcely  lay  down  any  general  rules  for  diagnosis,  since  tin- 
conditions  differ  in  almost  every  case.  If  we  feel  ;1  swelling,  its  pulsation 
is  the  symptom  which  points  most  to  an  aneurism,  but  we  must  be  certain 
that  the  pulsation  is  not  merely  transmitted,  bu1  that  it  really  takes  place 
in  all  directions  within  the  swelling  itself  [expansile  pulsation].  We  must 
also  consider  the  auscultatory  symptoms,  the  condition  of  the  heart  and  the 
arteries,  and  any  symptoms  of  compression,  and  above  all  the  result  of 
radiography. 

Treatment. — Many  attempts  have  been  made  to  bring  about  an  oblitera- 
tion of  the  aneurism,  and  thus  a  recovery.  Although  the  methods  of  treat- 
ment aiming  at  this  have  obtained  decisive  results  in  the  aneurisms  of  periph- 
eral arteries,  their  results  in  aneurism  of  the  aorta  are  still  of  a  very  doubtful 
character;  yet  we  are  always  justified  in  any  given  case  in  trying  one  of  the 
methods  recommended. 

Persistent  compression  by  a  pad  can,  of  course,  be  employed  only  in  those 
eases  where  the  aneurism  projects  at  one  part  of  the  chest  wall.  The  pressure, 
however,  usually  causes  great  pain,  and  hence  is  ill  borne. 

Tying  the  carotid,  the  subclavian,  or  both  vessels,  has  also  been  repeatedly 
performed  in  aneurism  of  the  arch  of  the  aorta,  sometimes  with  apparent 
success,  but  oftener  without  any  benefit. 

"Acupuncture"  of  the  aneurism  (Velpeau)  consists  in  inserting  a  needle 
or  an  iron  wire  into  the  aneurismal  sac  in  order  to  excite  coagulation  in 
it.  The  results  obtained  by  it  in  aneurism  of  the  aorta  are  not  very  en- 
couraging. 

Better  results  are  reported  from  galvano-puncture.  Two  needles  inserted 
into  the  aneurism  are  connected  with  the  poles  of  a  galvanic  battery,  by  which 
a  weak  current  is  passed  through  the  aneurism.  Here  we  must  regard  the 
chemical  and  electrolytic  action  of  the  current  as  well  as  the  mechanical 
action  of  the  needles.     At  present,  however,  the  method  is  scarcely  used. 

Injections  of  chemical  substances  into  the  aneurismal  sac,  in  order  to 
produce  coagulation,  are  dangerous,  since  the  coagula  caused  by  them  may 
give  rise  to  emboli.  Hence  we  have  abandoned  making  trial  of  liquor  ferri 
sesquichloridi  and  similar  substances.  We  can  better  recommend  injections 
of  ergotin  into  the  vicinity  of  the  sac,  2  to  5  gr.  (gm.  0.1  to  0.3)  of  the 
aqueous  extract  of  ergot  dissolved  in  water  or  glycerin,  injected  every  day 
or  two.  This  method  was  first  employed  with  success  by  Langenbeck  in 
peripheral  aneurisms. 

Most  used  at  present  is  the  injection  of  gelatin,  first  recommended  in 
France.  Every  five  to  eight  days  6.5  oz.  (gm.  200)  of  a  one-  to  two-per-cent 
gelatin  solution  is  injected  subcutaneously  into  the  breast,  but  not  in  the 
immediate   vicinity  of  the   aneurism.      Coagulation   in  the   aneurism   sac   is 


466  DISEASES   OF   THE   CIRCULATORY   ORGANS 

supposed  to  be  stimulated  by  the  gelatin.  We  have  obtained  some  apparently 
good  results  by  this  method,  though  we  have  also  had  numerous  failures. 

We  can  expect  little  action  on  an  aneurism  from  the  use  of  internal  reme- 
dies. Especially  recommended  is  the  long-continued  use  of  iodid  of  potas- 
sium, iodid  of  sodium,  sajodin,  etc.,  which  have  obtained  a  great  reputation 
in  all  arteriosclerotic  lesions  and,  in  particular,  in  syphilitic  disease  of  the 
arteries  (vide  supra,  astiology  of  aneurism) .  '  Yet  it  is  easy  to  see  why  one 
should  not  expect  too  much  from  the  iodids,  although  at  times  some  ameliora- 
tion of  the  symptoms  can  be  obtained  by  a  systematic  iodid  treatment.  The 
pains  may  cease  and  the  feeling  of  distress  may  be  alleviated. 

The  treatment  of  aneurism,  therefore,  will  be  mainly  symptomatic  and 
general.  The  main  thing,  as  soon  as  the  diagnosis  is  certain,  is  to  protect 
the  patient  as  much  as  possible  from  all  injurious  influences,  especially  bodily 
exertion.  Cold  applications,  locally  (ice  bag,  Leiter  coil),  sometimes  act  very 
favorably.  If  the  tumor  protrudes,  a  protective  pad  of  lead,  celluloid,  or 
the  like,  may  be  applied.  The  pains,  anginal  attacks,  and  dyspnoea  are  treated 
on  general  principles  (morphin,  nitroglycerin,  digitalis,  etc.).  Treatment  is 
powerless  against  internal  perforations. 

[TufnelPs  method,  so-called,  which  has  given  good  results  in  abdominal 
and  peripheral  aneurisms,  proves  sometimes  useful  in  palliating  the  symp- 
toms and  lengthening  the  course  of  aortic  aneurism.  The  aim  of  this  method 
is  to  diminish  the  force  and  rapidity  of  the  circulation,  and,  if  possible,  to 
increase  the  fibrinous  deposit.  It  is  carried  out  by  enforcing  absolute  rest  in 
the  recumbent  position,  and  by  limiting  the  amount  of  food,  especially  of 
liquids.  About  ten  ounces  of  solid  food  and  eight  of  liquid  are  allowed  daily, 
divided  into  three  meals.] 


CHAPTEE    III 

ANEURISMS    OF    THE    OTHER   VESSELS 

Aneurism  of  the  Abdominal  Aorta. — Its  favorite  seat  is  the  vicinity  of  the 
cceliac  axis.  In  many  cases  it  may  be  felt  through  the  abdominal  wall  as  a 
pulsating  tumor,  over  which  a  systolic  sound  or  a  whirring  murmur  can  be 
heard.  The  possible  symptoms  of  compression  are  very  numerous.  The 
stomach,  intestine,  and  liver  (jaundice)  may  be  implicated.  Pressure  of  the 
aneurism  upon  the  nerve  trunks,  or  even  pressure  on  the  spinal  cord  after 
gradual  erosion  of  the  vertebras,  with  consequent  severe  neuralgia,  paralysis, 
etc.,  has  been  repeatedly  observed.  Death  usually  ensues  from  rupture  of 
the  aneurismal  sac  and  internal  hemorrhage. 

Aneurism  of  the  trunk  of  the  innominate  is  rare.  Its  symptoms  are  very 
much  like  those  of  an  aneurism  of  the  arch  of  the  aorta.  If  we  feel  a  pulsat- 
ing tumor,  it  is  usually  situated  somewhat  higher  up  than  the  aneurism  of 
the  aorta,  in  the  first  right  intercostal  space,  or  the  tumor  even  extends  into 
the  supraclavicular  fossa.  In  rare  cases  aneurisms  of  the  subclavian  and 
of  the  carotid  have  been  observed.  We  have  ourselves  seen  an  aneurism  of 
the  internal  carotid  the  size  of  a  cherry  pressing  on  the  Gasserian  ganglion, 
which  caused  an  extremely  severe  trigeminal  neuralgia  lasting  for  years. 


NARROWING    OF  THE   AORTA  Jf.7 

Aneurism  of  the  pulmonary  artery  may  appear  as  a  pulsating  tumor  in 
the  second  left  intercostal  space.  It  is  usually  impossible  to  distinguish  it 
with  certainty  from  an  aneurism  of  the  aorta. 

We  have  already  mentioned,  in  the  description  of  pulmonary  tuberculosis, 
the  great  importance  of  small  aneurisms  of  the  branches  of  the  pulmonary 
artery  in  pulmonary  cavities  as  a  frequent  cause  of  hemorrhage. 

Aneurisms  of  the  arteries  of  the  brain,  which  are  relatively  most  frequent 
in  the  basilar  artery  and  the  artery  of  the  fissure  of  Sylvius  (the  middle 
cerebral  artery),  may  cause  severe  cerebral  and  bulbar  symptoms  (see  Vol.  11 ). 
As  has  already  been  mentioned,  miliary  aneurisms  of  the  cerebral  arteries 
play  an  important  part  in  the  aetiology  of  cerebral  hemorrhage  (q.  v.). 

The  symptomatology  and  treatment  of  aneurisms  of  the  peripheral  arte- 
ries belong  to  the  domain  of  surgery. 


CHAPTEE    IV 

RUPTURE  OF  THE  AORTA 

A  rupture  of  a  previously  healthy  aorta,  with  fatal  hemorrhage,  after 
violent  traumatic  influences,  has  been  seen  only  in  a  very  few  cases.  In  the 
majority  of  the  very  rare  cases  of  rupture  of  the  aorta  we  have  to  do  with  a 
vessel  that  is  already  atheromatous.  In  some  cases  a  special  exciting  cause 
is  present,  and  in  others  it  is  absent.  We  once  saw  sudden  death  caused  by 
rupture  of  the  ascending  aorta  in  a  young  man  about  twenty-five,  who  before 
that  seemed  perfectly  healthy.  ISTo  trace  of  atheroma  was  found;  but  at  the 
point  of  rupture  there  was  a  slight  protrusion  and  a  decided  thinning  of 
the  wall,  which  was  probably  congenital.  The  formation  of  a  so-called  dis- 
secting aneurism,  which  has  often  been  seen  in  the  aorta,  is  of  anatomical 
interest.  Here  only  the  intima  and  media  are  torn.  The  blood  burrows 
between  them  and  the  adventitia  or  between  the  layers  of  the  media.  Most 
of  the  cases  of  dissecting  aneurism  of  the  aorta  also  result,  like  rupture  of 
the  aorta,  in  sudden  death.  In  many  cases  death  results  from  the  secondary 
perforation  of  the  aneurism  into  the  pericardium.  On  the  other  hand,  a  sort 
of  recovery  from  dissecting  aneurism  may  occur.  A  secondary  perforation 
takes  place  into  another  part  of  the  aorta  itself  (Bostrom).  Cases  of  this 
sort  were  formerly  more  than  once  mistaken  for  double  aorta.  If  the  capsule 
containing  the  blood  is  preserved  for  a  considerable  length  of  time,  the  symp- 
toms may  assume  the  character  presented  in  ordinary  aortic  aneurism. 


CHAPTER    V 

NARROWING    OF    THE    AORTA 

Congenital  narrowness  of  the  aorta  and  its  branches  is  a  condition  to 
which  Rokitansky  first,  and  later  Virchow,  have  directed  attention.  We  find 
this  anomaly  especially  in  those,  mostly  women,  who  during  life  have  shown 


468  DISEASES   OF  THE   CIRCULATORY   ORGANS 

the  signs  of  persistent  chlorosis.  Sometimes  such  persons  are  backward  in 
their  whole  development;  they  retain  a  puerile  habit,  and  show  a  defective 
development  of  the  genitals.  They  often  suffer  from  palpitation,  faintness, 
and  a  tendency  to  hemorrhages.  In  many  cases  the  heart  is  also  small,  but 
in  others  it  is  dilated  and  hypertrophiecl.  We  have  already  pointed  out 
(page  428)  that  congenital  hypoplasia  of  the  aorta  may  be  regarded  as  the 
cause  of  certain  cases  of  "  idiopathic  hypertrophy  of  the  heart."  Valvular 
disease  of  the  heart  has  been  repeatedly  found  combined  with  general  narrow- 
ness of  the  arterial  system.  During  life  this  anomaly  of  the  vascular  system 
may  sometimes  be  suspected,  but  it  can  never  be  recognized  with  certainty. 

Narrowing  of  the  aorta  at  the  point  of  insertion  of  the  ductus  arteriosus 
is  a  lesion  observed  in  rare  cases,  whose  origin  probably  always  falls  in  the 
period  directly  after  birth,  and  is  associated  with  obliteration  of  the  fetal 
ductus  arteriosus.  Other  congenital  anomalies  of  the  heart  are  usually  present 
at  the  same  time.  If  the  narrowing  of  the  aorta  is  not  very  marked,  it  may 
be  properly  compensated  by  a  secondary  hypertrophy  of  the  left  ventricle  and 
the  development  of  a  collateral  circulation.  The  latter  is  brought  about  by 
dilatation  of  the  anastomoses  between  the  first  intercostal  artery,  the  dorsalis 
scapula?,  the  subscapularis,  and  the  transversalis  colli  on  one  side,  and  the 
lower  intercostal  arteries,  which  come  off  from  the  descending  aorta  below 
the  narrowing,  on  the  other.  Anastomoses  are  also  formed  between  the  mam- 
mary and  the  superior  epigastric  on  one  side  and  the  lumbar  and  femoral 
arteries  on  the  other.  During  life  the  dilated  arteries  are  prominent,  in  part 
abnormally  tortuous,  and  perceptibly  pulsating,  especially  the  dorsales  scapu- 
lae, the  subscapulars,  the  mamillaries,  and  the  epigastrics.  In  some  cases  a 
systolic  murmur  has  been  heard  over  some  of  these  vessels.  The  pulse  in  the 
arteries  of  the  lower  extremities,  the  femoral  and  popliteal,  is  very  weak  and 
scarcely  perceptible. 

In  many  cases  the  collateral  circulation  is  so  complete  that  the  person 
affected  may  feel  no  subjective  disturbance  at  all,  and  may  attain  an  advanced 
age,  but  in  other  cases  disturbances  of  the  circulation  appear  sooner  or  later, 
and  the  patient  finally  succumbs  to  dropsy.  Sudden  death  from  rupture  of 
the  heart  or  of  the  aorta  has  also  been  observed. 


IV.    DISEASES   OF   THE   DIGESTIVE   ORGANS 


SECTION   I 
Diseases  of  the  Mouth,  Tongue,  and  Salivary  Glands 

CHAPTER    I 

CATARRHAL    STOMATITIS 

(Catarrhal  Inflammation  of  the  Mucous  Membrane  of  the  Mouth) 

^Etiology. — Inflammation  of  the  buccal  mucous  membrane  is  not  infre- 
quently the  direct  result  of  mechanical  or  chemical  causes.  As  mechanical 
causes  we  may  mention  particularly  the  sharp  edges  of  broken  or  carious 
teeth.  It  should  be  said  that  often  infectious  organisms  (vide  inf?'a)  are 
active  at  the  same  time,  because  they  gain  a  much  easier  foothold  on  account 
of  the  presence  of  bad  teeth.  Chemical  irritation  may  come  from  highly 
spiced  food,  or  from  tobacco-chewing  or  excessive  smoking.  Chemical  and 
mechanical  irritation  provokes  stomatitis  in  many  trades  which  expose  the 
artisan  to  lime,  copper,  coal,  or  other  varieties  of  dust.  In  drunkards  we  find 
not  infrequently  a  chronic  stomatitis,  which  is  characterized  by  a  thickly 
coated,  moist,  and  shiny  tongue,  which  is  somewhat  swollen  and  exhibits  in- 
dentations on  its  side  due  to  its  pressure  against  the  teeth.  Inflammation 
of  the  mucous  membrane  of  the  mouth  from  poisoning  with  corrosive  acids 
or  alkalies  is  also  the  result  of  direct  chemical  irritation.  It  may  take  the 
form  of  severe  ulcerative  stomatitis  (see  the  following  chapter).  The  mer- 
curial stomatitis,  which  results  from  acute  or  chronic  poisoning  with  mercury, 
is  caused  indirectly  by  the  particles  of  mercury  deposited  from  the  blood  in 
the  mucous  membrane.  This  mercurial  'stomatitis  when  severe  always  takes 
the  form  of  ulceration  or  necrosis.  The  stomatitis  attendant  upon  the  cut- 
ting of  teeth  in  children  will  be  discussed  below. 

In  many  instances  stomatitis  comes  from  a  direct  propagation  of  inflam- 
mation from  neighboring  parts.  It  thus  forms  a  frequent  complication  of 
pharyngeal  catarrh,  and  less  often  of  rhinitis. 

Infection  plays  an  important  part  in  the  aetiology  of  stomatitis.  The  local 
inflammation  may  be  merely  part  of  a  constitutional  infectious  disease,  as  in 
measles,  variola,  and  syphilis.  Stomatitis  is  still  more  frequently  a  compli- 
cation of  some  severe  and  protracted  illness,  when  the  mouth  is  not  properly 
attended  to  and  cleansed.  The  bits  of  food  and  the  mucus  quickly  begin  to 
decay,  Great  numbers  of  fungi  and  bacteria  invade  the  buccal  cavity,  and 
30  469 


470  DISEASES   OF   THE   DIGESTIVE   ORGANS 

excite  inflammation  in  its  mucous  membrane.  Even  the  cases  of  primary 
stomatitis  which  sometimes  occur  are  probably  all  of  an  infectious  character. 
They  usually  soon  assume  the  ulcerative  form. 

Clinical  History. — The  usual  symptoms  of  an  inflammation  of  mucous 
membrane — namely,  redness,  swelling,  and  increased  secretion — are  exhibited 
in  stomatitis.  The  redness  is  usually  most  intense  on  the  inside  of  the  cheeks 
and  on  the  gums.  Indeed,  we  have  the  special  name — gingivitis — for  inflam- 
mation of  the  latter.  The  swelling  is  best  shown  by  the  indentations  made  by 
the  teeth  in  the  cheeks  and  the  edges  of  the  tongue.  The  tongue  and  gums 
are  smeared  with  mucus.  There  is  often  considerable  salivation.  If  the  in- 
flammation is  more  active,  we  find  a  mucopurulent  coating  on  a  greater  or 
less  portion  of  the  membrane.  The  tongue  is  almost  always  thickly  coated. 
If  we  scrape  off  a  little  of  the  coating  and  put  it  under  the  microscope,  we 
find  a  great  abundance  of  pavement  epithelium,  in  part  fatty  degenerated,, 
pus,  micrococci,  and  remains  of  food.  White  spots  made  up  of  epithelium 
may  also  be  seen  on  various  parts  of  the  oral  mucous  membrane.  Here  and 
there  little  vesicles  appear  which  burst  and  leave  superficial  ulcers. 

The  local  discomfort  of  severe  stomatitis  is  by  no  means  trifling.  There 
is  burning  pain,  which  interferes  with  taking  food,  and  usually  the  processes 
of  decomposition  occasion  a  constant  bitter  or  disgusting  taste  in  the  mouth, 
as  well  as  a  foul  and  offensive  breath. 

The  duration  of  the  disease  depends  on  the  nature  of  the  immediate  cause 
or  the  character  of  the  primary  disorder.  Usually  a  stomatitis  which  gets 
well  in  one  or  two  weeks  is  called  acute,  and  a  more  tedious  attack,  chronic. 
The  chronic  form  is  seen  in  topers,  inveterate  smokers?  and  persons  with  bad 
teeth.  It  may  last  for  years,  with  the  symptoms  described  above,  only  milder. 
(For  lingual  psoriasis,  vide  infra). 

Treatment. — If  the  inflammation  is  considerable,  the  diet  must  be  liquid. 
Sometimes  cold  drinks  are  most  agreeable,  but  usually  lukewarm  are  pre- 
ferred. Often  the  pain  is  relieved  by  taking  from  time  to  time  a  sip  of  iced 
water  or  a  bit  of  ice;  but  in  most  cases  the  patient  will  prefer  to  rinse  the 
mouth  with  lukewarm  water.  The  local  use  of  cocain  acts  beneficially  in 
severe  pain.  The  important  indication,  to  keep  the  mouth  as  clean  and  pure 
as  possible,  is  best  met  by  having  the  mouth  frequently  rinsed  out  with  a 
two-per-cent  solution  of  chlorate  of  potash,  or  one  or  two  teaspoonfuls  of  a 
one-per-cent  solution  of  permanganate  of  potash  in  a  glass  of  water.  It  is 
also  advisable  to  rinse  the  mouth  with  a  two-per-cent  solution  of  peroxid  of 
hydrogen  (preferably  chemically  pure  hydrogen  peroxid  (Merck),  dispensed 
in  thirty-per-cent  solution),  and  with  thymol,  which  latter  is  the  chief  con- 
stituent of  Miller's  mouth  wash,  the  ingredients  of  which  are :  Thymol,  0.25 
part;  benzoic  acid,  30  parts;  tincture  of  eucalyptus,  4  parts;  distilled  water, 
750  parts.  In  children  who  cannot  do  this,  the  mouth  is  to  be  carefully 
washed  or  sprayed.  If  the  gums  are  spongy,  they  should  be  painted  with  a 
mixture  containing  equal  parts  of  tincture  of  myrrh  and  tincture  of  rhatany.. 
If  there  are  superficial  ulcers  scattered  about,  it  is  sometimes  an  excellent 
plan  to  pencil  them  with  a  ten-per-cent  borax-glycerin  solution  or  to  touch 
them  lightly  with  lunar  caustic,  to  hasten  their  healing. 

Chronic  stomatitis  is  often  very  obstinate,  resisting  all  sorts  of  treatment 
for  a  long  time.     The  first  thing  is  to  remove  any  such  injurious  agencies  as. 


ULCERATIVE   STOMATITIS  471 

tobacco  or  bad  teeth.    It  is  recommended,  besides  the  above-mentioned  reme- 
dies, to  swab  out  the  mouth  with  a  solution  of  corrosive  sublimate  ( 1  to  5,000) 

or  of  lunar  caustic  (1  to  30  to  50). 


CHAPTEE    II 

ULCERATIVE    STOMATITIS 
(Stomacace) 

iEtiology. — By  ulcerative  stomatitis  is  meant  a  severe  disease  of  the  buccal 
mucous  membrane,  with  superficial  necrosis  and  the  consequent  formation  of 
ulcers.  The  abnormal  processes  are  not  in  all  cases  identical,  and  their  course 
may  vary.  Still,  it  is  probable  that  infection  is  the  important  factor,  at  least 
in  the  primary  cases.  The  disease  has  repeatedly  been  epidemic,  chiefly  among 
soldiers  in  barracks  or  on  a  campaign,  and  among  the  inmates  of  jails.  We 
have  repeatedly  seen  sporadic  cases  of  primary  ulcerative  stomatitis  with 
fever.  In  children  the  disease  is  especially  common  at  the  time  of  the  second 
dentition.  Here,  too,  endemic  and  contagious  influences  are  frecjuently  in 
evidence. 

Mercurial  stomatitis  is,  from  a  practical  point  o£  view,  the  most  im- 
portant of  those  forms  of  ulcerative  stomatitis  which  are  referable  to  definite 
chemical  action.  It  is  due  to  the  inhalation  of  the  fumes  of  mercury  in  those 
whose  trade  or  scientific  occupation  exposes  them  to  this  clanger,  and  very 
frequently  also  to  the  therapeutic  employment  of  mercury  in  the  form  of 
calomel  or  mercurial  ointments,  and  the  like.  (For  the  scorbutic  form,  see 
chapter  on  Scurvy.) 

Symptoms. — The  disease  usually  attacks  the  gums  of  the  lower  jaw  first, 
gradually  spreading  thence  to  neighboring  portions  of  the  lips  and  cheeks. 
Those  portions  of  the  mucous  membrane  of  the  mouth  where  the  teeth  are 
absent  are,  strange  to  say,  almost  always  spared.  The  tongue  and  palate  are 
likewise  generally  not  very  much  affected,  though  often  the  seat  of  a  simple 
catarrhal  inflammation.  In  severe  mercurial  stomatitis  the  gums  are  es- 
pecially apt  to  be  affected.  The  ulcers  also  show  a  preference  for  the  angles 
of  the  lower  jaw,  and  those  portions  of  the  mucous  membrane  of  the  cheeks 
which  rest  upon  the  teeth. 

Inspection  shows  that  the  mucous  membrane  in  the  places  mentioned  has  a 
pasty,  purulent  coating.  The  gums  are  swollen,  spongy,  and  red,  and  bleed 
easily.  The  mucous  membrane  on  the  edges  of  the  gums  becomes  necrotic, 
giving  rise  to  profuse  purulent  secretion  and  the  formation  of  ulcers.  The 
teeth  are  so  loosened  by  gingivitis  that  they  .may  even  fall  out.  There  is  usu- 
ally profuse  salivation.  The  lymph-glands  at  the  angle  of  the  lower  jaw 
and  on  the  chin  are  generally  swollen.  The  breath  is  very  offensive,  poison- 
ing the  air  of  the  whole  room. 

The  local  discomfort  of  the  patient  is  the  same  as  in  simple  stomatitis, 
only  much  worse.  It  is  very  difficult  to  take  nourishment.  In  many  cases 
there  are  marked  constitutional  symptoms.  The  patient  feels  very  weak  and 
languid.      The  primary,   and   sometimes   also   the   toxic,   cases   of  ulcerative 


472  DISEASES   OF   THE   DIGESTIVE   ORGANS 

stomatitis  are  associated  with  moderately  high  fever — 100.5°  to  102°  E.  (38°  to 
39°  C).  Xow  and  then  severe  symptoms  of  constitutional  sepsis  have  fol- 
lowed the  disease. 

The  course  of  ulcerative  stomatitis  is  favorable  in  the  great  majority  of 
cases.  With  good  treatment  and  nursing,  the  ulcers  gradually  clean  up,  and 
at  the  end  of  one  or  two  weeks  recovery  is  complete.  Exceptionally,  the  dis- 
ease may  be  more  chronic.  The  most  frequent  way  in  which  recovery  is 
delayed  is  that  the  disease  extends  to  the  periosteum  of  the  lower  jaw,  caus- 
ing necrosis  of  small  portions  of  the  bone,  which  must  be  expelled  before 
the  patient  gets  well. 

Treatment. — The  treatment  does  not  differ  essentially  from  that  of  the 
milder  forms  of  stomatitis.  The  mouth  must  be  still  more  carefully  and 
more  frequently  cleansed  and  disinfected.  Good  results  are  obtained  from 
potassium  chlorate,  permanganate  of  potash,  boric  acid,  peroxid  of  hydrogen, 
and  similar  remedies.  Some  authors  recommend  the  simultaneous  internal 
administration  of  potassium  chlorate  on  account  of  its  subsequent  excretion 
through  the  saliva,  but  it  is  usually  useless  and  not  entirely  devoid  of  danger, 
as  it  has  repeatedly  caused  poisoning. 

As  to  prophylaxis,  we  should  mention  that  all  patients  who  are  using  mer- 
cury should,  whenever  possible,  have  their  teeth  first  put  in  good  order  by  a 
dentist,  and  should  employ  a  gargle  of  potassium  chlorate  faithfully  from  the 
beginning  of  treatment,  in  order  to  prevent  the  occurrence  of  mercurial 
stomatitis.     If  salivation  occurs,  the  mercury  must  be  stopped. 


CHAPTEE    III 

APHTHOUS    STOMATITIS 

(Aphthce.     Disseminated  Fibrinous  Stomatitis) 

Aphthous  stomatitis  is  characterized  by  roundish  spots  upon  the  mucous 
membrane,  grayish  white,  and  of  small  size,  unless  made  larger  by  the  con- 
fluence of  several  into  one  another.  They  usually  have  a  narrow,  red  areola. 
They  are  most  numerous  on  the  edges  and  dorsum  of  the  tongue  and  on  the 
frsenum,  but  they  also  occur  on  the  lips  and  cheeks.  The  attempt  to  remove 
the  white  spot  with  forceps  never  succeeds,  but  it  causes  bleeding.  In  addition 
to  the  genuine  aphthae  there  are  almost  always  the  signs  of  a  common  stoma- 
titis, which  may  be  mild  or  severe.  The  white  spots  are  due  in  part  to  a 
thickening  and  opacity  of  the  epithelium,  and  in  part  are  said  to  be  caused 
by  the  formation  of  a  fibrinous  exudation,  which  penetrates  the  most  super- 
ficial la}rers  of  the  mucous  membrane.  If  the  necrotic  epithelium  is  cast  off, 
the  aphthous  spot  develops  into  a  little  ulcer,  which  often  heals  promptly,  but 
which  may  be  very  obstinate. 

The  disease  occurs  chiefly  in  children,  and  especially  frequently  at  the 
time  of  the  first  dentition.  The  child  is  usually  restless,  often  somewhat 
feverish,  and  evidently  suffers  pain  when  nursing.  Generally  there  is  con- 
siderable salivation.  The  lymph-glands  may  be  a  little  enlarged.  On  the 
outer  skin  in  the  neighborhood  of  the  mouth  there  may  also  appear  a  few 


APHTHOUS   STOMATITIS  473 

blisters  and  pustules.     These,  as   a    rule,   have  no  connection   with   hei 
although  a  real  mucous-membrane  herpes  does  exist,  and  now  and  then  gen- 
uine herpes  may  appear  in  association  with  aphthous  stomatitis.     The  disease 

is  not  rare  in  adults.  Many  individuals  are  especially  Liable  to  it,  and  v<.Ty 
frequently  have  little,  white,  and  often  very  painful  spots  here  and  there  on 
the  tongue  or  elsewhere  in  the  mouth.  These  have  a  tendency  to  develop 
into  ulcers  which  are  usually  superficial,  but  sometimes  deep.  They  may 
prove  very  troublesome,  from  their  frequent  recurrence  and  the  hindrance 
they  cause  to  speaking  and  mastication. 

With  the  exception  of  the  form  just  described,  which  is  constantly  re- 
lapsing, aphtha?  almost  always  run  a  favorable  course.  There  is  usually  com- 
plete recovery  in  a  week  or  two.  The  treal  ment  of  children  consists  in  carefully 
washing  out  the  mouth  with  cold  water  or  mild  disinfecting  lotion-.  If  the 
spots  do  not  disappear,  we  can  paint  them  with  a  solution  of  borax  (1  to  30), 
of  permanganate  of  potash  (1  to  150),  a  five-per-cent  solution  of  sulphate  of 
zinc.  If  some  of  the  places  are  especially  painful,  particularly  in  adults,  we 
may  touch  them  with  lunar  caustic,  when  they  usually  are  soon  cured. 

It  is  often  a  very  difficult  matter  to  treat  chronic,  recurrent,  aphthous 
stomatitis,  and  the  ulcerations  which  are  occasioned  by  it  in  adults.  Cauter- 
ization with  lunar  caustic,  chromic  acid,  and  similar  agents  usually  does 
more  harm  than  good.  Xone  of  the  ordinary  mouth  washes  has  any  great 
effect.  A  much-praised  remedy  is  the  chewing  of  bilberries,  either  fresh  or 
boiled,  for  several  minutes  several  times  a  day,  and  we  have  ourselves  tested 
it  in  some  cases  with  good  results.  Some  physicians  also  recommend  the  in- 
ternal use  of  iodid  of  potassium,  or  small  doses  of  calomel.  It  is  remarkable 
that  habitual  aphthous  stomatitis  sometimes  ceases  completely  for  months — 
for  example,  upon  change  of  residence  or  during  a  visit  to  the  country — but 
then  appears  afresh  without  special  cause. 

In  conclusion,  as  to  astiolog}^  infection  is  a  most  likely  cause,  if  we  con- 
sider that  small  epidemics  or  endemics  have  repeatedly  occurred.  Lately  at- 
tention has  been  called  to  the  possibility  that  the  milk  of  cows  suffering  from 
hoof-and-mouth  disease  may  be  a  source  of  infection.  That  infection  of  this 
sort  may  occur  seems  to  us  indubitable,  from  the  experience  of  others,  as  well 
as  our  own.  In  such  cases  there  is  not  only  a  severe  aphthous  stomatitis,  but 
a  development  of  vesicles,  pustules,  or  even  extensive  purulent  inflammation 
affecting  the  fingers  and  nails,  and  occasionally  the  hands,  arms,  and  feet, 
and  other  parts  of  the  body  surface.  Frequently,  at  the  same  time,  slight 
febrile  symptoms  and  gastro-intestinal  disturbances  occur.  Most  cases  of  this 
kind,  though,  pursue  a  favorable  course,  but  a  few  epidemics  have  been  described 
in  which  the  disease  became  dangerous  to  life  because  of  constitutional  sepsis. 

Of  course,  it  is  obvious  that  not  all  cases  of  aphthous  stomatitis  have  an 
aetiological  relationship  to  the  hoof-and-mouth  disease  of  animals.  In  the 
usual  milder  forms  there  are  probably  other  perhaps  not  always  identical  in- 
fection agents. 

There  is  a  special  form  known  as  Bednar's  aphtha?.  In  newborn  children 
white  patches  are  not  infrequently  found  lying  symmetrically  on  both  halves 
of  the  hard  palate  near  the  alveolar  processes,  and  persisting  till  about  the 
third  month.  These  plaques  are  not  syphilitic,  although  they  were  formerly 
in  some  cases  thought  to  be  so.    They  are  probably  due  merely  to  the  tongue 


474 


DISEASES   OF   THE   DIGESTIVE   ORGANS 


pressing  upon  the  thin  mucous  membrane  during  nursing.  Generally  they 
do  no  harm ;  but  in  marantic,  neglected  children,  they  may  develop  into  quite 
deep  ulcers.  In  that  case,  repeated  cauterization  with  a  five-per-cent  solution 
of  argentic  nitrate  is  required. 


CHAPTER    IV 


THRUSH 
(Soor.     Muguet.     Sprue) 

iEtiology. — Weak  and  artificially  nourished  children  are  particularly  liable 
to  this  disease;  but  it  also  attacks  adults  who  are  suffering  from  phthisis, 
carcinoma,  and  severe  typhoid  or  typhus  fever.  In  it  grayish-white  deposits 
are  developed  upon  the  buccal  and  pharyngeal  mucous  membrane.  The  mi- 
croscope shows  these  collections  to 
be  fungi  (Fig.  68)  ;  there  are  a 
multitude  of  oval  spores,  or  conidia, 
and  a  tangled  mass  of  long  myce- 
lium threads.  The  botanical  posi- 
tion of  the  thrush  fungus  (oidium 
albicans)  is  not  yet  entirely  clear. 
Grawitz  maintained  that  the  thrush 
fungus  is  a  sprouting  fungus,  and 
nearly  related  to  the  mold  fungi 
(mycoderma  vini,1  or  saccharomyces 
albicans — Rees).  ,  It  seems  to  be  a 
sort  of  transitional  form  between 
the  sprouting  fungi  and  the  thread 
fungi,  inasmuch  as  it  appears  both 
in  the  yeast  form  and  also  in  the 
form  of  thread-like  mycelia.  Plant, 
according  to  his  investigations, 
makes  the  thrush  fungus  identical  with  the  monilia  Candida,  which  belong 
to  the  Torulaceae.  At  any  rate,  the  thrush  fungus  is  widely  distributed,  for 
the  development  of  thrush  upon  the  mucous  membrane  of  the  mouth  and 
throat  is  a  frequent  phenomenon,  especially  in  ill-nourished  children.  Nurs- 
ing bottles  and  the  nipples  used  upon  them  are  probably  not  infrequently 
the  agents  by  which  the  disease  is  conveyed. 

Symptoms. — The  mucous  membrane  of  the  tongue,  cheeks,  and  soft  palate 
is  usually  somewhat  red  and  swollen.  Upon  it  we  see  at  first  small,  punctate, 
white  spots,  which  may  gradually  spread.  When  this  coating,  which  is  at 
first  white,  becomes  more  extensive,  it  assumes  a  more  dirty  yellow  or  brown- 
ish color.  Microscopic  investigations  have  shown  that  the  fungus  develops 
first  in  the  middle  layers  of  the  epithelium.  From  this  starting  point  it 
grows  not  only  upward,  but  also  downward  into  the  mucous  membrane.  If 
the  growth  is  abundant,  it  is  easy  to  scrape  off  the  upper  layers,  and  make  a 


Fig.  68. — Thrush  fungus  from  mouth. 


1  Mycoderma  vini  is  that  fungus  which  is  found  in  the  development  of  vinegar  from  alcohol, 
when  alcoholic  beverages  sour. 


DISEASES' OF  THE  TONGUE  475 

diagnosis  by  aid  of  the  microscope.  In  exaggerated  cases  the  growth  may 
even  extend  from  the  pharynx  into  the  upper  part  of  the  oesophagus  and  the 

entrance  of  the  larynx;  hut  we  only  rarely  find  thrush  in  the  larynx  itself, 
or  the  nostrils,  or  the  stomach  and  intestines — briefly,  in  places  where  there 
is  cylindrical  epithelium.  In  exceptional  cases  the  thrush  fungus  may  ex- 
tend its  growth  through  the  wall  of  a  blood  vessel,  and  so  reach  the  circula- 
tion. Usually  thrombosis  of  the  affected  vessel  takes  place,  but  the  metastasis 
of  thrush  to  the  brain  and  the  kidneys  has  been  observed.  If  abscesses  are 
associated  with  these  processes  they  depend  upon  the  simultaneous  intrusion 
of  pyogenic  cocci. 

As  a  rule,  thrush  is  accompanied  by  a  more  or  less  severe  stomatitis.  The 
fluids  of  the  mouth  have  an  acid  reaction.  Nursing,  or  chewing,  and  swal- 
lowing are  painful.  Still,  it  is  a  question  whether  the  stomatitis  is  due  to 
the  fungus,  or  whether  it  prepares  the  territory  for  the  fungus  to  settle  in. 
Nursing  infants,  who  suffer  from  thrush,  often  have  diarrhea  or  marasmus 
at  the  same  time,  which  latter  affections  are  more  probably  the  cause  than 
the  result  of  the  thrush.  If  vigorous  and  healthy  sucklings  are  attacked  by 
thrush,  the  disease  is  usually  quite  harmless,  quickly  vanishing  if  proper 
cleanliness  is  maintained.  In  sickly  children,  particularly  if  bottle  fed,  the 
appearance  of  the  disease  is  very  ominous.  The  children  become  very  restless 
and  hoarse.  The  mucous  membrane  of  the  mouth  and  pharynx  is  dry  and  of 
a  dark  color.  The  ingestion  of  food  is  almost  impossible.  In  adults,  as  we 
have  said,  thrush  is  with  few  exceptions  confined  to  persons  greatly  prostrated 
by  such  diseases  as  severe  typhoid  fever  or  tuberculosis,  and  from  this  point 
of  view  it  is  an  unfavorable  symptom. 

Treatment. — To  prevent  the  development  of  thrush  in  children,  the  mouth 
must,  if  possible,  be  wiped  out,  each  time  they  drink,  with  a  cloth  wet  in  cold 
water;  and  if  adults  are  very  ill,  they  require  equal  attention  in  this  regard. 
As  soon  as  we  see  the  first  traces  of  the  disease,  we  should  touch  the  parts 
attacked  with  a  brush  wet  in  an  aqueotts  solution  of  borax  (1  to  20).  Honey 
should  not  be  added  to  the  borax  solution,  as  is  often  unwisely  done.  Another 
good  solution  is  bicarbonate  of  soda  (1  to  10),  permanganate  of  potash  (1  to 
150),  or,  in  severe  cases,  bichlorid  of  mercury  (1  to  100,000).  If  the  thrush 
extends  into  the  oesophagus  an  efficient  remedy  (Baginsky)  is  said  to  be  the 
internal  administration  of  resorcin,  in  a  one-half-  to  one-per-cent  solution, 
the  dose  being  a  teaspoonful  every  two  hours.  The  food  should  contain  as 
little  sugar  as  possible,  as  this  furnishes  a  favorable  culture  medium  for  the 
thrush  fungus.  Mild  cases  can  usually  be  cured  by  the  remedies  named.  If 
the  thrush  has  once  got  a  vigorous  start  in  the  mouth  of  marantic  children, 
or  of  adults  suffering  from  an  incurable  disease,  it  must  be  confessed  that  we 
often  fail  to  check  its  growth. 


CHAPTER    V 

DISEASES    OF   THE    TONGUE 

Inflammation-  of  the  true  lingual  parenchyma  is  quite  rare,  although  the 
tongue's  mucous  surface  is  frequently  involved  in  the  various  diseases  of  the 
mouth. 


476  DISEASES   OF  THE   DIGESTIVE   ORGANS 

1.  Acute  Parenchymatous  Glossitis. — This  is  the  name  given  to  an  inflam- 
matory infiltration  of  the  whole  or  a  part  of  the  tongue,  usually  ending  in 
abscess.  A  frequent  cause  is  the  sting  of  a  bee  or  wasp,  or  it  may  follow 
burns  or  severe  cauterization.  In  the  rare  instances  when  it  is  apparently 
spontaneous,  it  is  probable  that  some  little  wound  has  afforded  ingress  to  the 
inflammatory  poison. 

An  important  role  seems  to  be  pla}red  by  the  lymph  follicles  in  front  of 
the  attachment  of  the  epiglottis — the  so-called  lingual  tonsil,  which  may 
serve  as  a  port  of  entrance  for  the  infectious  material. 

The  symptoms  of  acute  glossitis  are  very  violent  in  the  severer  cases.  The 
tongue  is  enormously  swollen,  so  as  sometimes  to  protrude  from  the  mouth. 
It  has  a  thick,  soft,  purulent  coating,  and  sometimes  presents  excoriations  and 
ulcerations.  The  patient  has  violent  pain.  Talking  and  eating  are  almost 
impossible.  There  is  usually  catarrhal  inflammation  of  the  rest  of  the  mouth 
and  profuse  and  very  annoying  salivation.  The  tongue  may  swell  so  much 
as  to  cause  dyspnoea  and  more  or  less  suffocation.  The  submaxillary  lymphatic 
glands  are  also  more  or  less  swollen.    There  is  usually  fever. 

Treatment  consists  in  the  employment  of  ice  and  the  various  mouth  washes 
(vide  supra).  As  soon  as  fluctuation  is  obtained,  we  must  give  exit  to  the 
pus.     Often,  however,  the  abscess  opens  spontaneously. 

Frequently  the  swelling  is  very  distinctly  limited  to  one  half  of  the  tongue. 
Evacuation  of  the  pus  is  usually  followed  by  a  rapid  abatement  of  the  dis- 
comfort and  complete  recovery. 

2.  Glossitis  Dissecans. — This  is  a  chronic  disease,  of  comparatively  rare 
occurrence  and  unknown  aetiology.  It  causes  the  gradual  development  upon 
the  surface  of  the  tongue  of  a  number  of  deep  fissures  and  indentations,  giv- 
ing the  organ  an  uneven  and  ragged  look.  The  pain  is-  due  to  the  frequent 
presence  of  excoriations  and  ulcers  in  these  fissures. 

The  trouble  is  not  intrinsically  dangerous,  nor  does  it  need  special  treat- 
ment. We  must  try  the  same  remedies  which  have  been  mentioned  above  in 
connection  with  the  various  forms  of  stomatitis,  such  as  antiseptic  mouth 
washes,  the  chewing  of  bilberries,  etc.  If  ulcers  are  present  they  sometimes 
require  cauterization  with  lunar  caustic. 

3.  Lingual  Psoriasis.  (Tylosis;  Ichthyosis  Ungues  et  oris.)  Leucoplacia. 
— Psoriasis  lingua,  again,  is  a  superficial  disease,  the  aetiology  of  which  is  un- 
known. It  consists  in  localized  circular  hyperplasias  of  the  epithelium  of  the 
tongue,  rarely  conjoined  with  similar  spots  upon  the  cheeks  and  lips.  The 
central  portion  of  mucous  membrane  which  is  surrounded  by  this  whitish, 
slightly  raised,  and  more  or  less  circular,  wall  of  epithelium,  is  abnormally 
smooth  and  of  a  reddish  color.  Usually  the  tongue  takes  on  a  resemblance  to 
a  map  (lingua  geographica).  The  disease  generally  persists  for  years,  and 
without  symptoms  except  in  severe  cases.  Often  it  is  found  by  chance  in  in- 
dividuals who  have  known  nothing  about  the  unusual  appearance  of  their 
tongues.  Still,  it  may  cause  a  hypochondriac  endless  anxiety,  especially  if 
he  takes  it  to  be  syphilitic. 

This  last  statement  applies  still  better  to  a  peculiar  disease  allied  to 
psoriasis.  It  is  called  leucoplacia,  and  affects  the  mucous  membrane  of  the 
tongue  and  mouth.  Usually  it  causes  the  appearance,  on  the  lateral  borders 
of  the  tongue,  of  dull  whitish  spots,  which  have  the  look  of  scars,  and  are 


'  NOMA  477 

generally  somewhat  notched.     As  a  rule,  the  lower  surface  of  the  tongue  and 
the  cheeks  display  at  the  same  time  similar  white  spots,  which  ai  atly 

due  merely  to  thickening  of  the  epithelium.  Certain  spots  may  disappear, 
hut  they  are  sure  to  he  replaced  hy  others,  so  that,  so  far  as  has  yet  been  ob- 
served, the  disease  must  he  regarded  as  incurable.  Still,  it  is  not  of  gt 
importance,  as  a  rule,  for  in  many  cases  the  local  discomfort  is  very  slight. 
If  the  indentations  along  the  sides  of  the  tongue  become  cracked  or  ulcerated, 
then  there  may  be  great  pain.  Leucoplacia  is  very  often  associated  with  bodily 
states  of  neurasthenia,  or  hypochondriasis,  particularly  if  the  malady  appears 
in  a  person  with  a  syphilitic  taint,  which  happens  with  remarkable  frequen 
But  it  is  certainly  not  to  be  regarded  as  a  tertiary  symptom,  rather  perhaps 
as  a  sort  of  sequel  to  syphilis,  although  many  cases  have  no  connection  what- 
ever with  the  latter  disease.  Antisyphilitic  treatment  is  invariably  useless. 
It  is  for  this  very  reason  important  that  the  physician  should  be  well  ac- 
quainted with  leucoplacia,  that  he  may  spare  his  patient  needless  anxiety  and 
ineffectual,  or  perhaps  actually  harmful,  treatment  with  mercury.  The  dis- 
ease has  no  relation  to  excessive  smoking,  one  proof  of  which  is  that  we  have 
seen  the  condition  in  women.  The  only  danger  of  leucoplacia  is  that  some- 
times lingual  carcinoma  may  eventually  develop  on  the  spot  affected  with  it. 
We  have  in  this  case  to  deal  with  a  process  which  is  analogous  to  the  devel- 
opment of  ventricular  carcinoma  in  the  scars  of  old  ulcers,  or  of  cancer  of 
the  gall  bladder  subsequently  to  gallstones.  Treatment  is,  as  we  have  said, 
usually  unsuccessful.  Still,  thorough  cleanliness  and  good  care  of  the  mouth 
may  avert  any  great  discomfort.  "We  may  try  the  effect  of  painting  the  spots 
with  a  four-per-cent  solution  of  borax,  or  a  five-per-cent  solution  of  chromic 
acid.  The  use  of  an  alcoholic  solution  of  salicylic  acid  (salicylic  acid,  1  part 
to  5  parts  each  of  spirit  of  wine  and  distilled  water)  is  said  to  he  still 
more  efficient.  Lately  the  frequent  chewing  of  boiled  bilberries  has  been 
recommended  for  leucoplacia,  and  we  have  had  good  results  from  this  pro- 
cedure. 

4.  The  Black-Hair  Tongue.  (Melanotrichia  lingua;.) — Sometimes  we  find 
at  the  base  of  the  tongue  a  circumscribed  area  which  appears  to  be  covered  with 
short  black  hairs.  Closer  examination  shows  that  we  have  to  deal  with  unu- 
sually long  and  dark  pigmented  filiform  papillse.  The  condition  is  entirely 
harmless  and  causes  no  symptoms  or  only  insignificant  ones.  It  is  usually 
cured  by  painting  with  a  ten-per-cent  alcoholic  solution  of  salicylic  acid,  or, 
if  need  be,  by  curetting  with  a  sharp  spoon.  Another  variety  of  black  pig- 
mentation of  the  tongue  has  been  occasionally  observed  due  to  a  black  fungus 
(mucor  niger). 


CHAPTEE   VI 

NOMA 

(Cancrum  oris.     Water-cancer) 

Noma  is  a  gangrene  of  the  cheek,  attacking  chiefly  feeble   and   sickly 
children.     The  disease  is  rare.     It  may  be  primary,  but  it  is  usually  a  sequel 


478  DISEASES   OF   THE   DIGESTIVE   ORGANS 

of  severe  diseases,  such  as  measles,  scarlet  fever,  typhus  and  typhoid  fevers, 
and  pneumonia.  Now  and  then  it  has  been  observed  in  adults.  A  priori,  it 
is  extremely  probable  that  noma  is  due  to  some  parasitic  microorganism,  al- 
though the  infectious  agents  have  not  been  definitely  determined.  Several 
investigators  have  suggested  the  hypothesis  that  the  exciting  cause  of  noma 
is  identical  with  the  infectious  agent  of  the  so-called  "  calf  diphtheria,"  the 
Bacillus  necroseos.  It  deserves  mention  that  noma  is  said  to  occur  with  much 
greater  relative  frequency  in  moist  regions  along  the  coast — for  example,  in 
Holland — than  in  German}^. 

The  disease  begins,  without  any  evident  occasion,  in  an  insignificant  spot 
of  gangrene  on  the  inner  surface  of  the  cheek — that  is,  in  the  mucous  mem- 
brane. It  is  usually  situated  near  the  corner  of  the  mouth.  Externally,  the 
parts  are  soon  swollen  by  collateral  oedema,  and  the  whole  cheek  gradually 
becomes  hard  and  infiltrated.  At  first,  all  we  see  upon  the  mucous  membrane 
is  a  dirty  greenish  spot  not  much  larger  than  a  silver  dime,  but  soon  the  whole 
cheek  and  the  neighboring  parts  are  one  mass  of  gangrene.  Bits  of  dead 
tissue  come  away,  and  foul-smelling  ichor  flows  constantly  into  the  mouth. 
The  collateral  oedema  may  finally  pervade  the  entire  half  of  the  face.  The 
neighboring  lymph-glands  are  always  greatly  swollen. 

This  condition  is,  as  a  rule,  accompanied  by  fever,  often  reaching  or  ex- 
ceeding 104°  F.  (40°  C).  The  general  health  may  indeed  for  a  time  be  aston- 
ishingly little  affected;  but  gradually  prostration  comes  on,  or  even  general 
sepsis  develops,  with  fever,  stupor,  and  delirium.  Frequently  lobular  pneu- 
monia, which  may  have  a  gangrenous  character,  is  produced  by  the  inhalation 
of  sloughing  bits  of  tissue;  and  often  the  ichor,  being  swallowed,  excites  vio- 
lent and  offensive  diarrhea.  The  local  discomfort  is  not  really  very  consid- 
erable in  most  cases,  compared  to  the  severity  of  the  disease.  There  may  even 
be  no  pain  felt  whatever. 

The  prognosis  is  almost  always  fatal.  Death  sometimes  occurs  suddenly 
from  collapse.  Sometimes  it  comes  at  the  end  of  three  or  four  weeks,  from 
a  gradual  sinking  of  the  bodily  powers.  Eecovery  has  been  seen  in  only  a 
few  cases ;  there  is  a  line  of  demarcation  formed,  the  sloughs  come  away,  and 
a  slow  convalescence  follows,  leaving  extensive  and  usually  very  disfiguring 
scars  behind. 

Treatment  must  have  for  its  chief  object  to  check  further  extension  of  the 
gangrene,  by  removing  all  parts  that  are  already  destroyed.  Local  cauteriza- 
tion with  concentrated  hydrochloric  acid,  or  fuming  nitric  acid,  or  lunar 
caustic,  or  chlorid  of  iron,  is  usually  futile.  It  is  probably  the  best  way  to 
remove  all  the  gangrenous  portion  by  means  of  Paquelin's  thermocautery. 
At  least  in  the  early  stages  of  noma  we  may  hope  something  from  this  method 
of  treatment;  but  if  the  case  is  far  advanced,  we  can  hardly  expect  to  accom- 
plish much. 

We  should  also  disinfect  the  mouth  as  thoroughly  as  possible.  The  most 
efficient  means  is  to  syringe  it  out  with  solutions  of  peroxid  of  hydrogen  or 
permanganate  of  potash.  We  should  do  our  best  to  maintain  the  patient's 
strength. 


PAROTITIS  479 


CHAPTER    VII 

PAROTITIS 

(Mumps) 

Parotitis,  or  inflammation  of  the  parotid  gland,  appears  not  only  as  a 
peculiar,  primary,  infectious  disease,  usually  epidemic,  but  also  as  a  secondary 
complication  of  numerous  other  severe  diseases.  These  two  forms  should  be 
considered  separately. 

1.     IDIOPATHIC,  PRIMARY  PAROTITIS  (EPIDEMIC  MUMPS) 

etiology. — The  disease  occurs  in  epidemics  that,  although  not  very  fre- 
quent, may  be  quite  extensive.  Endemics  also  occur,  in  barracks  and  schools; 
and  here  and  there  a  sporadic  case  is  seen.  Children  and  young  adults  are 
most  liable  to  it.  Nursing  infants  enjoy  a  marked  immunity,  as  well  as 
elderly  persons.    Males  are  much  oftener  attacked  than  females. 

There  can  be  no  doubt  that  mumps  is  a  specific  infectious  disease,  and 
claims  have  already  been  made  of  the  discovery  of  its  specific  bacillus,  but 
these  lack  confirmation.  Still,  it  is  natural  to  suppose  that  the  infectious 
matter  reaches  the  gland  by  way  of  Steno's  duct.  Numerous  observations  sup- 
j3ort  the  view  that  the  disease  is  directly  contagious;  but  the  degree  of  con- 
tagiousness is  not  great.  Perhaps  the  saliva  of  patients  has  something  to 
do  with  the  extension  of  epidemic  mumps  through  coughing,  etc.  The  period 
of  incubation  seems  to  vary.     On  the  average,  it  is  about  fourteen  days. 

Clinical  History. — There  may  be  a  prodromal  stage  of  one  or  two  days, 
with  mild  feverish  symptoms.  The  disease  itself  begins  with  swelling  of  one 
parotid  gland.  The  swelling  is  directly  below  and  in  front  of  the  lobe  of 
the  ear,  which  is  gradually  pushed  upward.  In  the  next  few  days  the  swell- 
ing rapidly  increases,  and  it  and  the  collateral  oedema  of  the  cheek  and  floor 
of  the  mouth  may  become  very  considerable.  The  face  is  much  distorted,  but 
often  makes  a  very  comical  impression,  especially  as  everybody  knows  how 
harmless  the  disease  is.  In  most  cases  the  other  gland  also  swell's  a  few  days 
later. 

Suppuration  scarcely  ever  occurs  in  genuine  mumps.  If  it  is  seen  as  a 
rare  exception,  it  is  probably  due  to  secondary  infection.  The  swelling  often 
becomes  \~ery  hard.  Generally  it  has  a  somewhat  doughy  consistency.  The 
corresponding  portion  of  skin  is  usually  pale  and  shiny.  The  submaxillary 
gland  not  infrequently  swells  also  in  addition  to  the  parotid,  and  this  may 
occur  upon  one  or  both  sides  of  the  neck.  Penzoldt  has  observed  cases  in 
which  the  submaxillary  and  sublingual  were  swollen,  but  not  the  parotid.  We 
ourselves  have  seen  a  swelling  of  the  submaxillary  precede  the  parotitis.  The 
sublingual  gland  also  seems  sometimes  to  be  involved  with  the  parotid. 

The  local  discomfort  is  moderate  in  most  cases.  There  are  local  pain  and 
difficulty  in  chewing,  but  less  in  swallowing  and  talking.  Often  quite  a  severe 
stomatitis  develops,  with  foul  breath. 

There  sometimes  seems  to  be  almost  no  fever.  Usually  there  is  a  mod- 
erate elevation  of  temperature.     Often,  however,  it  reaches  102.5°  to  104°  F. 


480  DISEASES   OF   THE   DIGESTIVE   ORGANS 

(39°  to  40°  0.).  Only  occasionally  has  there  been  a  case  with  grave  typhoidal 
symptoms.  We  have  frequently  observed  herpes  labialis  in  mumps.  In  rare 
cases  a  splenic  enlargement  can  be  demonstrated. 

Complications. — It  is  not  rare  for  men  to  have  a  swollen  testicle  with  in- 
flammatory serous  exudation  into  the  tunica  vaginalis,  which  may  be  quite 
painful,  but  which  usually  subsides  in  a  few  days.  The  orchitis  is  usually 
ushered  in  with  a  fresh  rise  of  fever.  Eesultant  suppuration  is  a  rare  occur- 
rence. Once  we  saw  the  orchitis  appear  several  days  before  the  swelling  of 
the  parotid  gland.  Double  orchitis  is  rare.  In  boys  this  complication  is  much 
more  exceptional  than  in  adults.  Some  observers  have  mentioned  analogous 
swellings  of  the  female  genitals  (oophoritis)  and  mammae,  but  this  is  doubt- 
ful. Other  complications,  as  facial  paralysis,  acute  nephritis,  pneumonia, 
etc.,  are  rare. 

Prognosis. — The  prognosis  of  epidemic  parotitis  is,  as  we  have  said,  almost 
always  favorable.  The  trouble  seldom  lasts  more  than  a  week  or  ten  days, 
when  the  swelling  goes  down,  and  the  patient  completely  recovers.  Possible 
but  exceptional  sequelae  are :  ptyalism,  cessation  of  the  salivary  secretion, 
chronic  swelling  of  the  parotid,  deafness,  and  atrophy  of  the  testicle. 

Diagnosis. — The  diagnosis  is  easy.  The  only  thing  to  exclude  is  swelling 
of  the  lymph-glands,  and  they  never  have  exactly  the  same  location  as  the 
parotid. 

Treatment. — Special  treatment  is  hardly  necessary.  Children  should  be 
kept  in  bed.  Usually  some  salve  (lanolin)  is  applied  to  lessen  the  feel- 
ing of  tension.  If  resolution  is  tedious,  we  may  paint  the  swelling  with 
iodized  vasogen  or  with  tincture  of  iodin;  or  we  may  prescribe  iodoform 
ointment  (1  to  15).  If  there  is  orchitis,  the  testicle  must  be  elevated,  as 
by  a  suspensory  bandage.  If  the  pain  and  swelling  are  marked,  an  ice 
bag  should  be  applied. 

2.     SECONDARY   SUPPURATIVE   PAROTITIS 

This  secondary  form  may  be  a  complication  of  any  grave  disease.  In  most 
cases  it  is  due  to  inflammatory  agents,  probably  staphylococci  in  most  cases, 
generated  by  decomposition  of  the  contents  of  the  mouth,  which  agents  reach 
the  gland  through  Steno's  duct.  It  was  formerly  the  universal  belief  that  the 
infection  was  metastatic,  being  conveyed  through  the  blood  vessels;  but  it 
is  not  certain  whether  this  occurs.  It  is  probable  that  the  pyaemic  form  is  in 
many  instances  thus  produced.  Secondary  parotitis  is  most  frequently 
observed  in  typhus  and  typhoid  fevers.  It  is  also  seen  occasionally  in  all 
other  severe  acute  diseases,  and  in  phthisis  and  carcinoma. 

The  parotid  gland  swells,  just  as  in  the  primary  disease.  It  is,  however, 
much  oftener  of  excessive  size,  and  in  the  majority  of  cases  suppurates.  If 
one  has  an  opportunity  to  make  an  autopsy  on  such  a  case  of  secondary  paro- 
titis in  its  early  stages,  the  cross-section  of  the  swollen  gland  presents  a  large 
number  of  rather  small  discrete  abscesses.  These  finally  unite  to  form  one 
larger  abscess,  which  usually  discharges  outward  through  the  skin  or  into  the 
external  auditory  meatus.  Sometimes  the  parotid  suffers  from  gangrenous 
inflammation,  and  there  is  often  extensive  sloughing.  If  such  a  case  finally 
gets  well,  still,  as  a  rule,  some  permanent  injuries  have  been  inflicted:  there 


ANGINA   LUDOVICI  481 

is  facial  paralysis,  clue  to  destruction  of  the  facial  nerves,  or  deafness,  caused 
by  an  extension  of  the  inflammation  to  the  middle  ear. 

The  treatment  of  secondary  parotitis  is  that  of  any  suppurative  inflamma- 
tion.    We  may  at  first  try  to  scatter  the  swelling  by  ice  or  a  compress  wet 
with  alcohol,  but  this  usually  fails.     As  soon  as  fluctuation  is  detected,  the 
spot  must  be  incised,  and  a  drainage-tube  inserted.     The  prognosis  depi 
chiefly  on  the  nature  and  course  of  the  original  disease. 

3.     MIKULICZ'S    DISEASE 

This  is  a  rare  and.  still  very  obscure  malady,  which  is  characterized  by  a 
chronic  swelling  of  the  salivary  glands,  particularly  the  parotids,  hut  also 
involving  the  submaxillary  and  the  sublingual  glands,  and  occasionally  the 
lachrymal  glands.  In  addition,  there  is  usually  a  general  anamiia.  The 
patients  very  frequently  develop  tuberculosis  later.  Treatment  has  little 
effect  and  must  be  purely  symptomatic.  The  attempt  to  reduce  the  swollen 
glands  by  regular  X-ray  treatment  is  to  be  recommended. 


CHAPTER    VIII 
ANGINA   LUDOVICI 

The  name  angina  Ludovici  is  applied  to  a  rather  rare  phlegmonous  in- 
flammation of  the  floor  of  the  mouth,  first  described  by  the  Wiirttemberg 
physician,  Ludwig.  Probably  this  is  not  occasioned  by  a  specific  cause,  but 
is  only  a  special  localization  of  the  ordinary  germs  which  occasion  sup- 
puration. Its  starting  place  seems  to  be  the  submaxillary  gland,  at  least 
in  most  cases.  It  may  be  primary,  or  a  complication  of  other  severe  acute 
diseases. 

Angina  Ludovici  usually  begins  with  swelling  in  the  neighborhood  of  the 
submaxillary  gland.  The  swelling  rapidly  increases,  and  comes  to  involve  the 
whole  floor  of  the  mouth  and  the  anterior  surface  of  the  throat.  It  causes 
great  discomfort.  Talking,  chewing,  and  swallowing  are  almost  impossible. 
There  is  usually  fever,  and  sometimes  we  find  the  symptoms  of  general  sepsis. 
There  may  be  great  dyspnoea,  due  either  to  compression  of  the  larynx  or  to 
oedema  of  the  glottis.  The  final  result  in  some  cases  is  an  extensive  sloughing 
of  the  soft  parts.  This  has  the  special  name  of  cynanclie  gangrenosa.  In 
other  cases  an  abscess  forms,  and  points  outward  or  into  the  oral  cavity.  The 
swelling  is  sometimes,  though  seldom,  reabsorbed. 

The  prognosis  should  always  be  guarded,  for  severe  constitutional  symp- 
toms and  a  fatal  ending  are  not  infrequently  seen,  particularly  if  the  patient 
has  a  weakly  constitution.  There  may  also  be  repeated  exacerbations  and 
relapses. 

Treatment. — At  the  commencement  of  the  disease  we  may  make  the  at- 
tempt, in  .suitable  cases,  to  check  the  process  by  local  depletion  and  by  ice; 
but,  as  soon  as  suppuration  or  gangrene  begins,  the  case  becomes  a  surgical 
one.     Xow  and  then  the  threatening  asphyxia  demands  tracheotomy. 


482  DISEASES   OF   THE   DIGESTIVE   ORGANS 


CHAPTEE    IX 

ANOMALIES    OF   DENTITION 

(Difficult  Dentition) 

The  processes  of  dentition  play  so  important  a  role  in  the  disorders  of 
childhood  that  we  feel  obliged  to  discuss  the  subject,  at  least  briefly. 

The  first  appearance  of  any  of  the  milk  teeth  usually  takes  place  when  the 
child  is  seven  to  nine  months  old;  it  may,  however,  occur  either  earlier  (be- 
tween the  fourth  and  seventh  months)  or  even  later  than  this  period.  As  a  rule, 
the  two  lower  central  incisors  are  cut  first;  then  the  upper  central  incisors 
appear,  a  few  weeks  later,  and  next  the  lateral  incisors  of  the  upper  jaw.  In 
the  beginning  of  the  second  year  come  the  lower  lateral  incisors,  and  some- 
what later  the  four  anterior  molars.  The  four  canine,  or  "  eye ,?  and 
"  stomach  "  teeth,  are  cut  in  the  second  half  of  the  second  year ;  and  last  of 

all   comes   the   eruption   of   the   four  pos- 
iiuiViniii  s  terior     molars.      The     first     dentition     is 

therefore  completed  by  the  end  of  the  sec- 
ond or  in  the  beginning  of  the  third  year, 
with  the  development  of  all  the  twenty  milk 
teeth.     The  accompanying  diagram    (Fig. 
69),  after  Vogel,  represents  the  order  in 
which  the  separate  teeth  appear.     In  the 
sixth  or  seventh  year  the  milk  teeth  begin 
to  be  replaced  by  the  permanent  teeth  of  the  second  dentition.    The  milk  teeth 
fall  out  in  about  the  same  order  as  they  appear.     "  Trouble  with  teething," 
however,  almost  invariably  refers  to  anomalies  of  the  first  dentition. 

Noticeable  delay  in  teething  is  frequent  in  constitutionally  weakly.,  and  par- 
ticularly in  rachitic  children,  in  whom  the  teeth  may  develop  not  in  pairs  and 
in  symmetrical  groups,  as  in  healthy  children,  but  in  irregular  succession.  In 
such  cases,  sometimes,  all  the  teeth  are  not  cut  till  the  end  of  the  third  year. 
On  the  other  hand,  it  sometimes  happens  that  certain  teeth  appear  very 
early,  or  even  are  present  at  birth.  If  an  abnormally  early  tooth  is  only 
loosely  inserted  in  the  gums,  it  should  be  removed  with  the  forcejjs;  for  it 
interferes  with  nursing,  and  injures  the  opposing  surface  of  the  mouth;  but 
if  the  tooth  is  firm  in  its  place,  we  let  it  be. 

During  the  eruption  of  the  teeth  there  is  in  every  child  considerable  red- 
ness of  the  mucous  membrane  and  an  increased  flow  of  saliva.  The  child 
evidently  feels  an  itching  in  the  mouth,  and  therefore  a  constant  desire  to 
bite  something.  It  is  more  restless,  especially  at  night,  and  does  not  take 
food  as  well  as  usual.  This  simple  catarrh  is  sometimes  accompanied  by  a 
slight  rise  in  temperature.  Occasionally  there  is  a  severe  stomatitis,  with 
which  fever  and  thrush  may  be  associated.  These  troubles  should  be  treated 
as  already  described. 

In  consequence  of  the  salivation,  and  the  large  amount  of  saliva  which  is 
swallowed,  in  which  the  processes  of  decomposition  are  apt  to  develop,  we 
often  see  gastro-intestinal  diseases  in  teething  children.  In  most  children  a 
temporary  and  mild  diarrhea  occurs.     We  should  be  particularly  careful  at 


VARIOUS   FORMS   OF  SORE  THROAT 

this  period  about  the  child's  nourishment,  and  in  treating  an}'  marked  gastro- 
intestinal symptoms.  Experience  shows  also  that  teething  children  are  unu- 
sually liable  to  simple  or  even  capillary  bronchitis,  and  catarrhal  pneumonia. 

Nervous  disturbances  are  often  referred  to  dentition.  The  most  important 
symptom  of  this  kind  is  eclampsia.  The  attacks  are  sometimes  called  "  teeth- 
ing convulsions/'  Although  the  laity  go  too  far  in  ascribing  all  sorts 
nervous  disorders  to  teething,  still  experienced  specialists  do  recognize  the 
possibility  of  such  an  origin  for  many  cases.  Some  of  the  convulsions-may  in 
fact  be  regarded  as  reflex  (vide  infra  the  chapter  on  the  Convulsions  of  Chil- 
dren, Vol.  II). 

When  the  upper  canines,  or  "  eye  teeth,"  are  being  cut,  there  is  sometimes 
a  unilateral  purulent  conjunctivitis,  which  is  perhaps  to  be  explained  as  an 
extension  of  the  inflammation  by  way  of  the  antrum  of  Highmore  and  the 
nostrils.  Eczema  and  other  cutaneous  eruptions  have  been  often  ascribed  to 
dentition,  whether  justly  or  not  is  doubtful.  Yet  it  is  remarkable  that  little 
children  sometimes  have  an  eruption  of  facial  eczema  with  the  appearance 
of  every  tooth. 

Even  healthy  children  frequently  show  a  marked  circumscribed  hyper- 
asmia  of  the  cheek  during  the  eruption  of  a  tooth. 

There  is,  of  course,  no  special  treatment  for  difficult  dentition.  Scarifi- 
cation of  the  gums  to  help  the  eruption  of  the  teeth  should  never  be  practiced. 
The  various  disturbances  appearing  during  dentition  are  to  be  treated  on 
general  principles. 


SECTION    II 


Diseases  of  the  Soft  Palate,  Tonsils,  Pharynx,  and 
Nasopharynx 

CHAPTEE   I 

VARIOUS    FORMS    OF    SORE    THROAT 
(Inflammation  of  the  Soft  Palate  and  of  the  Tonsils) 

AETIOLOGY 

Acute  inflammation  of  the  soft  palate  and  tonsils,  in  its  various  forms, 
is  one  of  the  commonest  of  diseases.  Almost  everybody  has  had  personal 
experience  with  it.  It  is  chiefly  a  disease  of  early  life,  being  infrequent  after 
the  thirty-fifth  year.  Individual  predisposition  to  it  varies  greatly.  There 
are  persons  who  have  one  or  more  attacks  almost  every  year,  while  with  others 
attacks  are  rare  and  insignificant.  In  many  instances  exciting  causes  have 
evidently  been  potent.  Chief  among  these  is  catching  cold ;  the  sufferer  has 
had  wet  feet,  or  has  been  talking  in  a  damp,  cold  atmosphere.  Most  cases, 
therefore,  occur  in  cool  weather,  although  now  and  then  attacks  may  occur 
in  the  hottest  days  of  summer.  Again,  direct  injuries  of  the  pharynx  may 
produce  the  disease — e.  g.,  the  smoky  atmosphere  of  inns,  combined  with  loud 


484  DISEASES   OF   THE   DIGESTIVE   ORGANS 

talking  or  shouting;  the  inspiration  of  poisonous  vapors;  cauterization  of  the 
mucous  membrane  with  concentrated  acids,  alkalies,  and  other  chemical  agents ; 
.and  burns. 

Apart,  however,  from  these  last-named  external  irritants  we  have  many 
cases  of  primary  angina,  for  which  we  must  assume  an  infectious  origin.  This 
supposition  is  suggested  by  the  severity  of  the  constitutional  disturbance,  with 
fever,  the  nature  of  the  local  process  (giving  rise  to  suppuration),  and  the 
■occasional  appearance  of  the  disease  in  an  epidemic  or  endemic  form.  At  the 
same  time,  exposure  to  cold  and  the  other  exciting  causes  above  mentioned, 
may  often  favor  its  development.  With  regard  to  the  nature  of  the  infectious 
organism,  if  the  tonsillitis  is  of  the  suppurative  parenchymatous  variety,  it  is 
certain  that  we  have  to  deal  with  the  ordinary  pus  organisms  (usually  staphy- 
lococci). The  same  is  also  true  of  follicular  tonsillitis,  although  several  dif- 
ferent kinds  of  pathogenic  organisms  may  be  concerned;  thus  we  may  find 
not  only  staphylococci,  streptococci,  and  particularly  diplococci,  but  probably, 
in  many  cases,  even  the  genuine  diphtheria  bacillus. 

Frequently  the  inflammation  is  due  to  extension  from  neighboring  parts, 
as  in  coryza,  laryngitis,  and  stomatitis.  In  many  cases  both  affections  are 
simultaneous  results  of  one  common  cause.  Finally,  sore  throat  may  be  a 
symptom  of  many  acute  infectious  diseases,  such  as  scarlet  fever,  measles, 
smallpox,  and  erysipelas. 

To  distinguish  between  an  inflammation  of  the  soft  palate  by  itself  and 
an  affection  of  the  tonsils  is  not  practicable.  In  most  cases  the  tonsils  are 
the  stronghold  of  the  disease;  less  often  we  find  the  inflammation  limited 
to  the  soft  palate. 

CLINICAL   HISTORY 

The  most  important  subjective  symptom  of  sore  throat,  and  that  by  which 
it  is  usually  first  recognized,  is  the  difficult  and  painful  deglutition.  The 
pain  is  sometimes  manifest  before  any  objective  changes  are  to  be  seen.  It 
may  in  a  severe  case  be  very  violent  and  distressing.  The  pain  has  a  "  dart- 
ing "  character,  or  sometimes  is  "  burning  " ;  and  it  is  most  acute  whenever 
the  patient  swallows,  although  in  well-marked  cases  it  seldom  entirely  inter- 
mits. Swallowing  is  not  only  painful,  but  it  is  laborious;  it  requires  more 
than  usual  effort  and  time.  The  patient  feels  constantly  as  if  he  had  to 
swallow  a  big  lump.  This  sensation  is  worse  if  the  tonsils  are  swollen.  It 
is  a  matter  of  experience  that  not  infrequently  an  "  empty  n  swallowing  hurts 
more  than  swallowing  a  liquid  or  some  half-solid  substance. 

Talking  is  also  difficult.  Every  word  may  be  painful,  so  that  the  patient 
expresses  his  wishes  as  briefly  as  possible.  Even  in  a  mild  case,  speaking  for 
any  length  of  time  will  produce  a  burning  pain  in  the  throat.  The  impaired 
mobility  of  the  soft  palate  often  prevents  the  complete  cutting  off  of  the 
nasal  passages  in  talking,  so  that  the  voice  has  a  nasal  twang;  and  it  sounds 
as  if  the  patient  were  talking  with  his  mouth  full :  he  has  the  "  voice  of 
sore  throat." 

Further  local  discomfort  results  from  the  mucus  and  saliva  collecting  in 
the  mouth.  Salivation  is  not  infrequent,  probably  as  a  result  of  the  stomatitis 
usually  present.     In  other  cases  the  patient  complains  that  his  mouth  feels 


VARIOUS   FORMS  OF  SORE  THROAT  485 

dry  and  sticky.  Frequently  there  is  a  persistent  bad  taste  in  the  mouth,  and 
the  breath  is  disagreeable. 

With  these  local  disturbances,  more  or  less  severe  constitutional  symptoms 
are  almost  always  conjoined.  Indeed,  these  latter  may  begin  a  day  or  two 
earlier  than  the  local  symptoms.  The  patient  is  indisposed,  languid,  has 
anorexia  and  headache.  The  general  disturbance  may  be  surprisingly  great 
in  comparison  with  the  slight  objective  changes  in  the  tonsils. 

There  is  fever  in  most  of  the  well-marked  cases;  it  may  even  be  quite 
high.  Temperatures  of  103°  or  104°  F.  (39.5°  to  40°  C.),  or  even  higher, 
are  not  rare.  Sore  throat  cannot  be  said  to  have  one  particular  type  of  fever. 
Usually  the  fever  appears  rather  abruptly,  remains  high  for  several  days, 
with  an  occasional  slight  interruption,  and  then  falls  with  equal  abruptness 
to  normal  again. 

The  entire  attack  usually  lasts  only  a  few  days,  seldom  more  than  a  week. 
Even  when  a  person  is  quite  ill  for  several  days,  convalescence  is  almost 
always  rapid  and  complete — that  is,  if  the  patient  has  a  good  constitution. 

Special  complications  are  rare,  except  that  the  neighboring  parts — the 
larynx,  mouth,  and  throat — are  not  seldom  involved.  The  condition  of  the 
urine  must  be  noted,  as  occasionally,  after  an  apparently  mild  sore  throat, 
an  acute  nephritis  may  develop.  It  is  worthy  of  mention  that  herpes  labialis 
is  quite  frequent. 

VARIETIES    OF   SORE   THROAT 

The  symptoms  thus  far  mentioned  are  much  the  same  in  all  cases  of  sore 
throat,  varying  only  in  intensity  and  duration.  But  the  objective  changes  to 
be  observed  in  the  soft  palate  and  tonsils  are  noticeably  different  in  different 
cases.  Whether  the  aetiology  differs  also  we  have  no  certain  information.  In 
some  instances  it  seems  probable  that  it  does. 

We  shall  distinguish  five  chief  varieties  of  acute  sore  throat.  Transitional 
forms  are,  however,  by  no  means  rare.  Genuine  diphtheria,  which  is  a  spe- 
cific, acute,  infectious  disease,  and  which  has  already  been  discussed,  does  not 
need  to  be  brought  up  again  here. 

1.  Catarrhal  Sore  Throat  (Simple  Catarrhal  Inflammation  of  the  Mucous 
Membrane  of  the  Soft  Palate). — There  is  a  more  or  less  vivid  reddening  of 
the  mucous  membrane,  either  uniform  or  in  patches.  The  swelling  is  most 
marked  in  the  pillars  of  the  fauces  and  the  uvula.  The  surface  of  the  tonsils 
is  likewise  reddened;  their  size  may  be  somewhat  increased,  or  remain  un- 
changed. The  mucous  membrane  of  the  palate  and  uvula  may  be  covered  here 
and  there  with  a  thin  layer  of  mucopus,  which  can  easily  be  wiped  off.  The 
tonsils  may  present  small  superficial  erosions  scattered  about.  These  little 
ulcers  are  apt  to  lie  at  the  openings  of  the  follicles.  The  small  "  blisters  " 
which  are  often  seen  on  the  mucous  membrane  of  the  soft  palate  are  caused 
in  various  ways.  Either  they  are  mucous  glands  or  solitary  follicles,  swollen; 
or,  rarely,  they  are  real  vesicles  filled  with  a  clear  fluid  and  produced  by  a 
raising  up  of  the  epithelium.  The  cervical  lymph-glands  are  usually  but 
slightly  swollen  if  at  all. 

This  is  the  common  and  mildest  form  of  sore  throat;  and  it  may  be  over 
in  a  day  or  two.  In  some  instances,  however,  it  causes  considerable  local 
31 


486  DISEASES   OF  THE   DIGESTIVE   ORGANS 

and  general  discomfort;  but  the  disease  seldom  lasts  longer  than  five  to 
eight  days. 

2.  Follicular  Tonsillitis. — In  this  frequent  and  practically  important  form 
there  is  not  only  more  or  less  catarrhal  inflammation  of  the  soft  palate,  but 
a  decided  swelling  of  one  or  both  tonsils.  On  the  reddened  surface  of  these 
swollen  bodies  are  whitish-yellow  spots,  varying  in  number  from  two  or  three 
to  ten  or  more,  and  corresponding  to  the  follicles.  These  spots  are  often 
seen  to  be  plugs  projecting  from  the  openings  of  the  follicles.  It  is  usually 
easy  to  press  out  the  pasty  contents  of  the  follicle,  represented  by  the  white 
speck,  with  a  spatula.  The  microscope  shows  it  to  consist  of  numerous  epi- 
thelial cells  and  pus  corpuscles,  bacteria,  and  detritus,  and  sometimes  there 
are  also  crystals  of  the  fat  acids  and  cholesterin.  The  pus  corpuscles  may  so 
predominate  that  we  may  have  small  follicular  abscesses,  which,  on  being 
opened,  leave  superficial  ulcers  behind.  The  parenchyma  of  the  tonsil  is 
swollen  with  a  serous  and  cellular  infiltration,  increasing  the  bulk  of  the 
part.  The  trouble  is  usually  bilateral,  though  often  more  marked  and  extensive 
on  one  side  than  on  the  other.  In  the  severer  cases  the  cervical  lymph-glands 
are  usually  moderately  swollen. 

The  local  symptoms  and  still  more  the  constitutional  disturbance  in  fol- 
licular tonsillitis  may  be  decided.  The  fever  not  infrequently  reaches  104°  F. 
(40°  C.)  or  even  higher.  The  patient  feels  very  languid,  has  no  appetite, 
and  complains  of  headache;  but  there  are  mild  as  well  as  severe  cases.  The 
disease  never  lasts  longer  than  a  few  days,  even  when  the  fever  is  high  at 
first.  The  yellow  spots  vanish  from  the  tonsils,  and  there  is  rapid  recovery; 
severe  complications  are  hardly  ever  seen.  Often  there  is  a  herpes  labialis 
and  there  may  be  slight  albuminuria,  but  this  very  rarely  amounts  to  a  genu- 
ine acute  nephritis.  It  should  be  mentioned  that  sometimes  the  contents  of 
a  few  of  the  follicles  remain  in  them  for  a  considerable  length  of  time,  and 
become  inspissated  and  calcified.  It  is  not  a  rare  thing  to  find  such  plugs 
in  the  tonsils  of  those  who  are  subject  to  sore  throat.  Timid  and  hypochon- 
driacal individuals  are  sometimes  badly  frightened  by  expectorating  these 
old  chalky  plugs,  which  they  believe  to  be  "  tubercles  " ! 

From  an  setiological  standpoint,  follicular  tonsillitis  is  in  most  cases  en- 
tirely distinct  from  genuine  diphtheria,  and  so  far  the  search  for  the  Klebs- 
Loffler  bacillus  in  the  plugs  contained  in  the  follicles  has  almost  invariably 
proved  negative.  Still,  it  is  noteworthy  that  precisely  at  the  time  of  diphtheria 
epidemics  follicular  tonsillitis  is  remarkably  frequent.  It  is  also  bacteriolog- 
ically  determined  that  the  mildest  degrees  of  diphtheria  present  themselves 
in  the  garb  of  an  apparently  simple  follicular  tonsillitis. 

3.  Tonsillar  and  Peritonsillar  Abscess  {Parenchymatous  Sore  Throat; 
Quinsy). — In  this  form  the  swelling  of  the  tonsils  and  the  surrounding  tissues 
is  the  most  striking  symptom.  They  may  be  more  than  twice  their  natural 
size.  The  anterior  pillars  of  the  fauces  are  pushed  forward  and  become 
convex.  The  swelling  extends  so  far  toward  the  median  line  that  the  tonsil 
touches  the  uvula ;  or,  if  the  affection  is  bilateral,  the  two  tonsils  press  against 
each  other,  grasping  the  uvula  between  them,  or  pushing  it  forward.  The 
soft  palate  is  very  much  reddened,  particularly  at  first.  Its  surface  is  usually 
thickly  covered  with  mucus.  If  this  be  wiped  off,  the  mucous  membrane  is 
seen  to  have  a  moist,  cedematous  luster.    The  mucous  membrane  of  the  tonsils. 


VARIOUS   FORMS   OF   SORE   THROAT  487 

not  infrequently  suffers  a  superficial  necrosis.  Follicular  and  parenchymatous 
tonsillitis  are  often  combined. 

In  well-marked  cases  of  abscess  the  local  discomfort  is  usually  great.  With 
every  attempt  to  swallow  there  is  pain  which  shoots  into  the  ear.  The  patient 
is  in  a  pitiable  condition;  he  can  neither  talk,  nor  swallow,  nor  gargle.  The 
few  words  which  he  painfully  utters  have  in  an  extreme  degree  the  nasal 
quality  of  the  "  voice  of  sore  throat." 

In  the  milder  cases  the  trouble  seldom  lasts  but  a  few  days  before  the 
swelling  goes  down,  and  the  discomfort  and  usually  rather  moderate  fever 
gradually  abate.  In  other  cases  an  abscess  of  the  tonsil  develops,  usually  on 
one  side  only,  but  it  would  be  more  correct  to  say  a  peritonsillar  abscess,  for 
the  pus  usually  collects  mainly  in  the  connective  tissue  between  the  tonsil 
and  the  arch  of  the  palate.  In  such  cases  the  mucous  membrane  bulges  out, 
usually  at  a  point  in  the  velum  of  the  palate,  and  on  palpation  there  is  a 
sense  of  fluctuation,  and  finally  the  abscess  ruptures.  In  other  cases,  how- 
ever, a  tonsillar  abscess  forms,  as  a  rule,  on  only  one  side.  The  mucous 
membrane  bulges  out  more  in  one  spot;  distinct  fluctuation  is  detected;  and, 
finally,  the  abscess  breaks.  With  the  discharge  of  the  pus  the  pain  is  relieved 
very  rapidly,  or  it  may  vanish  at  once.  The  rest  of  the  tonsil  soon  regains 
its  former  size,  and  in  a  few  days  the  patient  is  well.  Eelapses  are  possible, 
but  rare. 

Phlegmonous  sore  throat,  in  which  the  soft  palate  and  not  the  tonsil  is 
chiefly  affected,  is  infrequent.  Its  usual  cause  is  some  severe  external  injury, 
such  as  burns,  and  cauterization  with  concentrated  acids  or  alkalies.  The 
swelling  extends  deep  down  into  the  submucous  tissue.  The  uvula  may  have 
the  diameter  of  one's  finger.  There  is  intense  hypersemia.  Sometimes  there 
are  hemorrhages  into  the  mucous  membrane :  this  is  called  hemorrhagic  sore 
throat.1 

4.  Necrotic  Tonsillitis  (Necrotic  Sore  Throat). — This  name  is  applied  to 
a  disease  which  is  not  infrequent,  and  in  which  the  tonsils  are  the  main  seat 
of  the  pathological  processes.  The  pillars  of  the  fauces  and  the  uvula  are 
but  slightly  affected  with  a  simple  catarrhal  inflammation.  The  tonsils  are, 
as  a  rule,  moderately  swollen,  seldom  attaining  great  size.  The  mucous  mem- 
brane covering  them  presents  a  whitish  or  grayish-white  discoloration,  often 
quite  extensive,  and  most  marked  on  the  side  toward  the  uvula.  A  careful 
investigation  shows  that  there  is  in  reality  no  "  coating,"  but  a  necrosis.  The 
process  may  be  superficial;  sometimes  it  reaches  quite  deeply  into  the  struc- 
ture of  the  mucous  membrane.  It  is  not  possible  to  pull  off  this  white  mat- 
ter, as  one  can  loosen  croupous  membranes,  although  little  bits  may  perhaps 
be  scratched  off  with  a  spatula  or  a  pair  of  forceps.  These  particles  are  found, 
on  microscopic  examination,  to  be  made  up  of  detritus,  bacteria,  epithelium, 
and  pus  corpuscles.  The  necrosis  is  almost  invariably  confined  to  the  tonsils, 
and  a  sharp  boundary  line  separates  it  from  the  reddened  and  inflamed  pillars 
of  the  fauces.  After  a  few  days  the  slough  may  come  away,  leaving  behind 
an  ulcer,  which,  though  usually  shallow,  has  sometimes  a  considerable  depth. 
This  generally  cleans  up  rapidly.     In  severe  cases,  however,  the  floor  of  the 

1  Another  form  of  hemorrhagic  sore  throat  occurs  where  there  is  violent  tonsillitis  with 
necrosis  or  gangrene.  There  is  also  a  necrotic,  hemorrhagic  sore  throat  accompanying  scurvy 
and  leukaemia. 


488  DISEASES  OF  THE   DIGESTIVE   ORGANS 

nicer  consists  for  a  number  of  days  of  a  dirty  necrotic  material,  which  comes 
away  only  gradually.  The  worst  cases  may  be  properly  called  "  gangrenous 
tonsillitis." 

Necrotic  tonsillitis  is  almost  always  attended  by  considerable  fever  and 
marked  constitutional  disturbance.  Children  particularly  seem  very  ill  in 
the  first  days  of  the  attack.  The  cervical  glands  are  usually  swollen,  but 
seldom  as  much  so  as  in  genuine  diphtheria. 

Despite  the  rather  ominous  commencement,  the  disease  does  not  last  a 
great  deal  longer  than  the  other  forms  of  sore  throat.  It  seldom  continues 
more  than  five  to  eight  days  before  a  speedy  convalescence  begins. 

The  necrotic  tonsillitis  is  distinguished  from  the  follicular  form  by  the 
greater  area  of  the  white  or  grayish-white  spots.  Still,  it  should  be  particu- 
larly noted  that  sometimes  combinations  of  these  two  varieties,  or  transitional 
forms,  occur. 

Only  the  bacteriological  examination  can  decide  with  certainty  the  aetiology 
of  necrotic  tonsillitis.  In  some  cases  diphtheria  bacilli  can  be  demonstrated. 
Then,  of  course,  the  infection  is  a  true  diphtheria  which  presents  the  ana- 
tomical picture  of  a  necrotic  tonsillitis.  In  other  cases  there  are  present  no 
diphtheria  bacilli,  but  only  the  ordinary  inflammatory  organisms,  particularly 
streptococci. 

At  this  point  we  wish  to  refer  briefly  to  the  so-called  Plaut-Vincent's  An- 
gina, a  form  of  tonsillitis  first  described  by  Plaut  and  Vincent  in  1898,  and 
which  in  many  respects  resembles  diphtheria.  A  grayish-white  coating  devel- 
ops on  one  or  both  tonsils ;  after  this  separates  there  remains  a  superficial 
erosion  of  the  mucous  membrane,  or  occasionally  a  deeper  ulcer  (ulcero- 
membranous tonsillitis).  The  constitutional  manifestations  (fever,  glandular 
swellings,  joint  pains,  albuminuria,  etc.)  may  be  quite  severe.  The  disease 
runs  its  course  in  about  one  to  one  and  one  half  weeks.  The  bacteriological 
examination  shows  no  diphtheria  bacilli  but  generally  the  so-called  Bacillus 
fusiformis,  together  with  numerous  spirilla?  and  other  bacteria.  Of  late, 
small  epidemics  of  this  form  of  tonsillitis  have  been  repeatedly  observed. 

DIAGNOSIS   AND   PROGNOSIS 

It  is  never  very  difficult  to  recognize  a  sore  throat,  and  a  little  practice 
makes  it  easy  in  most  cases  to  decide  what  particular  variety  is  present,  if 
we  examine  the  objective  changes  carefully.  It  is  very  important  in  practice 
to  distinguish  diphtheria  from  the  benign  forms  of  inflammation.  Follicular 
and  necrotic  tonsillitis  are  very  frequently  mistaken  for  diphtheria — an  error 
which  explains  the  success  of  a  large  number  of  remedies  said  to  cure  diph- 
theria. Many  physicians  call  every  case  of  sore  throat,  where  there  is  any- 
thing white  to  be  seen,  "  diphtheria."  Certainty  in  diagnosis  of  genuine 
diphtheria  can  be  gained  only  by  practice;  no  description,  however  complete, 
can  take  the  place  of  personal  observation.  It  may  be  a  help  to  remember 
that  in  both  follicular  and  necrotic  tonsillitis  the  white  spots  are  usually 
limited  to  the  tonsils,  while  in  croupous  sore  throat  the  deposits  are  generally 
from  the  very  first  also  situated  upon  the  pillars  of  the  fauces  and  the  uvula. 
The  white  spots  of  the  follicular  variety  can  generally  be  at  once  recognized 
by  their  arrangement.     The  plugs  and  areas  of  suppuration  are  seen  pro- 


CHRONIC   HYPERTROPHY  OF  THE   TONSILS  489 

jecting  from  their  follicles.  In  necrotic  sore  throat  there  is  never  a  sepa- 
rable croupous  membrane  with  its  characteristic  histological  structure,  but 
there  is  simply  a  superficial  necrosis  of  the  raucous  membrane  and  paren- 
chyma. The  condition  of  the  cervical  lymph-glands  is  not  unimportant; 
as  a  rule,  they  are  much  more  affected  in  diphtheria  than  in  the  benign 
cases. 

It  is  further  to  be  noted  that  the  fever  in  true  diphtheria  rarely  reaches 
the  point  that  it  does  in  the  tonsillitis  produced  by  pus  organisms.  A 
tonsillitis  that  begins  at  once  with  fever  of  about  104°  F.  is  rarely  a  true 
diphtheria. 

Still,  the  fact  must  again  and  again  be  emphasized  that  only  the  bacterio- 
logical examination  can  definitely  decide  each  individual  case.  It  certainly 
is  worth  while,  especially  with  children,  to  isolate  all  cases  that  are  in  any  way 
doubtful. 

TREATMENT 

These  troubles  usually  run  so  favorable  a  course  that  active  treatment  is 
very  seldom  needed.  The  gargle  usually  prescribed  generally  gives  the  patient 
more  discomfort  than  relief.  The  most  common  prescriptions  are :  Solutions 
of  potassium  chlorate  (10  to  300)  diluted  with  lukewarm  water,  peroxid  of 
hydrogen,  etc.  To  paint  the  parts  is  a  useless  and  now  almost  obsolete  proceed- 
ing. Inhalations  of  spray  are  better,  with  alkaline  solutions  or  tannin.  The 
use  of  formamint  tablets  is  also  serviceable.  They  are  allowed  to  dissolve 
slowly  in  the  mouth.  It  is  beneficial  to  put  a  cold  or  hot  wet  compress  around 
the  throat.  Children  must  be  kept  in  bed,  and  adults  are  generally  forced  to 
go  to  bed,  if  the  constitutional  symptoms  are  well  marked.  If  the  febrile 
symptoms  are  marked,  antipyretics  (antipyrin,  phenacetin,  and  aspirin)  some- 
times afford  relief. 

We  try,  unfortunately  often  without  result,  to  relieve  the  symptoms  of 
parenchymatous  tonsillitis  with  ice  pellets  or  warm  mouth  washes.  If  there 
is  evident  fluctuation,  we  can  make  an  incision  with  a  spear-pointed  bistoury, 
after  guarding  a  portion  of  the  blade  with  sticking  plaster.  The  best  place  is 
almost  always  in  the  velum  palati,  corresponding  to  the  outer  boundary  of  the 
tonsil.  Great  relief  follows ;  and  even  if  there  is  no  distinct  abscess  an  incision 
will  usually  give  relief,  if  there  is  excessive  swelling,  and  if  there  is  a  deeply 
seated  abscess  will  facilitate  its  spontaneous  discharge.  Punctures  of  this  sort 
cause  scarcely  any  pain. 

[Hoffman  has  pointed  out  that  in  some  cases  permanent  recovery  can  be 
attained  by  breaking  down  the  partitions  between  the  crypts  of  the  tonsils,  thus 
establishing  thorough  discharge  of  their  secretions.] 


CHAPTEE    II 
CHRONIC   HYPERTROPHY    OF    THE    TONSILS 

Chronic  hypertrophy  of  the  tonsils  occurs  not  only  in  those  who  have  had 
repeated  attacks  of  tonsillitis,  but  also  in  cases  in  which  no  occasion  for  it  can 


490  DISEASES   OF   THE   DIGESTIVE   ORGANS 

be  found.  Even  in  childhood  there  is  not  infrequently  a  well-marked  hyper- 
trophy, which  must  be  due  to  a  special  congenital  predisposition. 

The  condition  is  at  once  revealed  by  inspection.  There  may  be  no  signs 
whatever  of  any  acute  or  chronic  inflammation,  or  there  may  be  an  accompany- 
ing chronic  pharyngitis.  The  tonsils  bulge  out  in  two  great  lumps.  They  may 
be  so  large  as  to  touch  the  uvula  on  each  side.  Histologically,  there  is  a  gen- 
uine hypertrophy  of  the  organ — that  is,  an  increase  of  all  its  component 
tissues. 

In  many  cases,  where  the  swelling  is  moderate,  there  is  no  discomfort. 
The  possessor  of  the  tonsils  is  not  aware  that  they  are  enlarged.  In  other  cases 
the  hypertrophy  proves  of  clinical  importance,  inasmuch  as  all  forms  of  sore 
throat  are  found  to  occur  more  frequently  if  the  tonsils  are  enlarged,  and  to 
cause  more  trouble  when  they  do  appear.  The  hypertrophied  organs  may  also 
be  the  seat  of  a  chronic  catarrh,  which  by  extension  gives  rise  to  chronic  nasal 
catarrh,  catarrh  of  the  Eustachian  tubes,  or  hoarseness. 

If  the  hypertrophy  is  considerable,  the  local  discomfort  may  be  quite 
marked.  Swallowing  is  rendered  difficult,  if  not  painful.  Frequently  there 
is  evident  dyspnoea.  The  patient  has  to  breathe  through  his  mouth,  and  some- 
times when  asleep  snores  and  snorts  in  a  way  to  frighten  one.  Children  are 
particularly  apt  to  suffer  in  this  manner.  Many  instances  of  pavor  nocturnus, 
or  "  night  terrors,"  in  children  are  referable  to  this  cause.  We  have  already 
mentioned  that  cases  of  bronchial  asthma  sometimes  seem  to  be  connected  with 
hypertrophy  of  the  tonsils. 

Treatment. — The  attempt  to  reduce  the  enlargement  by  applying  lunar 
caustic,  tincture  of  iodin,  etc.,  usually  fails.  If  there  is  much  distress,  if  the 
patient  is  subject  to  frequent  sore  throats,  or  if  the  hypertrophy  of  the  tonsils 
keeps  up  a  chronic  nasal  or  pharyngeal  catarrh,  then  the  only  remedy  is  to 
remove  the  tonsils  by  operation.  The  operation  should  not  be  undertaken, 
however,  without  sufficient  reason. 


CHAPTEE    III 
CHRONIC    PHARYNGITIS 

AETIOLOGY 

It  is  not  practicable  to  distinguish  between  chronic  catarrh  of  the  soft 
palate  and  of  the  pharynx,  for,  as  a  rule,  the  two  are  combined.  Sometimes  the 
condition  is  the  result  of  repeated  acute  attacks;  sometimes — and  probably 
oftener — it  is  due  to  persistent,  injurious,  local  influences.  A  large  number  of 
cases  originate  in  bad  habits,  or  in  abuse  incident  to  certain  vocations.  Ex- 
amples are  seen  in  smokers,  drunkards,  singers,  preachers,  teachers,  and  men 
who  work  outdoors.  In  talking  and  singing,  the  soft  palate  is  strained;  or 
the  disease  is  excited  by  breathing  cold  or  impure  air,  or  by  such  chemical 
irritants  as  alcohol  or  tobacco.  In  many  cases,  chronic  pharyngitis  follows 
chronic  rhinitis  or  chronic  laryngitis.  The  general  passive  congestion  due  to 
cardiac  disease  or  pulmonary  emphysema  may  sometimes  promote  the  develop- 
ment, or  prolong  the  existence,  of  a  chronic  pharyngitis. 


CHRONIC   PHARYNGITIS  491 

SYMPTOMS 

The  local  discomfort  is  often  slight.  The  patient  gets  used  to  it,  and  does 
not  mind  it  except  when  there  is  some  exacerbation.  It  becomes  a  more  im- 
portant matter  if  the  calling  of  the  patient  is  interfered  with,  as  in  a  preacher, 
singer,  or  teacher. 

Deglutition  is  seldom  impaired.  There  is  often,  however,  a  constant  feel- 
ing of  dryness,  burning,  or  scratching  in  the  throat.  The  patient  has  to  clear 
his  throat  frequently,  and  often  acquires  an  habitual,  short,  sudden  cough, 
which  may  or  may  not  be  dry.  The  expectoration,  if  there  is  any,  is  almost 
pure  mucus.  When  there  are  violent  efforts  to  clear  the  throat,  there  may  be  a 
slight  hemorrhage  from  the  dilated  blood  vessels  of  the  posterior  wall  of  the 
pharynx,  explaining  the  presence  of  small  amounts  of  blood  in  the  expectora- 
tion. This  blood  often  has  a  dried-up  look,  as  if  not  fresh.  It  sometimes 
leads  overanxious  patients  and  physicians  to  suspect  pulmonary  hemorrhage. 
The  uvula  becomes  so  long  that  its  tip  rests  on  the  tongue  or  the  posterior  wall 
of  the  pharynx;  and  this  gives  rise  to  a  peculiar  and  disagreeable  sensation 
of  tickling.  All  these  uncomfortable  feelings  are  temporarily  increased  if  any- 
thing affects  the  throat  unfavorably;  and  they  are  generally  at  their  worst  on 
rising  in  the  morning,  apparently  because  the  mucous  membrane  has  become 
dry,  or  a  collection  of  tough  mucus  has  formed  during  the  night.  Everyone 
knows  how  drunkards  have  to  hawk  and  cough  in  the  morning,  so  that  often 
they  almost  strangle  or  vomit. 

On  inspection,  we  generally  find  the  mucous  membrane  reddened.  Very 
often  a  number  of  dilated  and  tortuous  veins  are  visible  both  on  the  soft  palate 
and  in  the  back  of  the  throat.  Of  equal  frequency  is  the  appearance  of  numer- 
ous small  gray  projections,  corresponding  usually  to  swollen  follicles  or  else 
to  hypertrophied  mucous  glands.  This  is  called  granular  pharyngitis.  Small 
follicular  ulcers  are  not  infrequent.  Exceptionally  there  are  more  extensive 
catarrhal  ulcers.  The  mucous  membrane  of  the  posterior  wall  of  the  pharynx 
may  present  patches  of  opaque  or  thickened  epithelium,  giving  the  surface  a 
grayish-white  appearance. 

Frequently  chronic  pharyngitis  is  combined  with  chronic  laryngitis,  evi- 
denced by  hoarseness ;  or  with  posterior  nasal  catarrh,  or  catarrh  of  the  Eu- 
stachian tube,  producing  deafness  and  ringing  in  the  ears. 

VARIETIES   OF   CHRONIC   PHARYNGITIS 

1.  Chronic  Catarrh  of  the  Nasopharynx,  or  Chronic  Posterior  Nasal  Ca- 
tarrh.— This  has  the  same  aetiology  as  the  ordinary  form.  It  is  practically 
important  because  the  nose  and  ear  are  frequently  involved. 

The  anatomical  changes  are  essentially  those  already  depicted  under 
chronic  pharyngitis.  The  region  affected  cannot  be  seen  by  direct  inspection, 
so  that  accuracy  in  diagnosis  requires  the  use  of  a  nasal  speculum  (see  par- 
ticulars in  the  works  mentioned  on  page  164).  The  ordinary  examination  of 
the  throat  may  reveal  a  condition  which  is  quite  characteristic  of  posterior 
nasal  catarrh:  a  collection  of  mucopus,  or  of  firmly  adherent  dry  crusts,  is 
seen  on  the  posterior  wall  of  the  pharynx,  and  extends  upward  toward  the 
nasopharynx. 


492  DISEASES   OF  THE   DIGESTIVE   ORGANS 

The  local  discomfort  is  somewhat  similar  to  that  experienced  in  chronic 
pharyngitis.  There  is  a  scratchy  feeling,  or  a  feeling  as  if  there  were  a 
foreign  body  in  the  back  of  the  throat,  accompanied  by  a  constant  desire 
to  blow  the  nose,  hawk,  or  cough.  Dried  and  decomposing  secretion  often 
causes  extremely  foul  breath.  There  is  often  also  vertigo  and  occipital 
headache. 

In  many  cases  the  nostrils  are  stopped  up.  The  posterior  opening  of  the 
nostrils  is  closed  in  part  by  the  swelling  and  hypertrophy  of  the  mucous  mem- 
brane, and  in  part  by  the  accumulated  secretions.  The  patient,  therefore, 
usually  has  to  breathe  through  the  mouth.  The  ear  is  frequently  involved. 
The  catarrh  extends  into  the  Eustachian  tubes  and  the  tympanic  cavity,  or 
the  opening  of  the  tubes  is  occluded  with  the  secretions.  For  a  detailed  con- 
sideration of  the  deafness,  tinnitus,  etc.,  thus  produced,  consult  works  on 
otology. 

2.  Pharyngitis  Sicca,  or  "  Dry  Atrophic  Catarrh  of  the  Throat  and  Naso- 
pharynx."— This  name  is  applied  to  an  atrophic  disease  of  the  mucous  mem- 
brane, which  sometimes  is  spontaneous  and  sometimes  is  a  sequel  of  chronic 
pharyngitis.  The  whole  mucous  membrane  of  the  pharynx  and  the  naso- 
pharynx (seen  with  the  rhinoscope)  seems  pale,  smooth,  and  perfectly  dry, 
and  has  a  peculiar  luster,  as  if  varnished.  Here  and  there  tortuous  veins 
project  from  the  general  anaemic  surface. 

If  an  opportunity  is  afforded  to  examine  the  mucous  membrane  micro- 
scopically, it  will  be  found  that  the  atrophy  involves  all  the  elements  of  the 
tissue,  though  the  follicles  and  mucous  glands  suffer  most. 

This  condition  may  not  cause  any  symptoms,  but,  in  many  cases,  the  pa- 
tient suffers  considerably.  The  chief  trouble  is  a  feeling  of  dryness  in  the 
throat,  rendering  deglutition  difficult  or  even  painful.  There  is  also  a  con- 
stant desire  to  clear  the  throat.  The  secretion  hawked  up  may  be  scanty  and 
tough  or  more  abundant,  and  it  is  often  tinged  with  blood.  Actual  coughing 
may  also  be  due  to  pharyngeal  trouble  ("throat  cough").  Talking  is  often 
rendered  difficult,  the  voice  grows  weak,  and  it  becomes  easily  tired.  In  severe 
cases  there  is  also  general  debility.  Not  infrequently  pharyngitis  sicca  is  as- 
sociated with  atrophic  rhinitis  (q.v.),  but  it  occurs  also  where  there  is  no 
nasal  disease. 

The  disease  is  most  frequently  seen  in  the  elderly,  but  it  also  occurs  in 
children  and  young  persons.  It  is  especially  common  in  ill-nourished  indi- 
viduals, or  in  those  who  are  suffering  from  such  diseases  as  tuberculosis  or 
chronic  nephritis. 

3.  Hypertrophic  Catarrh  in  the  Pharynx  and  Nasopharynx. — An  opposite 
condition  of  hypertrophy  sometimes  results  from  chronic  catarrh.  The 
changes  consist  mainly  in  hyperplasia  of  the  lymphatic  tissue,  and  they  are 
usually  termed  "  adenoid  growths."  The  choanse  and  the  posterior  extremity 
of  the  nasal  septum  may  be  almost  completely  hidden  by  these  growths,  as; 
they  extend  down  from  the  roof  of  the  pharynx  in  grayish-red,  uneven  masses. 
In  the  majority  of  cases  the  hypertrophy  seems  to  originate  chiefly  in  Kolli- 
ker's  "  pharyngeal  tonsil." 

The  adenoid  growths  are  especially  common  in  childhood.  The  symptoms 
consist  in  a  change  of  the  voice  (which  loses  its  reverberating  quality  and  be- 
comes nasal),  frequent  snuffling  and  hawking,  and  a  tough  mucous  secretion, 


CHRONIC   PHARYNGITIS  403 

often  tinged  with  blood.    Not  infrequently  there  is  headache.     Of  greater  im- 
portance is  ear  trouble,  which  is  often  occasioned  by  the  growth.-. 

An  accurate  diagnosis  requires  rhinoscopy.  Positive  results  are  also  often 
obtained  by  palpation.  The  index  finger,  being  pressed  backward  and  bent 
upward,  can  touch  the  protuberances  and  the  enlarged  pharyngeal  tonsil  in 
the  nasopharynx. 

PROGNOSIS 

In  all  varieties  of  chronic  pharyngeal  catarrh,  the  prognosis  as  to  re- 
covery is  doubtful,  for  in  all  severe  cases  the  process  is  very  obstinate,  and 
permanent  restoration  to  health  exceptional.  It  is  essential  for  the  best  re- 
sults that  all  injurious  influences  should  be  removed.  Even  if  decided  im- 
provement occurs  there  is  a  tendency  for  the  trouble  to  grow  worse  again, 
and  for  acute  exacerbrations  to  occur. 

TREATMENT 

Many  of  the  milder  cases  never  apply  to  a  physician.  The  patient  uses 
some  domestic  remedy  or  gargle,  or  becomes  so  accustomed  to  the  disagreeable 
sensations  that  he  does  not  consider  it  necessary  to  do  anything  in  particular 
about  them. 

The  treatment  of  a  well-developed  case  requires  great  patience  and  per- 
sistence on  the  part  of  all  concerned.  If  there  is  some  underlying  disease, 
such  as  pulmonary  or  cardiac  disease,  that  must  be  treated.  All  exciting 
causes  must  be  avoided.  Energetic  local  treatment  is  also  indispensable.  I 
cannot,  however,  refrain  from  calling  attention  to  the  fact  that  the  local 
treatment  can  also  be  overdone.  Not  very  infrequently  patients  with  chronic 
pharyngeal  catarrh  are  painted  or  cauterized  locally  for  months  without  any 
particular  benefit.  Such  a  long-drawn-out  treatment  is,  particularly  in  worri- 
some neurasthenics,  sometimes  more  harmful  than  beneficial.  Regarding  the 
methods  of  local  treatment,  the  following  remarks  will  meet  the  requirements 
of  ordinary  practice : 

Gargles  are  seldom  satisfactory,  for  they  never  reach  farther  than  the  soft 
palate.  Inhalations  are  better;  we  may  use  solutions  of  alum  or  tannin,  or, 
in  mild  cases,  of  common  salt.  Still  more  efficient  is  the  painting  of  the  en- 
tire surface  of  the  pharynx  with  some  concentrated  solution.  The  physician 
usually  has  to  perform  this,  although  some  patients  learn  to  do  it  for  them- 
selves. Proper  solutions  are:  Argentium  nitrate,  five  or  ten  per  cent;  tannin, 
eight  to  twenty  per  cent ;  tincture  of  iodin,  either  pure  or  diluted ;  or  iodized 
glycerin,  composed  of  pure  iodin,  parts  0.5;  iodid  of  potassium,  2;  glycerin 
20,  with  the  addition,  if  desired,  of  two  drops  of  oil  of  peppermint.  These 
applications  must  reach  all  the  diseased  surface.  If  the  nasopharynx  is  in- 
volved, the  brush  must  accordingly  be  bent  upward,  to  reach  that  region. 
For  this  a  mirror  may  be  needed.  It  is  very  important  to  make  the  applica- 
tions to  the  mucous  membrane  itself,  freed  from  any  interposing  secretions. 

In  the  treatment  of  chronic  posterior  nasal  catarrh  the  nasal  douche  (vide 
diseases  of  the  nose)  plays  an  important  part.  It  should  be  used  two  or  three 
times  a  day.  It  not  only  removes  the  collected  secretions,  but  it  is  a  means 
of  making  local  applications.     The  instrument  is  merely  a  fountain  syringe. 


494  DISEASES   OF  THE   DIGESTIVE   ORGANS 

The  nozzle  must  be  of  a  size  to  fill  the  nostril  completely.  The  force  of  the 
current  should  always  be  moderate,  and  the  patient's  head  should  be  sharply 
flexed  forAvard.  The  fluid  used — the  best  is  a  one-per-cent  solution  of  sodic 
chloric!  or  bicarbonate — must  have  about  the  temperature  of  the  body.  Other 
medicated  solutions  must  be  very  weak,  such  as  sulphate  of  zinc,  1  to  1,000. 

The  insufflation  of  powders  into  the  throat  can  be  made  through  any  small 
glass  tube  three  to  six  times  a  week.  Alum  or  tannin  may  be  used,  either 
pure  or  mixed  with  equal  parts  of  pulvls  gummosus  [P.  G.,  made  of  gum 
arabic,  3  parts;  licorice  root,  2  parts;  and  sugar,  1  part],  or  3  to  5  parts  of 
nitrate  of  silver  to  100  of  starch.  For  the  nasopharynx,  a  bent  tube  of  glass 
or  hard  rubber  is  to  be  introduced  through  the  mouth.  There  are  numerous 
"  insufflators  "  to  be  had  at  the  instrument  makers. 

Many  baths  enjoy  a  great  reputation  for  the  cure  of  chronic  pharyngitis. 
Besides  Ems,  there  are  Eeichenhall,  Kreuznach,  Salzungen;  the  cold  sulphur 
springs,  such  as  Weilbach,  and  many  others.  Good  results  are  also  achieved 
in  Kissingen  and  Marienbad,  if  these  places  are  favorable  to  the  patient's  gen- 
eral constitution. 

In  pharyngitis  sicca,  the  nasal  douche  with  a  one-per-cent  salt  solution  is 
to  be  recommended.  It  is  sometimes  also  beneficial  to  paint  the  parts  with 
solution  of  argentic  nitrate,  iodized  glycerin,  etc.  Many  irritating  influences 
which  do  harm  in  common  pharyngitis  seem  sometimes  actually  to  benefit  this 
form — such  as  smoking  and  taking  snuff. 

In  treating  the  hypertrophic  forms  of  pharyngitis  and  the  adenoid  growths, 
cauterization  with  nitrate  of  silver  suffices  for  the  milder  cases  alone.  A 
thorough  and  permanent  cure  can  be  achieved  only  by  removing  the  growths 
through  operation. 

[To  Hooper,  of  Boston,  belongs  the  credit  of  showing  that  a  radical  opera- 
tion for  the  removal  of  adenoid  growths  of  the  nasopharynx  can  safely  be 
done  under  anaesthesia.  The  blood  does  not,  as  was  feared,  run  into  the  air- 
passages,  but  either  into  the  stomach  or  outwardly.  Anaesthesia  thus  renders 
it  possible  to  scrape  away  with  the  finger  or  tear  away  with  forceps  the  hyper- 
trophied  tissue  at  one  sitting,  and  to  do  it  in  the  child  before  secondary 
changes  have  taken  place  in  the  facial  expression,  the  jaw,  the  ears,  or  the 
form  of  the  chest.] 


CHAPTEE    IV 

RETROPHARYNGEAL   ABSCESS 

Retropharyngeal  abscess  is  formed  by  a  suppurative  inflammation  of 
the  connective  tissue  lying  between  the  posterior  wall  of  the  pharynx  and  the 
spinal  column.  It  is  a  serious  disease,  although  a  rare  one.  If  unrecognized, 
it  proves  fatal  in  many  instances;  while,  if  a  correct  and  timely  diagnosis  is 
made,  the  patient  can  usually  be  easily  cured.  It  is  commonest  in  childhood, 
and  before  the  second  year.  It  almost  always  appears  as  a  primary,  acute  dis- 
ease, without  any  special  cause  being  evident.  Probably  the  agents  which 
excite  the  inflammation  penetrate  into  the  tissue  from  the  pharynx.  The  idea 
that  the  inflammation  originates  in  the  small  lymphatic  glands  which  lie  in 
front  of  the  vertebrae  lacks  proof  as  yet. 


RETROPHARYNGEAL   ABSCESS  495 

The  disease  attacks  not  only  weakly  children,  but  those  who  have  been 
perfectly  healthy  and  vigorous.  The  child  grows  restless  and  fretful,  and 
does  not  nurse  well.  Apparently,  deglutition  soon  becomes  painful,  but  one 
cannot  be  certain  about  this  except  in  older  children.  Generally^  the  respira- 
tion quickly  takes  on  a  peculiar  stertorous  character,  particularly  during 
sleep.  Mucus  collects  in  the  mouth  and  throat.  Upon  swallowing  there  is 
often  regurgitation  through  the  mouth  or  nose,  or  some  of  the  food  gets  into 
the  windpipe  and  causes  violent  coughing.  The  lymph-glands  of  the  jaws  are 
usually  somewhat  swollen,  and  the  neighboring  parts  may  seem  slightly 
^edematous.  After  a  week  or  two  the  dyspnoea  gradually  increases.  Eespira- 
tion  becomes  more  and  more  laborious,  with  loud  rattling,  and  signs  of  ste- 
nosis. The  jugular  veins  become  distended,  the  lips  cyanotic,  and  portions  of 
the  thorax  are  retracted  during  inspiration.  The  voice  is  feeble,  and  may  be 
hoarse  and  indistinct. 

The  correct  interpretation  of  these  symptoms,  which  are  common  to 
various  disorders,  requires  a  careful  examination  of  the  throat.  It  must  be 
confessed  that  this  has  its  difficulties  in  an  infant.  Still,  we  can  sometimes 
see  distinctly  a  swelling  in  the  posterior  wall  of  the  pharynx.  This  may  be 
either  in  the  median  line  or  on  one  side.  All  doubt  is  removed  by  digital  ex- 
amination, in  making  which,  however,  we  must  insert  a  wedge  between  the 
teeth,  to  avoid  being  bitten.     The  finger  detects  fluctuation. 

The  diagnosis  once  established,  the  abscess  must  be  opened  at  once.  We 
should  not  delay,  even  if  the  dyspnoea  has  not  yet  become  extreme.  To  use  the 
finger  nail  for  the  purpose,  as  has  been  recommended,  is  permissible  only  in  an 
emergency.  As  a  rule,  incision  is  made  with  a  bistoury,  of  which  all  but  the 
point  is  guarded  with  sticking  plaster.  The  left  index  finger  is  placed  upon 
the  abscess,  and  used  as  a  guide.  Meanwhile,  the  child's  head  is  kept  upright, 
and,  as  soon  as  the  cut  is  made,  bent  over  forward.  The  pus  pours  out  in  abun- 
dance. It  is  advisable  to  syringe  out  the  mouth  repeatedly  with  lukewarm 
water.  The  threatening  symptoms  vanish  almost  instantly  upon  the  escape 
of  the  pus.    Exceptionally,  the  abscess  refills  and  requires  a  second  incision. 

If  the  trouble  is  not  correctly  diagnosticated,  or  if  the  abscess  is  not  opened 
promptly,  the  patient  may  suffocate.  The  abscess,  however,  may  burst  sponta- 
neously; then  there  is  either  speedy  recovery  or  asphyxia  from  the  pus  filling 
the  larynx.  In  some  instances,  when  a  retropharyngeal  abscess  has  not  been 
properly  treated,  the  pus  has  gravitated  far  down  into  the  neck  and  posterior 
mediastinum.  The  recognition  and  incision  of  the  abscess  may  prove  very 
difficult  if  from  the  start  it  is  situated  lower  down  in  the  throat  than  usual. 

Analogous  to  this  acute  idiopathic  abscess  of  which  we  have  been  speaking 
is  the  chronic  abscess  due  to  caries  of  the  cervical  vertebras.  This  occurs  in  chil- 
dren as  well  as  adults.  Incision  of  such  abscesses  is  indicated  only  when  there 
is  danger  of  suffocation.  Because  of  their  tuberculous  character,  the  prognosis 
is,  of  course,  much  more  unfavorable  than  in  ordinary  suppurative  inflam- 
mation. 

Eetropharyngeal  abscesses  sometimes  occur  in  pyaemia  or  other  severe  acute 
infectious  diseases,  but  they  have  hardly  any  interest  except  to  the  pathologist.1' 

1  Tuberculosis  of  the  pharynx  is  spoken  of  in  the  chapter  on  Pulmonary  Tuberculosis.     New- 
growths  in  the  mouth  or  pharynx  belong  to  the  domain  of  surgery. 


496  DISEASES   OF   THE   DIGESTIVE   ORGANS 

SECTION   III 

Diseases  of  the  (Esophagus 

CHAPTEE   I 

INFLAMMATION   AND    ULCER    OF  THE    (ESOPHAGUS 

iEtiology  and  Pathology. — The  various  forms  of  oesophageal  inflammation 
and  ulceration  are  not  of  very  great  clinical  importance.  The  processes  are  sel- 
dom of  a  severe  grade,  or,  if  so,  they  are  generally  a  part  of  some  complicated 
disease,  to  which  they  seldom  contribute  prominent  symptoms.  Very  likely  the 
milder  forms  of  inflammation  occur  frequently,  but  the  symptoms  are  hardly 
ever  characteristic. 

A  simple  catarrhal  inflammation  of  the  oesophageal  mucous  membrane  may 
be  caused  by  swallowing  substances  which  are  injurious  mechanically,  chem- 
ically, or  from  their  temperature.  It  may  also  occur  in  the  general  infectious 
diseases,  such  as  typhoid  and  typhus  fevers,  and  the  acute  exanthemata.  Any 
inflammation  of  neighboring  tissues  may  extend  into  the  oesophagus.  Chronic 
catarrh  is  seen  in  heart  disease,  from  the  passive  congestion.  It  is  also  found 
in  the  vicinity  of  other  chronic  oesophageal  diseases,  particularly  cancers  and 
diverticula  (vide  infra). 

The  acute  catarrh  is  distinguished  by  not  having  the  usual  increase  of  secre- 
tion. The  epithelium  grows  spongy,  as  a  rule,  and  is  cast  off  more  rapidly  than 
usual,  so  as  to  suggest  the  name  of  a  desquamative  catarrh.  It  is  in  only  a  few 
cases  that  the  scanty  mucous  glands  become  swollen  and  look  like  papules  upon 
the  surface  of  the  membrane ;  this  form  is  called  follicular  catarrh.  In  limited 
areas  the  desquamation  may  be  complete,  giving  rise  to  small  catarrhal  erosions. 
Likewise,  the  swollen  follicles  may  break  down  into  small  follicular  ulcers. 

In  chronic  catarrh  there  is  a  moderate  increase  in  the  secretion  of  mucus, 
and  a  marked  thickening  of  the  epithelium.  In  very  protracted  cases  actual 
papillomata  may  finally  be  formed.    In  some  cases  ulcers  are  seen. 

Croupous  and  diphtheritic  inflammations  of  the  cesophagus  are  very  rare. 
We  have  already  said  that  the  specific  pharyngeal  diphtheria  frequently  ex- 
tends into  the  larynx,  but  only  exceptionally  into  the  gullet.  Still,  we  have 
ourselves  seen  in  children  several  cases  of  cicatricial  oesophageal  strictures  (vide 
infra)  subsequent  to  an  attack  of  diphtheria.  Isolated  cases  of  diphtheritic 
oesophagitis  have  also  been  seen  in  connection  with  severe  infectious  diseases, 
such  as  typhus,  typhoid,  smallpox,  cholera,  pyaemia,  and  pulmonary  tubercu- 
losis, as  well  as  in  the  course  of  Bright's  disease  and  cancer.  In  variola  it  is 
not  unusual  for  pocks  to  appear  upon  the  oesophageal  mucous  membrane. 

A  purulent,  phlegmonous  oesophagitis  now  and  then  attacks  the  submucous 
layer.  It  may  be  either  diffuse  or  circumscribed.  The  mucous  membrane  is 
dissected  up  from  the  muscular  layer  by  the  pus,  and  pushed  inward,  so  as  to 
diminish  the  lumen  of  the  oesophagus  more  or  less.  Most  of  the  cases  end  by 
the  discharge  of  pus  into  the  tube,  when  complete  recovery  may  ensue.  If 
the  mucous  membrane,  however,  has  been  extensively  undermined,  Zenker 


DILATATION   OF   THE   (ESOPHAGUS  497 

states  that  a  fissure-like  cavity  may  be  left  even  after  healing  has  taken  place. 
Its  walls  grow  smooth,  and  finally  acquire  a  layer  of  fresh  epithelium. 

Purulent  oesophagitis  is  caused  either  by  the  presence  of  foreign  bodies  in 
the  oesophagus,  or  by  purulent  inflammation  in  neighboring  parts,  as  in  glandu- 
lar abscess,  vertebral  abscess,  or  laryngeal  perichondritis.  It  has  now  and  then 
resulted  from  the  action  of  concentrated  acids  and  the  like  upon  the  mucous 
membrane. 

The  action  of  corrosive  poisons  (corrosive  oesophagitis)  is  to  cause  necrosis 
of  the  tissues,  which  in  its  turn  produces  inflammation.  The  inner  surface  of 
the  oesophagus  is  converted  into  a  rotten,  hemorrhagic,  sloughing  mass,  of  a 
dirty  gray  or  almost  black  color.  In  severe  cases  the  muscular  layer  itself 
may  be  partly  destroyed.  If  death  does  not  occur  speedily,  the  necrosed  por- 
tions come  away,  leaving  extensive  purulent  ulcers  behind.  These,  if  they  heal 
at  all,  cause  large  cicatrices  and  stenosis. 

Symptoms. — The  milder  cases,  as  we  have  stated,  produce  almost  no  dis- 
tinctive symptoms.  Possibly  there  may  be  pain  along  the  oesophagus,  or  at 
some  one  point  in  it,  during  deglutition.  In  a  more  severe  case  the  pain  may 
be  great ;  but  the  other  symptoms  are  usually  too  grave  for  this  to  excite  special 
attention.  Laborious  deglutition,  and  the  feeling  as  if  the  food  were  inclined 
to  stick  in  the  throat,  result  from  implication  of  the  muscular  layer.  A  diag- 
nosis of  the  particular  form  of  oesophagitis  is  attainable  only  when  the  aetiology 
guides  us  to  it. 

Treatment  must  be  purely  symptomatic.  No  solid  food  should  be  taken. 
The  pain  is  to  be  allayed  by  bits  of  ice  or  by  morphin. 


CHAPTEE    II 
DILATATION   OF    THE    (ESOPHAGUS 

1.     DIFFUSE   DILATATION 

Diffuse,  spindle-shaped  dilatation  of  the  oesophagus  is  observed  as  a  result 
of  organic  stricture  of  the  cardiac  orifice.  At  first  the  muscular  coat  hyper- 
trophies as  the  orifice  contracts,  and  is  able  to  overcome  the  obstruction,  so 
that  there  is  no  dilatation;  but  as  soon  as  the  muscles  are  paralyzed,  and  food 
collects  behind  the  stricture,  the  dilatation  begins  and  keeps  on  increasing. 
The  ectasis  is  greatest  at  the  lower  end  of  the  tube,  as  is  natural  from  its 
mode  of  origin,  and  gradually  diminishes  upward. 

There  have  been  a  very  few  well-substantiated  instances  of  this  diffuse 
spindle-shaped  dilatation,  without  any  demonstrable  anatomical  stenosis  of 
the  cardiac  orifice.  Their  mode  of  origin  is  still  doubtful.  At  present  most 
writers  assume  that  in  these  cases  there  exists  a  constant  abnormal  cramp  of 
the  cardia  (cardiospasm).  As  yet  there  has  been  no  certain  proof  of  this 
hypothesis.  In  favor  of  the  assumption  of  a  cardiospasm  is  the  observation 
that  the  bougie  in  these  cases  can  sometimes  be  easily  passed  into  the  stomach, 
while  at  other  times  this  is  impossible.  This  phenomenon  can  perhaps  be 
explained  by  other  kinds  of  mechanical  disturbance  at  the  lower  end  of  the 
oesophagus,  such  as  kinking,  pocket  formation,  etc.     Possibly  the  chief  factor 


498  DISEASES   OF   THE   DIGESTIVE   ORGANS 

is  a  congenital  deviation  in  the  formation  and  growth  of  the  oesophagus,  such 
as  the  development  of  a  so-called  "  proventriculus."  The  mucous  membrane 
of  the  oesophagus  is  usually  but  slightly  changed  in  these  cases,  but  the  mus- 
cularis  is  as  much  hypertrophied  as  in  genuine  stenosis  of  the  cardia. 

Actual  Cardiac  Strictures. — If  an  actual  stenosis  of  the  cardia  from  cica- 
trix or  carcinoma  is  present,  this,  and  not  the  secondary  dilatation  of  the 
oesophagus  is,  of  course,  the  real  cause  of  the  existing  dysphagia  and  the  sub- 
sequent regurgitation  of  any  ingested  food.  The  patients  themselves  often 
feel  that  food  sticks  in  the  gullet,  and  that  a  large  part  of  it  does  not  reacli 
the  stomach  at  all. 

It  is  much  more  difficult  to  explain  the  symptoms  in  diffuse  dilatations 
of  the  oesophagus  without  demonstrable  macroscopic  changes  at  the  cardia. 
The  malady  develops  very  gradually.  At  first  the  patients  complain  only  of 
indefinite  painful  sensations  at  the  sternum.  Gradually,  however,  difficulty 
in  swallowing  supervenes;  the  food  taken  does  not  reach  the  stomach  at  all,, 
or  only  a  very  small  part  of  it  does.  Very  soon  it  is  regurgitated.  Some- 
times it  remains  for  a  considerable  time  in  the  dilated  oesophagus,  and  is  ex- 
pelled only  by  straining  and  vomiting.  In  such  cases,  the  oesophageal  dis- 
ease is  sometimes  confounded  with  a  disease  of  the  stomach  (ulcer,  pyloric, 
stenosis,  etc.),  which  error  in  diagnosis  may  lead  to  incorrect  therapy.  The 
diagnosis  is  possible  only  when  the  results  obtained  by  using  the  sound  and 
by  washing  out  the  oesophagus  and  stomach  are  carefully  considered.  In  dif- 
ficult cases,  cesophagoscopy  and  the  X-ray  examination  of  the  oesophagus,  filled 
with  a  mixture  of  bismuth  and  mashed  potato,  must  be  resorted  to. 

As  soon  as  the  nutrition  is  permanently  disturbed,  there  is  loss  in  weight 
and  strength,  which  may  finally  reach  an  extreme  stage.  The  problem  facing 
the  physician  is  to  maintain  the  nutrition  by  means  of  the  stomach  tube.  If 
it  is  possible  to  introduce  the  tube  into  the  stomach,  then  the  condition  of  the. 
patient  will  be  rapidly  improved  through  the  newly  added  nourishment.  If 
for  any  reason  the  introduction  of  the  tube  into  the  stomach  is  impossible,, 
all  that  remains  to  be  done  is  rectal  feeding  {vide  infra)  (which,  after  all,, 
is  not  sufficient  for  any  length  of  time),  or  the  establishment  of  a  gastric 
fistula.  Upon  the  success  of  this  operation  and  the  nature  of  the  primary 
lesion  depends  the  ultimate  outcome  of  the  disease.  In  the  so-called  cardio- 
spasm, the  artificial  dilatation  of  the  cardia  has  been  repeatedly  practiced  with 
good  result.  A  collapsed,  small  rubber  balloon  is  introduced  into  the  cardia, 
and  gradually  inflated  with  air.  All  these  mechanical  methods  of  treatment, 
require  great  care,  if  we  do  not  wish  to  experience  unfortunate  consequences,, 
such  as  secondary  inflammation,  and  even  rupture  of  the  oesophagus,  which  I 
know  to  have  occurred  in  one  case.     [See  also  remarks  on  page  339.] 

2.     DIVERTICULA 

.ZEtiology  and  Pathology. — Circumscribed  pouches  in  the  wall  of  the- 
oesophagus  are  termed  diverticula.  They  are  divided  into  two  essentially  dis- 
tinct varieties,  according  to  their  mode  of  origin.  Zenker  has  given  them  the 
names  of  pressure  and  traction  diverticula. 

The  diverticulum  due  to  pressure  is  extremely  rare:  It  is  caused  by  pres- 
sure upon  the  mucous  membrane  from  within,  by  which  some  abnormally^ 


DILATATION   OF   THE   (ESOPHAGUS  499 

weak  spot  is  forced  outward.  All  cases  that  have  been  carefully  examined 
thus  far  have  shown  that,  histologically,  the  wall  of  the  diverticulum  is  not 
the  distended  but  otherwise  unchanged  wall  of  the  oesophagus,  but  is  com- 
posed exclusively  of  the  mucous  membrane  and  the  thickened  submucous 
coat.  We  are  therefore  obliged  to  suppose  that  the  mucous  membrane  is 
pushed  out  like  a  hernia  through  some  gap  in  the  muscular  coat.  It  is  only 
about  the  neck  of  the  diverticulum  that  any  muscular  fibers  are  found. 

The  original  factor,  therefore,  in  the  occurrence  of  a  pressure  diverticulum 
is  apparently  to  be  sought  in  some  circumscribed  lesion  of  the  muscular  coat. 
As  a  result  of  several  observations,  it  is  established  that  a  foreign  body,  stick- 
ing in  the  throat,  may  separate  some  of  the  muscular  fibers  and  push  the 
mucous  membrane  through  the  gap  thus  formed.  Or  a  severe  injury  leads  to 
a  trifling  rupture  of  the  muscular  coat,  and  then  the  food,  as  it  is  being 
swallowed,  presses  out  the  mucous  membrane  at  this  weakened  spot.  There 
are  still  many  other  cases  in  which  the  true  origin  of  the  diverticulum  re- 
mains obscure. 

As  soon,  however,  as  the  formation  of  the  pouch  has  once  begun,  there 
are  many  influences  to  make  it  grow  larger.  Each  successive  bit  of  food, 
as  it  glides  by,  presses  upon  this  yielding  and  inelastic  spot.  Gradually  a 
little  sac  is  formed,  in  which  bits  of  food  lodge.  These  exercise  a  constant 
pressure  upon  the  walls  of  the  pouch,  and  by  their  weight  drag  it  bodily  down- 
ward. The  larger  the  pouch  the  more  it  holds,  and  consequently  the  more  it 
grows.  Thus  a  pressure  diverticulum  of  the  smallest  size  originally  may 
gradually  attain  a  diameter  of  four  inches  or  more.  The  general  shape  of  the 
diverticulum  may  approach  the  hemispherical,  or  it  may  be  more  cylindrical 
or  pear-shaped. 

It  is  remarkable  that,  with  very  rare  exceptions,  these  pressure  diverticula 
are  always  situated  at  the  beginning  of  the  oesophagus,  or  rather  between  it 
and  the  pharynx,  and  almost  invariably  affect  the  posterior  wall.  The  pouch 
hangs,  therefore,  in  front  of  the  spinal  column.  It  pushes  out  through  the 
lowest  fibers  of  the  inferior  constrictor  of  the  pharynx;  and  the  feebleness  of 
this  muscle  is  apparently  a  potent  factor  in  determining  the  precise  point 
of  origin. 

The  cases  thus  far  seen  have  been  almost  all  in  men,  and  at  a  rather  ad- 
vanced age.    A  few  cases  have  occurred  in  children. 

Traction  diverticula  are  much  more  common,  but  in  most  instances  have 
little  interest  except  for  the  pathologist.  They  are  not  infrequently  found 
unexpectedly  at  the  autopsy.  Eokitansky,  and  later  Zenker,  have  given  ex- 
planations of  their  occurrence:  some  tissue,  which  has  formed  adhesions  to 
the  oesophagus,  contracts  and  gradually  pulls  out  the  oesophageal  wall  in  the 
shape  of  a  funnel.  Bronchial  glands  are  apt  to  be  the  seat  of  the  contractile 
change.  These  glands  are  situated  near  the  bifurcation  of  the  trachea,  and. 
accordingly  the  traction  diverticula  occur  oftenest  at  this  level.  There  may 
be  two  or  three  in  one  subject.  They  are  rarely  over  a  third  of  an  inch  in 
depth.  From  within,  the  mucous  membrane,  much  wrinkled  transversely,  is 
seen  to  be  drawn  toward  the  apex  of  the  diverticulum.  The  wall  of  the  latter 
consists  either  of  the  mucous  membrane  alone,  bulging  out  like  a  hernia,  or 
of  the  mucous  membrane  covered  by  the  muscular  layer.  Inasmuch  as  chil- 
dren quite  often  suffer  from  suppuration  and  caseation  of  bronchial  glands, 


500  DISEASES   OF   THE   DIGESTIVE   ORGANS 

with  subsequent  shrinkage,  we  see  why  traction  diverticula  are  frequent  in 
children. 

Clinical  History. — The  large  pressure  diverticula  always  cause  grave  symp- 
toms, for  they  obstruct  more  and  more  each  day  the  passage  of  food.  At 
first  there  is  scarcely  any  disturbance.  Gradually,  however,  deglutition  is 
impeded.  A  portion  of  the  food  lodges  in  the  pouch,  and  is  either  wholly  or 
in  part  regurgitated,  though  perhaps  not  immediately.  Decomposition  is  apt 
to  take  place  in  the  contents  of  the  diverticulum,  giving  rise  to  foulness  of 
the  breath  and  to  nausea.  The  danger  reaches  its  climax  when  the  distended 
sac  presses  sidewise  upon  the  oesophagus  and  closes  its  lumen,  so  that  no  food 
reaches  the  stomach.  After  protracted  strangling  and  vomiting,  the  material 
may  be  in  part  ejected,  and  the  patient  enabled  once  more  to  swallow. 

Of  course  the  symptoms  in  individual  cases  depend  upon  the  mechanical 
conditions  present,  and  they  may  vary  greatly.  Patients  contrive  all  sorts 
of  manipulations,  by  which  they  manage  to  get  at  least  some  portion  of  their 
food  down.  Such  individuals  may  maintain  a  tolerable  degree  of  nutrition 
for  years,  although  they  scarcely  ever  are  in  a  normal  condition.  But  at  last 
some  cause  or  other  renders  the  amount  of  food  ingested  inadequate,  where- 
upon a  rapidly  progressive  marasmus  sets  in,  and  the  patient  will  inevitably 
starve  to  death  unless  some  relief  is  afforded. 

The  most  valuable  objective  evidence  in  these  cases  is  gained  by  the  use 
of  the  oesophageal  sound.  If  the  sound  enters  the  sac  its  passage  is  impeded. 
If  it  happens  to  slip  by  the  mouth  of  the  diverticulum,  it  glides  readily  into 
the  stomach.  This  varying  result  may  sometimes  be  obtained  at  one  sitting 
by  repeated  trials,  and  is  of  the  greatest  importance  in  making  the  diag- 
nosis. 

In  some  instances  where  the  sac  was  large,  a  tumor  in  the  neck  has  been 
observed  at  one  side  of  the  trachea,  appearing  after  eating  and  disappearing 
when  the  sac  emptied  itself.  Symptoms  due  to  compression  of  the  recurrent 
and  phrenic  nerves  and  of  the  blood  vessels  have  been  noticed  in  some  cases. 

Auscultation  of  the  oesophagus  during  the  act  of  swallowing  has  been  prac- 
ticed, and  of  late  years  cesophagoscopyhas  been  used  in  the  diagnosis  of  these 
conditions.  Whether  these  methods  of  investigation  will  prove  valuable  for 
diagnosticating  diverticula,  experience  must  determine. 

The  traction  diverticula  are  usually  of  no  clinical  importance.  They  do 
not  affect  deglutition  at  all,  and  their  size  is  too  limited  to  permit  any  great 
accumulation  of  food  in  them.  There  is  but  one  way  in  which  they  are  dan- 
gerous :  the  apex  of  the  funnel  may  undergo  ulceration  and  perforation.  A 
foreign  body,  such  as  some  bit  of  food,  produces  necrosis  of  the  wall,  by  what 
is  probably  at  first  a  purely  mechanical  irritation.  The  tissue  ulcerates ;  and 
then  the  inflammation  may  gradually  progress  till  it  causes  a  severe  and 
often  fatal  illness.  The  most  frequent  event  is  perforation  into  a  bronchus, 
followed  by  the  aspiration  of  food  and  pulmonary  gangrene;  or  the  perfora- 
tion may  take  place  into  the  pleural  cavity,  exciting  an  ichorous  empyema. 
In  other  cases  the  pericardium  or  a  large  vein  has  been  perforated.  Many  a 
case  of  apparently  spontaneous  pulmonary  gangrene,  or  purulent  inflamma- 
tion of  the  anterior  mediastinum,  or  empyema,  has  been  found  at  the  autopsy 
to  have  been  brought  about  in  the  manner  above  indicated.  These  occurrences 
are  fortunately,  however,  exceptional. 


STENOSIS  OF  THE  (ESOPHAGUS  501 

Treatment. — The  only  possible  way  of  treating  the  large  pressure  diver- 
ticula successfully  is  by  operation.  If  surgical  treatmenl  cannot  be  carried 
out,  our  efforts  are  confined  to  sustaining  the  patient.  If  he  cannot  swallow, 
we  must  try  to  feed  him  through  a  tube.  As  long  as  this  is  possible,  starva- 
tion is  averted.  It  is  well  to  have  the  patient  pass  the  tube  himself.  He  will 
find  out  how  host  to  avoid  the  sac  and  reach  the  stomach.  If  food  can  no 
longer  he  given  in  this  way,  there  remain  two  alternatives:  rectal  feeding 
(vide  infra),  or  making  a  gastric  fistula.  As  to  the  Latter,  there  has  been  thus 
far  very  little  practical  experience,  because  cases  are  so  rare. 

The  traction  diverticula  admit  of  no  special  treatment.  If  the  events 
above  mentioned  occur,  we  must  endeavor  to  meet  the  indications  of  the  indi- 
vidual case. 


CHAPTER    III 
STENOSIS    OF    THE    CESOPHAGUS 

etiology  and  Pathology. — Contractions  of  the  oesophagus  occur  with  such 
relatively  great  frequency  that  they  are  the  most  important  of  all  its  disorders. 
They  originate  in  various  ways.  By  far  the  commonest  cause  is  ring-shaped 
carcinoma  of  the  tube.  The  new  growth  in  the  mucous  membrane  encroaches 
more  and  more  upon  the  lumen  of  the  oesophagus,  until  finally  it  fills  it.  Car- 
cinoma will  be  discussed  at  length  in  the  next  chapter.  We  shall  here  confine 
our  attention  to  its  purely  mechanical  action  in  causing  steno.-is. 

(Esophageal  tumors  other  than  cancer  are  very  rare.  Fibrous  peduncu- 
lated polypi  have  been  observed  a  few  times.  They  usually  originate  in  the  low- 
est portion  of  the  anterior  wall  of  the  pharynx,  hanging  down  into  the  oesopha- 
gus, which  they  may  thus  obstruct.  In  rare  cases  sarcoma  of  the  oesophagus 
has  been  observed. 

A  second  cause  of  stenosis  is  the  contraction  of  cicatrices  of  the  oesophageal 
wall.  The  most  frequent  occasion  for  this  is  the  extensive  ulceration  caused 
by  caustic  poisons,  such  as  concentrated  acids  or  alkalies.  If  the  victim  es- 
capes a  speedy  death,  he  is  almost  certain  to  have  extensive  scars  formed  in 
the  wall  of  the  oesophagus.  These  scars  radiate  irregularly  in  all  directions, 
and,  contracting,  may  almost  completely  close  the  tube. 

Ulcers  from  other  causes,  resulting  in  stenosis  due  to  the  scars  they  leave, 
are  among  the  rarities.  The  possibility  of  cicatricial  oesophageal  strictures 
subsequent  to  diphtheria  has  already  been  referred  to  (page  496).  Further, 
syphilis  has  been  the  well-established  cause  in  some  instances,  and  Quincke 
has  described  a  few  cases  in  which  there  were  ulcers  at  the  lower  end  of  the 
oesophagus  analogous  to  the  round  ulcer  of  the  stomach,  or  "  ulcer  due  to 
digestion"  (vide  infra).  These  ulcers  also  may  eventually  produce  cicatri- 
cial stenosis. 

A  third  and  rare  cause  of  stenosis  of  the  oesophagus  is  compression  from 
tumors  external  to  it.  Such  swellings  may  originate  in  the  thyroid  gland,  or 
in  the  lymph-glands  of  the  neck  or  the  anterior  mediastinum ;  or  the  swelling 
may  be  due  to  a  vertebral  abscess  or  an  aortic  aneurism.  This  form  of  stenosis 
is  seldom  extreme,  for  the  portion  of  the  tube  pressed  upon  is  usually  limited. 


502  DISEASES   OF  THE   DIGESTIVE   ORGANS 

Next  on  the  list  after  stenosis  due  to  compression  is  usually  placed  what  is 
called  intermittent  dysphagia  (dysphagia  lusoria).  This  term  is  applied  to 
the  difficulty  in  swallowing  which  is  said  to  be  caused  by  an  anomaly  in  the 
course  of  the  right  subclavian  artery.  The  artery  is  given  off  as  the  last 
branch  from  the  arch  of  the  aorta,  and  runs  toward  the  right  side  just  behind 
or  just  in  front  of  the  oesophagus.  It  seems,  however,  a  priori  improbable  that 
the  feeble  pressure  of  this  vessel  as  it  pulsates  should  impede  deglutition;  nor 
has  it  yet  been  proved  to  do  so.  It  would  be  more  natural  to  believe,  what 
was  indeed  the  original  explanation  of  the  phenomenon,  that  a  large  morsel 
of  food  passing  down  the  oesophagus  compresses  the  vessel  and  thus  excites 
uneasiness  and  palpitation ;  but  so  far  as  we  know  even  this  is  extremely  rare,, 
if  it  ever  occurs. 

Stenosis  due  to  foreign  bodies  belongs  to  surgery.  It  need  not  be  said 
that  the  clinical  symptoms  differ  greatly  in  different  cases.  Not  only  the 
obstruction,  but  also  a  possible  laceration  and  consequent  inflammation  are 
to  be  considered.  Occasionally  thrush  has  been  abundant  enough  to  cause 
pronounced  symptoms  of  stenosis. 

Above  the  point  of  stenosis,  no  matter  how  the  condition  arose,  if  only  it 
is  well  developed  and  has  lasted  a  certain  length  of  time,  the  circular  fibers 
of  the  muscular  coat  are  more  or  less  hypertrophied.  This  hypertrophy  is 
due  to  the  increased  muscular  contraction  required  to  propel  the  ingesta  down- 
ward.   In  many  cases  the  tube  is  also  diffusely  dilated  above  the  stenosis. 

Symptoms. — The  effect  of  every  oesophageal  stenosis  is  to  render  degluti- 
tion difficult.  If  the  case  is  a  mild  one,  the  patient  experiences  nothing  more 
than  a  moderate  pressure  in  the  oesophagus  upon  swallowing.  He  feels  that 
the  morsel  is  longer  than  usual  in  reaching  the  stomach.  Very  soon  he  notices 
that  solid  food  and  large  morsels  can  be  swallowed  only  with  difficulty.  Ac- 
cordingly, he  is  gradually  led  to  confine  himself  to  a  liquid  diet,  takes  small 
mouthfuls,  and  always  washes  down  any  solid  food  with  a  swallow  or  two  of 
liquid.  The  narrower  the  stenosis,  the  more  he  is  troubled.  Finally,  even 
liquids  can  be  taken  only  slowly  and  in  sips. 

It  must  not  be  thought  that  the  dysphagia  just  described  is  due  ex- 
clusively- to  the  mechanical  obstruction  of  the  lumen.  Sometimes  a  patient 
is  almost  entirely  unable  to  take  nourishment,  and  yet  at  the  autopsy  no  ade- 
quate mechanical  obstruction  is  found.  The  dysphagia  must  therefore  be  due 
to  some  lesion  of  the  muscular  coat  of  the  oesophagus.  The  impaired  con- 
tractility of  the  muscular  coat  at  the  affected  spot  is  always  a  potent  factor 
in  impeding  deglutition. 

As  soon  as  the  dysphagia  has  become  considerable  there  is  usually  regurgi- 
tation of  food.  At  first  only  a  portion  of  the  food  comes  up,  but  at  last  all 
of  it.  If  the  tube  has  become  dilated  above  the  stenosis,  food  may  collect  for 
some  hours,  and  then  be  regurgitated,  mixed  with  an  abundance  of  very 
tenacious  mucus.  We  saw  a  case  of  this  kind  in  which  the  patient  could  fill 
the  sac  above  the  stricture  with  quite  a  large  amount  of  fluid  without  a  drop 
reaching  the  stomach.  If  he  bent  his  head  sharply  forward,  the  collected 
fluid  would  run  out  again  through  his  mouth.  It  was  not  until  the  pouch 
was  completely  filled  that  a  small  amount  of  liquid  would  trickle  through  the 
stenosis  into  the  stomach. 

Although  the  dysphagic  symptoms  above  described  generally  imply  oeso- 


STENOSIS   OF   THE   (ESOPHAGUS  503 

phageal  stenosis,  the  diagnosis  cannot  be  really  established  without  using  a 
sound.  Upon  introducing  this,  it  is  usually  easy  to  detecl  the  obstacle,  which 
may  either  allow  the  instrument  to  pass  with  a  noticeable  jerk,  or  else  prevenl 

its  further  progress.  By  measuring  the  length  of  the  portion  introduced  be- 
fore the  stenosis  is  reached  we  can  learn  its  position.     On  the  average,  the 

entire  distance  from  the  teeth  to  the  cardiac  sphincter  is  in  adults  16 
inches  (40  cm.)  ;  from  the  teeth  to  the  beginning  of  the  oesophagus,  6  inches 
(15  cm.);  and  consequently  the  length  of  the  hitler  is  about  1"  inches  (25 
cm.).  If  we  succeed  in  passing  a  smaller  sound  through  the  stricture,  the 
feeling  as  we  move  it  back  and  forth  will  give  us  some  idea  of  the  length  of 
the  stenosis,  or  will  demonstrate  the  existence  of  several  lying  one  below  the 
other,  etc.  If  the  end  of  the  sound  can  be  moved  aboul  very  freely  above  the 
stenosis,  we  may  conclude  that  the  tube  is  dilated  there. 

Hamburger  has  employed  auscultation  of  the  oesophagus  for  diagnostic- 
purposes.  If  we  listen  behind,  to  the  left  of  the  upper  dorsal  vertebrae  during 
deglutition,  we  hear  a  gurgling  sound,  due  to  the  act  of  swallowing,  extending 
down  the  tube  to  the  stenosis,  but  no  farther.  Then  come  all  sorts  of  sounds, 
some  of  them  caused  by  the  fluid  trickling  slowly  through  the  narrow  part, 
and  some  caused  by  regurgitation.  In  general,  the  results  obtained  by  aus- 
cultation are  rather  variable  and  uncertain,  and  it  is  therefore  little  used  in 
practice. 

(Esophagoscopjr,  though  technically  difficult  of  application,  has  neverthe- 
less been  frequently  very  successful.  In  many  cases  the  X-ray  examination 
of  the  oesophagus,  filled  with  a  mixture  of  bismuth  and  mashed  potato,  gives 
very  clear  pictures.  The  retention  of  the  pasty  mass  above  the  stenosis  is 
distinctly  seen.  Fluoroscopy  after  the  swallowing  of  a  "bismuth  pill"  (a 
gelatin  capsule  filled  with  the  subnitrate  of  bismuth)  also  gives  important 
information.  It  is  possible  closely  to  follow  on  the  fluoroscopic  screen  the 
descent  of  the  pill,  its  arrest,  etc. 

Having  established  the  fact  of  the  existence  of  a  stenosis,  we  have  next  to 
determine  its  nature,  which  is  our  chief  guide  to  prognosis  and  treatment.  In 
certain  instances  the  history  of  the  case  gives  us  the  needed  information. 
The  diagnosis  of  cicatricial  stricture  can  hardly  be  made  unless  the  patient 
himself  tells  us  of  being  burned  or  injured  by  caustic  poisons.  The  previous 
history  is  likewise  of  great  importance  if  the  stenosis  be  due  to  foreign  bodies, 
to  diphtheria,  or  to  syphilis.  If  no  decisive  setiological  factor  can  be  elicited, 
we  must  carefully  examine  the  neck  and  thorax,  with  regard  to  the  possible 
existence  of  a  swelling  compressing  the  oesophagus.  When  an  aortic  aneurism 
has  acted  in  this  way,  a  rhythmical  movement  has  sometimes  been  communi- 
cated to  the  free  end  of  a  sound  introduced  as  far  as  the  stenosis.  If  the 
physical  examination  does  not  reveal  a  compressing  tumor,  and  particularly 
if  the  stenosis  has  developed  gradually  and  in  an  elderly  person,  we  are  almost 
compelled  to  assume  that  there  is  cancer  of  the  oesophagus.  This  is,  after 
all,  by  far  the  most  frequent  cause  of  oesophageal  stricture.  If  the  new  growth 
has  ulcerated,  a  little  portion  of  it  may  adhere  to  the  end  of  the  probe,  and,  on 
microscopic  examination,  render  our  diagnosis  of  carcinoma  certain.  CEso- 
phagoscopy  is  also  a  means  of  making  a  certain  diagnosis. 

The  prevailing  characteristic  in  stenosis  of  the  oesophagus  is  inanition, 
increasing  as  the  dysphagia  increases.     The  patient  gets  to  be  very  much 


504  DISEASES  OF  THE  DIGESTIVE  ORGANS 

emaciated,  and  so  feeble  that  he  cannot  leave  his  bed.  The  temperature  is 
subnormal;  for  weeks  it  keeps  at  95°  to  97°  F.  (35°  to  36°  C).  The  pulse 
grows  very  small  and  slow,  being  40  to  60  per  minute.  The  heart  sounds  are 
soft.  Bespiration  is  superficial  and  slow;  and  toward  the  close  of  life  short 
pauses  occur  after  expiration,  before  inspiration  begins.  The  stomach  and 
intestines  are  so  empty  that  the  abdomen  is  very  concave,  while  the  abdominal 
walls  usually  feel  tense  and  resistant.  In  all  cases  when  the  nature  of  the 
stenosis  precludes  the  possibility  of  cure  or  improvement,  death  results  from 
increasing  exhaustion,  the  lamp  of  life  gradually  nickering  out. 

Prognosis  and  Treatment. — In  prognosis  the  main  factor  is,  of  course,  the 
nature  of  the  stenosis.  If  it  is  due  to  foreign  bodies  or  to  cicatrices,  it  may 
be  completely  cured.  In  stenosis  from  other  causes  it  is  often  possible  to 
produce  considerable  improvement,  at  least  temporarily.  The  final  result 
must  be  confessed  to  be  usually  unfavorable,  as  we  should  expect  from  the 
nature  of  the  original  trouble. 

The  treatment  is  chiefly  mechanical.  We  shall  not  speak  of  operations 
for  the  removal  of  new  growths,  etc.  What  we  do  refer  to  is  a  methodical 
and  gradual  dilatation  of  the  stricture.  Its  results  are  sometimes  brilliant, 
particularly  in  cicatricial  stenosis.  Other  varieties,  such  as  the  stenosis  from 
cancer,  may  sometimes  undergo  considerable  though  but  temporary  improve- 
ment with  this  treatment. 

The  best  instrument  to  employ  is  the  flexible,  so-called  English,  oesophageal 
bougie.  It  is  made  in  all  sizes.  If  the  stenosis  is  very  narrow  indeed,  we 
may  have  to  resort  to  catgut  at  first.  Whalebone  bougies,  with  olive-shaped 
ivory  tips  of  various  sizes  to  screw  on  the  end,  are  also  good,  except  that,  being 
stiff er,  there  is  more  danger  in  using  them.  For  introduction  of  the  bougie, 
the  patient  should  be  seated,  with  the  head  slightly  extended  backward.  The 
first  two  fingers  of  the  left  hand  are  introduced  into  the  throat  and  guide  the 
instrument,  previously  Avell  oiled,  over  the  back  of  the  tongue  and  the  epiglot- 
tis into  the  oesophagus.  Of  course,  no  violence  must  be  used.  Otherwise  a 
perforation  might  occur  if  there  were  a  soft,  broken-down  cancer,  or  an  aortic 
aneurism.     However,  such  a  misfortune  is  very  exceptional. 

The  use  of  the  bougie  is  almost  invariably  beneficial  if  the  stricture  can  be 
passed.  The  patient  generally  finds  that  he  can  swallow  easier  than  before, 
and  will  himself  request  a  repetition  of  the  performance.  If  the  patient  is 
an  intelligent  person,  it  is  advisable  to  have  him  introduce  the  bougie  himself. 
Patients  often  acquire  even  greater  skill  with  it  than  the  physician  has.  The 
bougie  should  be  passed  regularly  once  a  day,  or,  at  most,  twice  daily;  and 
in  favorable  cases  we  shall  be  able  gradually  to  increase  the  size.  If  so,  the 
symptoms  speedily  abate,  and,  with  the  increased  ingestion  of  food,  the  pa- 
tient gains  flesh  very  fast. 

If  the  stenosis  is  extreme,  and,  although  it  admits  the  bougie,  does  not 
allow  of  sufficient  nourishment,  we  must  pass  a  tube  into  the  stomach  through 
which  to  introduce  liquid  food.  Milk  is  the  best  food  to  choose.  Raw  eggs, 
sugar,  wine,  etc.,  may  be  mixed  with  it.  The  various  infants'  foods  and  the 
artificial  proteid  preparations  are  also  excellent.  Their  consistence  is  favor- 
able for  the  purpose,  and  they  supply  a  considerable  amount  of  nourishment 
in  a  small  bulk.  Until  recently  the  sounds  and  dilators  employed  in  stenosis 
of  the  oesophagus  have  been  usually  introduced  by  the  mouth,  but  of  late 


CANCER  OF  THE  (ESOPHAGUS  .",()." 

the  practice  has  been  constantly  growing  of  treating  stenosis  through  an  arti- 
ficial opening  in  the  oesophagus  or  stomach.  Mechanical  dilatation  can  thus 
be  accomplished  with  much  greater  rapidity  and  completeness.  In  the  surgical 
wards  in  Erlangen  admirable  results  have  been  obtained  by  U3ing  sounds  after 
cesophagotomy  in  eieatrieial  stenosis;  whereas  in  carcinoma  of  the  cesophag 
the  improvement  is,  of  course,  merely  temporary,  although  the  symptoms  are 
greatly  alleviated.  Further  particulars  with  regard  to  the  surgical  treatment 
of  oesophageal  stenosis  are  to  be  sought  in  text-books  on  surgery.  [See  also 
remarks  on  page  339.] 

Thiosinamin  may  be  considered  in  the  treatment  of  the  eieatrieial  stenoses 
of  the  oesophagus.  A  fifteen-per-cent  alcoholic  solution  is  used,  and  about 
1  gr  (gm.  0.05)  of  thiosinamin  is  injected  every  other  day,  subcutaneously, 
into  the  front  of  the  chest.  The  cicatrices  are  supposed  to  become  so  dilatable 
that  the  introduction  of  even  large  bougies  is  easy,  and  thus  a  complete 
recovery  may  be  brought  about.  Considering  the  experience  to  date,  further 
trials  of  this  interesting  remedy  are  certainly  indicated. 

Finally,  we  desire  to  append  a  few  remarks  as  to  the  nourishment  of 
patients  by  enemata,  to  which  we  are  particularly  apt  to  have  recourse  in 
cases  of  oesophageal  disease. 

Brilliant  results  are  never  to  be  expected  from  rectal  feeding.  It  is  indeed 
probable  that  life  may  be  by  this  means  somewhat  prolonged,  but  not  indefi- 
nitely. The  moral  effect,  however,  is  very  valuable,  when  the  patient  could 
otherwise  receive  no  nourishment  whatever.  The  sufferer  feels  that  some- 
thing is  being  done  to  avert  absolute  starvation.  The  simplest  materials 
for  the  nutrient  enemata  are  milk,  solutions  of  grape  sugar,  eggs,  albuminous 
preparations,  and  the  like ;  to  which  we  may  add  pepsin  and  pancreatin  in 
the  hope  of  promoting  absorption.  Before  every  nutrient  enema,  the  rectum 
should  be  cleansed  by  an  enema  of  plain  water.  Too  large  an  amount  ought 
not  to  be  given  at  one  time,  say  about  2  oz.  (gm.  50),  and  the  fluid  must  be 
raised  to  about  the  temperature  of  the  body.  [The  limit  in  quantity  set  by 
the  author  is  smaller  than  many  patients  can  retain.  If  the  fluid  is  injected 
gently  and  slowly,  4  to  8  oz.  may  be  administered  every  six  hours,  and  cases 
are  on  record  of  patients  retaining  even  16  oz.  The  rectum  seems  capable 
of  a  certain  amount  of  training  in  this  regard,  so  that  the  amount  given  may 
eventually  be  greater  than  at  first.  Unusual  irritability  may  be  diminished 
by  adding  to  the  enema  about  5  minims  of  laudanum.] 


CHAPTEE    IV 


CANCER   OF    THE    OESOPHAGUS 


iEtiology  and  Pathology. — Cancer  is  the  most  important  and  most  fre- 
quent affection  of  the  oesophagus.  We  have  already  mentioned  in  the  preceding 
chapter  that  often  stenosis  is  the  result  of  carcinoma  in  the  oesophageal  walls. 

Little  is  known  about  the  astiology.  It  has  been  often  maintained  that 
mechanical,  chemical,  or  thermic  irritation  of  the  mucous  membrane  may 
result  in  the  development  of  cancer;  but  this  is  not  certain.  It  receives  some 
support  from  the  remarkably  frequent  occurrence  of  oesophageal  cancer  in 
hard   drinkers.     Now  and  then  the  patient  himself  will   allege  a  perfectly 


506  DISEASES   OF  THE   DIGESTIVE   ORGANS 

definite  cause  for  his  disease,  such  as  the  lodging  of  a  foreign  body,  or  the 
swallowing  of  a  very  large  or  very  hot  morsel.  Still,  it  is  hardly  possible  in 
any  particular  case  to  decide  how  much  value  such  statements  have.  Car- 
cinoma may  sometimes  develop  in  the  scar  of  an  old  ulcer.  This  is  of  interest 
when  we  recall  the  similar  fact  in  regard  to  gastric  carcinoma   (vide  infra). 

(Esophageal  cancer  follows  the  general  rule  in  being  most  frequent  in 
elderly  people — somewhere  between  forty  and  sixty  years  of  age.  The  male  sex 
is  decidedly  more  often  attacked  than  the  female. 

As  we  might  expect  from  the  histological  character  of  the  epithelium 
lining  the  oesophagus,  primary  cancer  here  is  invariably  composed  of  pavement 
cells.  The  new  growth  may  be  either  hard,  firm,  and  fibrous,  or  it  may  be 
soft,  succulent,  and  but  scantily  supplied  with  connective  tissue.  The  first 
variety  corresponds  to  the  "  scirrhus "  of  older  writers,  and  the  second  to 
"  medullary "  cancer.  Usually  the  new  formation  encircles  the  entire  tube 
like  a  ring,  extending  three  to  ten  centimeters  longitudinally.  Exceptionally 
a  still  larger  portion  of  the  oesophagus  is  involved,  sometimes  almost  all  the 
mucous  membrane.  The  tumor  is  usually  seated  in  the  lower  and  middle 
thirds  of  the  oesophagus,  being  much  rarer  above. 

Symptoms  and  Complications. — In  the  great  majority  of  cases  the  symp- 
toms are  those  of  a  gradually  increasing  stenosis,  with  its  results.  We  may 
therefore  refer  to  the  preceding  chapter  for  most  of  the  particulars.  There 
are,  however,  exceptional  cases  in  which  the  carcinoma  is  flat  and  entails  no 
dysphagia,  or  so  little  that  oesophageal  trouble  may  not  be  suspected.  We  have 
repeatedly  seen  cases  of  extensive  secondary  hepatic  cancer,  or  of  pulmonary 
gangrene  (vide  infra),  in  which  the  real  primary  disease  was  a  flat  cancer 
of  the  oesophagus,  which  gave  no  clinical  signs  of  its  existence,  and  was  there- 
fore not  diagnosticated. 

It  is  characteristic  of  the  stenotic  symptoms  produced  by  oesophageal  cancer 
that  sometimes  a  considerable  and  apparently  spontaneous  amelioration  oc- 
curs. This  is  because  of  a  superficial  ulceration  of  the  new  groAvth.  The 
tumor  is  transformed  into  an  ulcer,  and  one  can  easily  understand  how  this 
may  occasion  a  temporary  improvement  in  deglutition.  Not  infrequently, 
small  hemorrhages  may  occur  from  these  ulcerations. 

Important  clinical  symptoms  may  result  from  conditions  secondary  to  the 
new  growth.  The  cancer  may  extend  to  neighboring  organs.  Not  infrequently 
the  cardiac  extremity  of  the  stomach  is  thus  involved.  Sometimes  such  a 
tumor  may  be  felt  in  the  epigastrium;  but  in  most  cases  there  is  nothing 
to  indicate  that  the  stomach  is  attacked. 

The  neighboring  parts  of  the  trachea  or  bronchi  are  sometimes  affected, 
and  important  symptoms  result  from  such  a  complication.  If  perforation 
occurs,  there  is  a  pronounced  irritative  cough  almost  every  time  the  patient 
takes  food,  and  an  almost  certain  result  is  the  inhalation  of  food  or  of  decay- 
ing bits  of  the  tumor,  with  consequent  pulmonary  gangrene,  and,  as  a  rule, 
speedy  death.  Perforation  of  the  pleura  with  putrid  pleuritis  has  also  been 
•observed.  The  pericardium  and  the  aorta  may  likewise  be  attacked.  A  few 
instances  are  known  in  which  the  vertebra?  have  been  involved,  the  spinal  cord 
compressed,  and  paraplegia  thus  induced.  We  have  ourselves  seen  one  such  case. 

Quite  frequently  the  left  recurrent  nerve  is  affected,  and  a  paralysis  of  the 
vocal  cords  is  produced,  which  can  be  detected  by  the  laryngoscope.     This 


RUPTURE  OF  THE  (ESOPHAGI  8  507 

nerve  lies  so  close  to  the  oesophagus  that  it  is  peculiarly  exposed  to  injury 
from  the  new  growth  itself,  or  from  any  inflammatory  process  which  may 
be  se1  up  around  it. 

Metastatic  cancer  in  distant  organs  is  not  infrequent.  It  attack-  mosl  often 
the  liver;  the  lungs,  kidneys,  pancreas,  hones,  and  brain  are  also  liable  to  it. 

Pulmonary  gangrene  must  bo  mentioned  as  a  relatively  frequent  complica- 
tion, and  one  which  has  serious  consequences.  We  have  already  stated  that 
it  may  result  from  perforation.  Even  without  actual  perioral  ion,  an  infection 
of  the  air-passages  may  take  place.  A  still  more  frequent  cause  of  pulmonary 
gangrene  is  the  inspiration  of  decaying  masses  vomited  or  regurgitated. 

Clinical  History,  Termination,  Prognosis,  and  Treatment. — The  diseae 
incurable.  Operative  removal  lias  never  been  successful,  notwithstanding 
repeated  attempts  in  this  direction.  [Recently  attempts  at  radical  operation 
for  malignant  growths  situated  in  the  lower  and  more  accessible  portion  of 
the  oesophagus  have  been  made  by  Willy  Meyer,  of  New  York,  and  others, 
with  the  employment  of  an  air-pressure  apparatus.  Although,  thus  far,  the 
results  have  not  been  successful,  the  prospect  for  a  radical  cure  of  an  early 
case  is  very  promising.]  The  entire  duration  of  the  disease  seldom  exceeds  a 
year,  or  a  year  and  a  half.  At  the  end  of  this  period  the  patient  dies  either 
from  lack  of  nourishment  or  as  a  result  of  some  one  of  the  complications  above 
enumerated.  Treatment  is  purely  symptomatic.  Temporary  improvement 
may  be  obtained  by  mechanical  treatment  of  the  stenosis.  A  gastrostomy  is 
indicated  when  the  patient  is  no  longer  able  to  take  nourishment  by  mouth. 


CHAPTEE   V 


RUPTURE    OF    THE    (ESOPHAGUS 

Medical  literature  records  a  small  number  of  cases  which  prove  that  the 
sudden  rupture  of  the  oesophagus  in  persons  previously  perfectly  well  is  pos- 
sible, although,  of  course,  very  rare.  The  first  and  most  famous  instance  was 
described  by  Boerhaave  in  1724. 

The  symptoms,  according  to  the  observations  thus  far  reported,  usually 
commence  with  sudden  nausea  and  vomiting,  during  or  shortly  after  a  hearty 
meal.  There  is  simultaneously  an  extreme,  general  collapse.  There  is  pallor 
of  the  face  and  extremities,  cold  perspiration,  and  an  extremely  feeble  pulse. 
Sometimes  the  patient  feels  a  sudden  darting  pain  in  the  chest.  Almost 
invariably  an  extensive  emphysema  overspreads  the  neck  and  thorax.  Death 
results  in  a  few  hours,  or  at  latest  in  a  few  days. 

The  autopsy  reveals  a  tear  in  the  oesophagus,  invariably  situated  in  its 
lower  half.  It  may  be  five  centimeters  long,  and  it  is  almost  always  longi- 
tudinal. Food  has  usually  escaped  into  the  surrounding  tissues,  in  which 
case  a  secondary  purulent  inflammation  exists,  if  death  was  not  immediate. 

Zenker  has  attempted  to  explain  this  remarkable  phenomenon  by  a  sup- 
position that  cesophagomalacia  always  precedes  these  so-called  spontaneous 
ruptures.  The  cause  of  this  softening  of  the  oesophageal  walls  is  perhaps  the 
action  of  gastric  juice  escaping  into  the  tube  and  attacking  a  surface  which, 
through  some  temporary  disturbance  in  the  circulation,  has  lost  its  normal 
powers  of  resistance. 


508  DISEASES  OF  THE   DIGESTIVE   ORGANS 

CHAPTEE    VI 
NEUROSES    OF    THE    OESOPHAGUS 

1.  Spasm  of  the  (Esophagus. — In  rare  instances  oesophageal  disturbances 
are  observed,  which  appear  to  result  from  spasmodic  contraction  of  its  muscu- 
lar coat.  Nervous  and  lrysterical  subjects  are  particularly  apt  to  present 
temporarily  the  symptoms  of  extreme  stenosis,  for  which  there  is  no  ana- 
tomical basis.  Such  cases  are  termed  "  spastic  stenosis  "  of  the  oesophagus, 
or  "  cesophagismus."  It  is,  of  course,  possible  that  there  may  exceptionally 
be  some  real  lesion  at  the  foundation  of  the  trouble,  and  that  the  spasm  is. 
the  reflex  result  of  an  ulcer  or  inflammation  affecting  the  oesophagus.  It 
is  even  affirmed  that  the  reflex  influence  may  sometimes  originate  in  distant 
organs,  such  as  the  uterus;  but  the  exact  nature  of  these  reflex  spasms  is 
at  present  exceedingly  obscure  (see  chapter  on  Hysteria).  The  dysphagia 
is  usually  attended  by  a  painful  sense  of  constriction  in  the  throat  and  chest. 
The  bougie  comes  upon  an  obstruction,  which  usually  soon  yields.  This 
circumstance,  that  when  the  spasm  relaxes  it  is  possible  to  introduce  the 
bougie  without  any  difficulty,  confirms  the  diagnosis.  Other  important  fac- 
tors are,  the  character  of  the  symptoms  as  a  whole  and  the  other  attendant 
nervous  and  hysterical  disturbances.  Some  authors  also  explain  the  "  globus 
hystericus  " — that  feeling  as  if  a  lump  were  passing  up  or  down  in  the  throat 
and  chest — as  a  spasm  of  the  oesophagus. 

2.  Paralysis  of  the  (Esophagus. — Of  this  subject  we  have  little  accurate 
knowledge.  It  is  not  improbable  that  an  extensive  bulbar  paralysis,  affecting 
the  muscles  of  the  pharynx  and  larynx,  may  sometimes  involve  the  oesophagus ; 
although  such  a  disturbance  hardly  ever  gives  rise  to  prominent  symptoms  in 
this  disease.  Ziemssen  asserts  that  sometimes  the  oesophagus  seems  to  partici- 
pate in  post-diphtheritic  paralysis  when  extensive. 


SECTION   IV 
Diseases  of  the  Stomach 

CHAPTEE   I 

BRIEF  PRELIMINARY  REMARKS  ON  THE  EXAMINATION  OF  THE  GASTRIC 

CONTENTS  x 

When  a  disease  of  the  stomach  exists,  we  have  the  subjective  symptoms  to 
consider,  such  as  anorexia,  eructations,  vomiting,  and  gastric  pain,  together 

1  Complete  particulars  with  regard  to  the  methods  of  examining  the  gastric  contents  cannot 
be  given  here,  but  they  may  be  found  in  the  following  works:  Ewald,  "  Klinik  der  Verdauungs- 
krankheiten  " ;  Boas,  "  Diagnostik  und  Therapie  der  Magenkrankheiten  " ;  Leo,  "  Diagnostik  der 
Krankheiten  der  Verdauungsorgane";  Riegel,  "  Erkrankungen  des  Magens,  in  Nothnagel's 
Handbuch,"  etc. 


EXAMINATION   OF  THE   GASTRIC   CONTENTS  509 

with  the  external  physical  signs  obtained  by  inspection  and  palpation,  such 
as  tenderness,  distention,  peristaltic  motion,  swelling,  and  tumors;  and  we 
also  have  for  our  guidance  an  examination  of  the  stomach  and  the  stomach 
contents.  The  procedure  was  introduced  by  Leube,  followed  by  Ewald,  Boas, 
Kiegel,  and  many  others.  It  is  carried  out  by  menus  of  the  stomach  tube, 
and  is  now  universally  employed  among  physicians,  for  in  fact  its  results  are 
so  important  and  decisive  with  regard  to  diagnosis,  that  an  examination  of 
this  sort  is  at  the  present  day  indispensable  in  any  severe  case  of  persistent 
gastric  trouble.  The  inconvenience  of  the  investigation  for  the  patient  is 
comparatively  slight,  especially  now  that  a  soft  and  yielding  tube  (  Xelaton), 
or  the  so-called  Jacques'  patent  rubber  tube,  is  employed.  This  should  have 
free  apertures  at  its  lower  extremity,  and  it  is  introduced  into  the  stomach 
in  the  following  manner:  The  tube  is  moistened  with  water,  put  into  the 
patient's  mouth,  and  passed  backward  over  the  base  of  the  tongue,  and  he 
is  told  to  swallow  it,  as  it  were;  the  physician  at  the  same  time  aids  by  push- 
ing the  tube,  but  he  does  not  introduce  his  finger  into  the  patient's  mouth. 
In  this  way  it  is  almost  always  easy  to  introduce  the  instrument  into  the 
oesophagus,  and  so  into  the  stomach.  Most  patients,  if  the  tube  has  to  be 
employed  frequently,  soon  learn  to  guide  it  themselves.  Formerly  a  wire 
was  placed  inside  the  tube  so  as  to  stiffen  it  for  introduction,  but  this  is 
ordinarily  useless,  if  not  a  hindrance. 

If  the  tube  has  been  introduced  into  the  stomach,  and  we  wish  to  obtain 
a  portion  of  the  contents  of  that  organ  for  examination,  it  can,  in  most  cases, 
be  got  by  simple  "  expression."  If  the  patient  makes  his  abdominal  muscles 
tense  ("presses"),  or  if  he  makes  a  few  slight  efforts  to  vomit,  there  is  usu- 
ally a  sufficient  amount  of  the  gastric  contents  expressed  through  the  tube  into 
a  beaker  held  to  receive  it.  This  portion  of  the  gastric  contents  is  filtered, 
and  the  filtrate  subjected  to  examination.  If  we  wish  to  empty  the  stomach 
completely  ("rinse  it  out"),  the  upper  end  of  the  inserted  tube  is  connected, 
by  means  of  a  short  piece  of  glass  tubing  with  a  longer  rubber  tube  con- 
nected at  its  other  end  with  a  large  glass  funnel  which  holds  about  a  liter  of 
water.  If  warm  water  is  poured  into  the  funnel,  and  this  is  alternately  raised 
and  lowered,  we  shall  eventually  entirely  empty  the  stomach  (see  Fig.  70).  It 
is  advisable  to  insert  a  short  bit  of  glass  tubing  in  the  rubber  tube  (fenestra), 
so  as  to  observe  whether  the  fluid  runs  well  in  either  direction.  Kussmaul 
originally  employed  a  "  stomach  pump  "  for  rinsing  out  the  stomach,  but  this 
has  been  quite  universally  abandoned  for  the  simple  siphon  apparatus  sug- 
gested by  Hegar. 

By  using  the  stomach  tube  we  are  readily  enabled  to  settle  the  following 
important  points :  First,  the  chemical  and  other  constituents  of  the  gastric 
juice,  or  contents  (the  secretory  activity  of  the  stomach) ;  second,  the  motor 
activity  of  the  stomach ;  and  third,  the  size  and  position  of  the  organ. 

1.  General  Nature  of  Gastric  Contents. — Before  we  attempt  a  more  exact 
chemical  analysis  of  the  gastric  contents,  we  should  first  make  a  general  in- 
spection of  the  entire  amount  which  has  been  obtained  by  the  stomach  tube. 
The  macroscopic  differences  in  the  subdivision  of  the  food  are  in  themselves 
very  striking.  If  the  total  gastric  contents  is  changed  into  a  finely  granular 
mass,  this,  as  a  rule,  points  to  a  satisfactory  peptic  quality  of  the  gastric  juice 
and  a  normal  HC1  content.     In  anacidity  of  the  gastric  juice,  the  food  is 


510 


DISEASES   OF  THE   DIGESTIVE   ORGANS 


found  in  large  pieces,  just  as  it  has  been  swallowed.  In  such  cases,  the  open- 
ing of  the  tube  is  more  easily  occluded  than  it  is,  for  example,  in  cases  of 
hypersecretion,  where  the  entire  gastric  contents  are  changed  into  a  fine  pap. 
The  demonstration  of  the  presence  of  profuse,  stringy  mucus  in  the  gastric 
contents  is  likewise  of  importance.  This  can  be  easily  recognized  by  pouring 
the  contents  from  one  vessel  into  another.    If  there  has  been  gaseous  fermen- 


Fig.  70. — Method  of  washing  out  the  stomach.     (Erlangen  Medical  Clinic.) 


tation,  the  gastric  contents  present  a  foamy  appearance.  On  standing,  such 
gastric  contents  separate  into  three  layers :  an  upper  layer  of  foam,  a  mid- 
dle of  fluid,  and  a  bottom  layer  of  more  solid  particles.  We  must  look  very 
carefully  for  the  possible  presence  of  blood  (vide  infra).  The  odor  of  the 
gastric  contents  is  also  important.  Fatty  acids  are  usually  readily  recognized 
by  their  rancid  odor.  Also  in  putrid  decomposition,  which  occurs  frequently 
in  carcinoma,  the  odor  enables  us  to  recognize  the  condition.     In  gaseous 


EXAMINATION   OF  THE   GASTRIC   CONTENTS  511 

fermentation  there  is  a  slightly  pungenl  odor  of  carbon  dioxid  and  aromatic 

substances. 

We  shall  add  here  a  few  remarks  on  the  microscopic  examination  of  the 

gastric  contents.  This  enables  us,  first  of  all,  to  recognize  Food  remnants. 
With  profuse  HC1  secretion  the  meat  is  well  digested,  but  there  are  still 
many  starch  granules  present.  On  the  other  hand,  with  anacidity  the  diges- 
tion of  albumen  suffers  most.  We  often  find  fermentation  produces  yeast 
molds,  long-extended  bacilli  of  lactic-acid  fermentation,  or  sarcina;  (vide 
infra).  Finally,  we  occasionally  see  red  blood  corpuscles,  leucocytes,  epithelial 
cells,  or  tumor  particles.  The  diagnostic  significance  of  all  these  findings  is 
obvious. 

2  Free  Hydrochloric  Acid,  Pepsin,  and  Lactic  Acid.  Constituents  of  the 
Gastric  Juice. — In  a  healthy  person  the  stomach  is  almost  completely  empty  in 
the  morning  before  breakfast — i.e.,  some  ten  or  twelve  hours  after  the  pre- 
ceding evening  meal.  If  we  introduce  the  stomach  tube  we  obtain,  therefore, 
by  expression  either  nothing  at  all  or  a  very  small  amount  of  watery  mucus, 
of  neutral  reaction.  If  this  fluid  contains  a  little  hydrochloric  acid,  this  is 
not  necessarily  anything  abnormal,  but  if  there  is  a  large  amount  of  acid 
fluid  in  the  fasting  state,  disease  is  indicated.  The  healthy  stomach  contains 
in  the  morning  few  vestiges  of  the  food  swallowed  the  day  before.  If  we 
pour  in  some  water,  this  is  returned  almost  perfectly  clear.  If  now  the  sub- 
ject of  examination  eats  a  so-called  test  breakfast,  consisting  of  an  ordinary 
roll  and  a  large  cup  of  weak  tea,  at  once  the  stomach  begins  to  secrete  its 
peculiar  juice.  If  the  stomach  tube  is  introduced  an  hour  after  a  test  break- 
fast has  been  taken,  and  a  sufficient  amount  of  the  stomach  contents  is  ex- 
pressed and  filtered,  we  shall  obtain  a  fluid  of  acid  reaction,  and,  under 
normal  conditions,  invariably  containing  free  hydrochloric  acid  uncombined 
with  albumen.  It  is  the  comparatively  small  amount  of  the  test  breakfast 
which  makes  it  most  suitable  for  the  determination  of  the  important  question, 
whether  the  stomach  secretes  hydrochloric  acid  in  a  satisfactory  manner.  If 
we  introduce  into  the  stomach  a  larger  amount  of  food  ("test  meal/'  vide 
infra)  there  will,  indeed,  in  most  cases,  be  free  hydrochloric  acid  after  one 
or  two  hours,  but  the  amount  of  albuminous  material  present  is  so  great  that 
even  under  normal  circumstances  all  the  hydrochloric  acid  secreted  is  taken 
up  by  the  albuminous  substances,  and  consequently  there  is  no  hydrochloric 
acid  to  be  discovered  by  our  ordinary  chemical  tests.  If,  on  the  other  hand, 
we  do  not  find  any  free  hydrochloric  acid  in  the  gastric  contents,  or,  at  any 
rate,  merely  doubtful  traces  of  it,  an  hour  after  the  test  breakfast,  this  con- 
dition is  termed  anacidity,  or  subacidity,  and  it  must  be  regarded  as  ab- 
normal, particularly  if  repeated  examination  leads  to  the  same  result.  The 
term  acidity  in  this  connection  relates  to  the  hydrochloric  acid.  Even  if  this  is 
absent  it  is  perfectly  possible  that  there  may  be  other  organic  acids  in  the 
gastric  contents. 

The  test  for  the  presence  of  free  hydrochloric  acid  now  almost  universally 
employed  is  one  introduced  by  Giinzburg,  who  recommended  a  solution  of  2 
parts  of  phloroglucin  and  1  part  of  vanillin  in  30  parts  of  absolute  alcohol. 
If  we  mix  a  few  drops  of  this  phloroglucin-vanillin  in  a  saucer  with  a  few 
drops  of  the  filtered  gastric  contents  to  be  examined,  and  then  heat  the  mix- 
ture cautiously  so  as  to  avoid  charring,  there  will  immediately  develop  on  the 


512  DISEASES   OF   THE   DIGESTIVE   ORGANS 

edge  of  the  fluid  a  beautiful  red  border,  if  free  hydrochloric  acid  is  present. 
Another  good  reagent  for  free  hydrochloric  acid  is  methyl  violet.  This  re- 
quires an  accurate  comparison  of  colors,  so  that  the  weak  watery  solution  of 
methyl  violet  is  divided  into  two  portions  in  test  tubes.  If  now  we  add  to  one 
test  tube  some  of  the  gastric  contents  containing  free  hydrochloric  acid,  the 
violet  is  immediately  changed  into  a  distinct  blue  color,  which  is  evidently 
different  from  the  original  fluid  contained  in  the  other  test  tube.  For  a  third 
test  what  is  called  Congo  paper  is  employed — i.  e.,  strips  of  paper  colored  with 
an  aqueous  solution  of  Congo  red.  If  the  stomach  contents  contain  free 
hydrochloric  acid,  the  red  color  of  the  paper  is  changed  to  a  distinct  blue. 
There  is  a  certain  inaccuracy  in  this  last-mentioned  test  with  Congo  red,  as 
the  red  is  colored  blue  by  concentrated  solutions  of  other  acids,  particularly 
lactic  acid;  but,  as  a  matter  of  fact,  the  other  acids  are  scarcely  ever  present 
in  the  stomach  in  sufficient  amounts  to  invalidate  the  test;  so  that  in  actual 
practice,  if  the  Congo  paper  changes  to  a  distinct  blue,  we  may  almost  always 
infer  that  free  hydrochloric  acid  is  present.  Still,  it  is  advisable  in  every  case 
to  carry  out  the  two  other  tests  also,  which  are  almost  as  simple  and  en- 
tirely unambiguous.  There  is  a  reagent  often  employed  which  indicates  the 
presence  of  free  acids  in  general,  including  free  lactic  acid.  It  consists  of  an 
alcoholic  (or  aqueous)  solution  of  "  tropseolin  00."  The  yellow  color  of 
tropseolin  is  changed  to  a  beautiful  red  by  even  small  amounts  of  acid,  but 
still  more  readily  by  hydrochloric  acid  than  by  the  organic  acids.  Blue  lit- 
mus paper,  as  is  well  known,  is  colored  red  by  free  acids  as  well  as  by 
acid  salts. 

Sahli  has  suggested  an  ingenious  method  to  demonstrate  the  presence  of 
free  hydrochloric  acid.  He  prepared  small  bags  filled  with  methylene  blue 
and  tied  with  a  catgut  thread — so-called  desmoid  capsules.  If  the  patient 
swallows  such  a  capsule  after  a  meal,  then,  if  free  hydrochloric  acid  is  pres- 
ent, the  connective  tissue  of  the  catgut  is  digested,  the  methylene  blue  is  set 
free  in  the  stomach,  and  after  about  two  hours  the  urine  is  colored  a  distinct 
greenish  blue.  In  exceptional  cases  the  blue  discoloration  occurs  only  after 
the  addition  to  the  urine  of  acetic  acid.  If  the  stomach  contents  do  not  con- 
tain free  hydrochloric  acid,  the  catgut  will  remain  undigested,  the  capsule 
enters  the  intestine  unopened,  and  is  expelled  without  the  urine  becoming 
blue.  Because  of  its  great  simplicity,  this  test  can  very  well  be  used  in  prac- 
tice, although,  on  account  of  all  kinds  of  accidents,  there  are  decidedly  more 
sources  of  error  to  be  feared  than  in  the  direct  examination  of  the  siphoned 
gastric  contents.  In  the  Breslau  clinic  we  used  the  preferable  keratin  capsule 
instead  of  the  desmoid  capsule  of  Sahli. 

If  the  examination  of  the  contents  of  the  stomach  an  hour  after  the  test 
breakfast  shows  the  presence  of  free  hydrochloric  acid,  an  experienced  ob- 
server will  often  be  able  to  estimate  from  the  degree  of  the  qualitative  reaction 
whether  he  is  dealing  with  a  small  or  considerable  amount  of  hydrochloric 
acid.  An  accurate  quantitative  estimation  is  possible  by  titration  of  the 
stomach  contents  with  a  decinormal  soda  solution,  for  which  a  few  drops  of 
phenol-phthalein  solution  serve  as  index.1  The  amount  of  acid  determined 
by  this  process  is,  of  course,  the  sum  total  of  free  acids,  and  not  exclusively 

1  We  scarcely  need  to  describe  this  simple  process  more  fully. 


EXAMINATION-    OF   THE    GASTRIC    CONTENTS  513 

the  free  hydrochloric  acid.  Still,  provided  there  is  an  abundanl  amount  of 
hydrochloric  acid  in  the  gastric  contents,  the  results  obtained  may  be  ascribed 
without  great  error  to  hydrochloric  acid  alone;  for  experience  has  shown  that, 
when  there  is  a  considerable  amount  of  hydrochloric  acid  in  the  gastric  eon- 
tents  there  is  scarcely  ever  any  considerable  amount  of  organic  acids  (vide 
infra).  The  degree  of  acidity  of  the  gastric  fluid  is  usually  expressed  in  the 
number  of  cubic  centimeters  of  soda  solution  which  are  necessary,  as  shown 
by  the  titration,  to  neutralize  100  c.c.  of  the  gastric  fluid;  for  example,  if  we 
have  required  6  c.c.  of  soda  solution  to  neutralize  10  c.c.  of  the  gastric  con- 
tents, the  acidity  is  reckoned  at  GO.  In  terms  of  hydrochloric  acid  we  would 
have  GO  multiplied  by  3. Go,  equal  to  19  mgm.  of  hydrochloric  acid — that  is, 
0.22  per  cent.  The  degree  of  acidity  which  is  found  in  the  gastric  contents 
of  healthy  persons  after  the  test  breakfast  is  usually  55  to  G5 ;  amounts  of 
70  to  80  indicate  hyperacidity.  If  the  gastric  juice  contains  an  abundance 
or  an  excess  of  hydrochloric  acid,  the  further  question,  and  an  important  one, 
arises  whether  there  is  a  hypersecretion,  or,  more  correctly,  a  continuous  se- 
cretion of  gastric  juice.  As  we  have  already  mentioned,  the  normal  stomach 
does  not  ordinarily  secrete  except  when  its  mucous  membrane  is  affected  by 
food  swallowed,  or  by  other  stimulating  influences.  The  fasting  stomach  does 
not,  as  a  rule,  contain  any  hydrochloric  acid,  and  when  the  stomach  has  passed 
the  food  on  into  the  duodenum,  its  secretion  immediately  ceases.  In  order, 
then,  to  determine  the  existence  of  hypersecretion  or  continuous  secretion,  we 
must  examine  the  contents  of  the  fasting  stomach  at  last  six  or  seven  hours 
after  the  last  meal.  If  we  then  find  fluid  in  the  stomach,  with  distinct  or 
abundant  amounts  of  hydrochloric  acid  contained  in  it,  we  are  justified  in 
assuming  that  there  is  an  abnormal  hypersecretion  on  the  part  of  the 
stomach. 

Physiology  teaches  us  that  not  only  hydrochloric  acid,  but  pepsin  in  as- 
sociation with  it,  is  necessary  for  the  peptonizing  of  albuminoids.  The  demon- 
stration of  pepsin  in  the  gastric  contents  is,  therefore,  essential  to  a  determina- 
tion of  the  peptic  function  of  the  stomach.  Experience  has  shown,  however, 
that  pepsin  is  rarely  absent  from  the  gastric  juice,  and  if  there  is  a  distinct 
secretion  of  hydrochloric  acid  we  may  almost  always  assume  that  pepsin  is 
secreted,  without  making  anj^  special  examination.  Even  in  cases  of  anacidity 
pepsin  often  continues  to  be  secreted.  Still,  there  are  cases  when  the  direct 
demonstration  of  the  presence  or  absence  of  pepsin  in  the  gastric  juice  is  de- 
sirable. The  process  is  simple.  We  obtain  some  gastric  contents  in  the  ordi- 
nary way  after  a  test  breakfast,  filter  it  into  a  test  tube,  and  put  into  it  a 
square  shaving  of  the  white  of  a  hard-boiled  egg.  Normal  gastric  juice  con- 
taining Irydrochloric  acid  and  pepsin,  if  kept  at  a  temperature  of  98.6°  F. 
(37°  C.)  in  an  incubator,  will  dissolve  the  flake  of  albumen  completely  in 
from  thirty  to  sixty  minutes.  If  the  gastric  juice  contains  no  hydrochloric 
acid,  but  only  pepsin,  the  albumen  will  be  dissolved  if  we  add  a  few  drops  of 
dilute  hydrochloric  acid.  If,  however,  pepsin  also  is  absent  from  the  gastric 
juice,  the  bit  of  albumen  will  swell  up  but  will  not  be  actually  dissolved,  un- 
less we  add  artificial  pepsin. 

Besides  hydrochloric  acid  there  are  also  some  organic  acids  in  the  gastric 
juice;  the  most  important  of  these  is  lactic  acid.  The  lactic  acid  is  not  a 
product  of  the  gastric  mucous  membrane,  but  the  result  of  lactic-acid  fer- 


514  DISEASES   OF  THE   DIGESTIVE   ORGANS 

mentation  of  the  carbohydrates  in  the  gastric  contents,  except  for  small 
amounts  which  may  be  directly  introduced  with  the  food.  If  we  test  the 
gastric  contents  a  short  time  (fifteen  to  thirty  minutes)  after  a  test  break- 
fast, we  can  often  find  some  lactic  acid  present,  but  as  yet  no  hydrochloric 
acid.  This  corresponds  to  the  amylolytic  stage  of  gastric  digestion.  Later, 
when  the  secretion  of  hydrochloric  acid  has  begun,  the  lactic-acid  fermenta- 
tion promptly  ceases,  so  that  under  normal  conditions,  as  we  have  said,  we 
find  hydrochloric  acid  distinctly  present  an  hour  after  the  test  breakfast,  but 
usually  no  lactic  acid.  If  we  do  find  lactic  acid  it  is  always  an  indication  of 
•  an  impaired  production  or  absence  of  hydrochloric  acid.  There  is  a  condition 
which  is  especially  favorable  for  the  formation  and  collection  of  large  amounts 
of  lactic  acid  in  the  stomach.  This  is  when  the  absence  of  hydrochloric  acid 
is  associated  with  a  stagnation  of  the  ingesta  in  the  stomach.  This  combina- 
tion is  especially  frequent  in  the  case  of  carcinoma  of  the  pylorus  (q.  v.).  Un- 
der these  conditions  the  lactic-acid  fermentation  may  go  on  unchecked,  and 
we  find  an  abundance  of  that  acid  in  the  stomach  at  whatever  time  we  make 
a  test. 

The  qualitative  test  for  lactic  acid  is  by  means  of  Uffelmann's  reagent :  by 
adding  a  drop  of  ferric-chlorid  solution  to  a  three-  or  four-per-cent  solution 
of  carbolic  acid,  we  obtain  a  liquid  of  a  beautiful  steel-blue  color.  Upon  add- 
ing to  a  small  portion  of  this  blue  fluid,  contained  in  a  test  tube,  gastric 
contents  in  which  there  is  lactic  acid,  the  blue  color  changes  to  a  distinct  yel- 
low, or  yellowish-green.  The  test  should  not  be  regarded  as  positive  unless 
there  is  a  distinct  yellow  color.  We  may  first  agitate  the  gastric  fluid  with 
ether,  and  then  make  the  test  with  the  ether  extract,  as  ether  takes  up  the 
lactic  acid.  The  ether  extract  is  carefully  evaporated,  the  residue  is  dissolved 
in  water,  and  the  watery  solution  is  tested  with  Uffelmann's  reagent.  The 
quantitative  estimation  of  lactic  acid  is  tedious,  and  not  very  important  in 
practice. 

The  fatty  acids  and  acetic  acid  are  not  found  in  the  gastric  contents  unless 
there  is  marked  fermentation,  and  their  presence  therefore  indicates  a  stag- 
nation of  the  gastric  contents  (vide  infra),  and  the  absence  of  hydrochloric 
acid,  which  acts  as  an  antiseptic.  In  practice  we  form  an  opinion  as  to  the 
presence  of  these  acids  by  the  sense  of  smell,  since  their  demonstration  by 
direct  chemical  means  is  far  from  simple.  The  presence  of  the  volatile  fatty 
acids  is  recognized  by  heating  the  gastric  contents  in  a  test  tube,  and  at  the 
same  time  exposing  a  piece  of  moistened  blue  litmus  paper  to  the  vapors, 
which  turn  it  red. 

3.  Determination  of  the  Motor  Activity  of  the  Stomach. — The  employment 
of  the  stomach  tube  also  enables  us  to  form  with  ease  a  satisfactory  estimate 
of  the  motor  function  of  the  stomach,  and  this  is  an  extremely  important 
matter.  As  physiology  teaches  us,  the  pylorus  remains  firmly  closed  during 
the  first  part  of  gastric  digestion.  It  does  not  open  until  the  food  is  suffi- 
ciently prepared,  and  then  the  chyme  is  discharged  by  successive  jets  into  the 
duodenum.  For  practical  purposes  it  is  sufficient  to  know  that  the  examina- 
tion of  healthy  persons  has  shown  the  stomach  to  be  completely  empty  again 
about  two  hours  after  the  ingestion  of  a  small  amount  of  food — e.  g.,  after 
the  test  breakfast  (vide  supra).  If,  then,  we  rinse  out  the  stomach  two  hours 
after  a  test  breakfast  we  ought  not,  under  ordinary  circumstances,  to  find  any 


EXAMINATION  OF  THE  GASTRIC   CONTENTS  515 

large  amount  of  bread  in  the  wash  water.  Bui  ii  is  a  comparatively  easy  task 
for  the  stomach  to  make  away  with  the  test  breakfasl  ;  so  ii  is  more  suitable, 
if  we  desire  to  tesl  its  motor  powers,  to  administer  whal  is  called  a  test  meal, 
consisting  of  a  plate  of  broth,  150  gm.  (5  oz.)  of  underdone  broiled  steak 
(minced)  50  gm.  (2  oz.)  of  potato  puree,  and  a  roll.  A  meal  of  this  sorl 
disappears  from  the  stomach  often  in  three  or  four  horn--,  but  at  the  latest, 
under  normal  conditions,  in  seven  hours.  If  we  wash  oul  the  stomach  .-even 
hours  after  a  test  meal  and  still  find  any  considerable  amount  of  food,  it  is 
sure  proof  of  an  unsatisfactory  discharge  of  the  stomach  contents,  whether 
as  a  result  of  impaired  motor  power  or,  as  is  most  frequently  tin-  case,  of  a 
mechanical  stenosis  of  the  pylorus.  If  we  really  wish  to  know  how  long  por- 
tions may  be  retained  in  the  stomach,  we  may  add  to  the  meal  a  few  cran- 
berries or  green-colored  beans,  and  the  like.  Such  easily  recognizable  tilings 
may  sometimes  be  found  again  in  rinsing  out  the  stomach  several  days  after 
their  ingestion.  As  a  rule,  in  practice,  it  is  advisable  to  perform  the  first 
gastric  lavage  in  the  early  morning  before  the  patient  has  taken  food.  If  the 
stomach  still  contains  distinct  remnants  of  food  taken  the  previous  evening, 
this  in  itself  is  ample  proof  of  a  marked  retention  of  the  gastric  contents. 

In  this  connection,  however,  we  may  make  brief  mention  of  another  method 
originated  by  Ewald,  with  this  same  object  of  determining  the  motor  efficiency 
of  the  stomach.  The  patient  is  given,  early  in  the  morning,  a  gelatin  capsule 
containing  15  gr.  (gm.  1)  of  salol.  Salol  is  not  broken  up  until  it  reaches 
the  intestine,  when  it  separates  into  carbolic  and  salicylic  acids.  The  salicylic 
acid  is  then  immediately  excreted  in  the  urine,  and  readily  detected  by  chlorid 
of  iron.  If  the  stomach  does  not  empty  itself  in  a  normal  manner,  the 
salicylic  reaction  is  often  to  be  detected  in  the  urine  even  after  twenty-four 
or  thirty  hours,  at  which  time  it  would  have  vanished  under  normal  condi- 
tions. This  test  has  not  been  adopted  very  generally  in  practice,  because  it 
is  uncertain. 

4.  Estimation  of  the  Size  and  Position  of  the  Stomach. — Under  normal 
conditions,  the  stomach  lies  mainly  in  the  left  hypoehondrium,  directly  below 
the  vault  of  the  diaphragm,  and  nearly  vertical.  The  pylorus  lies  in  the 
epigastrium,  in  the  median  line  or  a  trifle  to  the  left.  There  are  many  indi- 
vidual variations  from  this  position,  such  as  displacement  from  pressure  of 
the  clothes,  etc.  Many  of  these  changes  of  position  have  really  no  great 
pathological  significance.  Still,  it  is  important  to  determine  these  points 
about  the  organ.  An  experienced  eye  not  infrequently  recognizes  the  position 
of  the  stomach  by  mere  observation  of  the  abdomen,  but  often  this  is  negative 
or  misleading.  By  percussion  we  may  distinguish  the  limits  of  the  deep 
tympanitic  resonance  of  the  stomach  from  the  usually  higher  tympanitic 
resonance  of  the  surrounding  intestines;  or  we  may  mark  the  lower  limit  of 
dullness  when  the  organ  is  full,  so  that  we  can  sometimes  form  a  tolerably 
certain  opinion  as  to  the  lower  border  of  the  stomach.  In  general,  these  re- 
sults are  also  deceptive  and  uncertain. 

With  the  aid  of  the  stomach  tube  the  matter  is  very  simple.  It  is  accom- 
plished by  blowing  up  the  stomach  with  air,  in  the  manner  first  proposed  and 
practiced  by  Runeberg.  This  is  done  by  means  of  the  ordinary  rubber  double 
balloon  bulb  [such  as  is  employed  with  the  Paquelin  cautery;  or  with  a  simple 
Davidson  syringe].   The  method  used  by  us  in  our  wards  almost  every  day  is  as- 


516  DISEASES  OF  THE   DIGESTIVE   ORGANS 

follows  :  The  patient  is  either  fasting  or  has  had  his  stomach  thoroughly  rinsed 
•out,  and  lies  as  nearly  horizontal  as  possible  upon  his  back.  The  stomach 
tube,  being  introduced,  is  connected  with  the  bulb  at  its  upper  end,  and  air 
is  pumped  in.  As  the  pylorus  is  almost  always  firmly  closed,  the  contours 
of  the  stomach  become  visible  very  shortly.  By  percussion  of  the  inflated 
stomach,  we  can  verify  the  results  of  simple  inspection. 

We  should  then  not  only  mark  the  position  of  the  greater  curvature  but 
also  that  of  the  lesser  curvature,  if  visible.  If  the  stomach  is  normal  in 
position  and  size,  the  protuberance  occupies  the  epigastrium  above  the  navel. 
If  the  stomach  is  dilated,  the  greater  curvature  reaches  below  the  navel; 
while  if  the  stomach  as  a  whole  is  displaced  downward  (vide  infra,  gastrop- 
tosis),  the  smaller  curvature  also  falls  to  the  neighborhood  of  the  navel  or 
below  it. 

As  soon  as  we  disconnect  the  bulb  the  air  escapes,  and  the  distended 
stomach  collapses.  We  can,  if  a  certain  degree  of  caution  is  used,  repeat  the 
procedure  more  than  once,  so  as  to  make  sure  of  our  results.  Of  course,  in- 
flation should  be  interrupted  immediately  if  the  distention  of  the  stomach 
becomes  painful ;  and  we  should  abstain  from  the  procedure  altogether  when- 
ever there  is  suspicion  of  an  ulcer,  because  the  artificial  distention  of  the 
stomach  in  this  case  might  do  harm.  In  some  cases,  direct  inflation  does  not 
render  the  contours  of  the  stomach  distinctly  prominent,  probably  because  of 
insufficiency  of  the  pylorus.  In  such  cases,  and  in  such  only,  we  should  em- 
ploy a  rubber  bag  (condom)  fastened  on  the  lower  end  of  the  tube,  having 
previously  tested  its  distensibility.  When  this  is  introduced  into  the  empty 
stomach  and  blown  up,  we  can  usually  discern  it  through  the  abdominal  walls 
and  determine  the  position,  but  of  course  not  the  size,  of  the  stomach.  For 
ordinary  cases  the  first-described  method  is  not  only  simpler  but  more  satis- 
factory, and,  so  far  as  the  patient  is  concerned,  less  disagreeable.  If  the 
abdominal  walls  are  thick  with  fat  the  method  fails,  but  such  a  condition  is 
very  rare  when  there  is  severe  gastric  disease. 

The  simple  method  just  described  seems  to  us  to  have  rendered  entirely 
superfluous  most  of  the  other  more  or  less  complicated  procedures  for  the 
determination  of  the  size  and  position  of  the  stomach,  especially  as  no  de- 
cidedly better  results  are  obtained  by  them.  This  last  statement  applies  es- 
pecially to  electric  transillumination  of  the  stomach  and  anterior  abdominal 
walls  by  means  of  an  incandescent  light  introduced  with  a  tube.  In  practice 
the  X-ray  examination  of  the  stomach  filled  with  a  bismuth-potato  pap  can 
usually  be  dispensed  with,  although  this  method  has  given  very  good  results 
(Eieder,  Holzknecht,  and  others). 

In  ordinary  practice  where  the  introduction  of  the  stomach  tube  is  not 
always  practicable,  the  old  method  recommended  by  Frerich  may  be  employed. 
For  carrying  this  out  it  is  best  to  have  the  patient  fasting,  and  in  a  horizontal 
position.  Seventy-five  to  one  hundred  and  fifty  grains  (gm.  5  to  10)  of  tar- 
taric acid  are  given,  and  immediately  after  an  equal  amount  of  bicarbonate 
of  soda,  each  drug  being  dissolved  in  half  a  glass  of  water.  At  once  there 
is  an  abundant  production  of  carbonic  dioxid.  The  stomach  is  blown  up 
and  its  outlines  become  sometimes  very  distinct,  both  for  observation  and 
for  percussion.  The  great  advantage  of  the  previously  described  method  of 
pumping  in  air  consists,  however,  in  the  fact  that  we  have  the  degree  of 


EXAMINATION   OF   THE   GASTRIC   CONTENTS  517 

distention  under  far  better  control,  and  that  we  can  repeat  the  process  several 
times  in  succession. 

5.  Testing  the  Absorptive  Powers  of  the  Stomach. — Brief  mention  should 
be  made  of  Penzoldt's  method  of  determining  the  absorptive  powers  of  the 
stomach.  A  gelatin  capsule  filled  with  iodid  of  potassium,  if  swallowed  by 
a  healthy  person  fasting,  will  give  rise  at  the  end  of  ten  or  fifteen  minutes 
to  a  reaction  for  iodin  in  the  saliva  and  in  the  urine  (by  adding  sulphuric 
acid  and  shaking  with  sulphid  of  carbon).  In  severe  diseases  of  the  stomach 
the  time  required  is  often  much  longer.  In  practice,  however,  the  method 
has  not  gained  any  great  importance,  particularly  since  the  examinations  of 
Mehring  have  shown  that  the  absorptive  powers  of  the  stomach  are  after  all 
slight.  Water  is  not  at  all  absorbed  from  the  stomach;  sugar,  peptone,  and 
salt  are  absorbed  to  a  slight  degree,  but  with  a  simultaneous  excretion  of 
watery  secretion.  Alcohol,  on  the  other  hand,  is  absorbed  in  large  amounts 
from  the  stomach. 

6.  Demonstration  of  Blood  in  the  Gastric  Contents. — Any  admixture  of 
blood  with  the  contents  of  the  stomach  is  of  great  importance  in  the  diagnosis 
of  certain  gastric  diseases,  particularly  ulcer  and  carcinoma.  If  there  is  fresh 
blood  mixed  with  the  vomitus  or  with  the  gastric  contents  obtained  by  wash- 
ing out  the  stomach,  it  is  often  directly  recognizable  from  its  characteristic 
appearance,  but  if  the  blood  is  already  decomposed  or  intimately  mixed  with 
the  food,  or  present  in  very  small  amounts,  we  need  special  methods  for  its 
certain  recognition.  Microscopic  examination  alone  is  insufficient,  for  the 
red  corpuscles  are  soon  destroyed  in  the  stomach.  The  method  of  spectrum 
analysis  requires  a  special  spectroscope.  We  search  for  the  characteristic 
bands  of  hematin  in  an  ethereal  extract,  made  by  shaking  up  a  portion 
of  the  gastric  contents,  to  which  a  few  drops  of  glacial  acetic  acid  have  been 
added,  with  ether.  For  medical  practice  the  most  useful  and  simple  method 
is  Van  Deen's  test,  with  fresh  tincture  of  guaiac  and  turpentine.  A  small 
amount  of  a  mixture  of  equal  portions  of  these  two  liquids  is  poured  into  a 
test  tube  upon  a  portion  of  the  gastric  contents.  If  blood  is  present,  there  ap- 
pears at  once,  or  after  a  short  time,  an  intense  blue  color  at  the  junction  of  the 
two  fluids.  As  certain  other  matters  contained  in  the  food  may  cause  this  same 
color  reaction,  it  is  more  satisfactory  first  to  decompose  the  gastric  contents 
with  a  few  drops  of  glacial  acetic  acid,  then  extract 

with  ether  and  perform  the  guaiac-turpentine   test  ^      jm      ^ 

with  the  ether  extract.   This  test  is  especially  distinct  %^^  ^     a^Jp 

if  there  are  organic  acids  present,  as  in  case  of  car-  x0Jpg     g       ^ 

cinoma,  in  which  disease  the  stomach  contains  blood  .#-        A  0mM 

in  association  with  lactic  acid,  but  no  hydrochloric  /  ^   "%>    %a       ^ 

acid.     On  the  other  hand,  in  our  experience,  the  test  jr7    $      ^ 

is  often  uncertain  in  the  case  of  ulcer,  because  the  W     J^     w  ^ 

JUL  mi       ^C 
presence  of  hydrochloric  acid  is  a  hindrance.   Another  &  F 

common  method  is  to  see  if  we  can  produce  Teich-        pIG_  71. Hemin  crystals. 

mann's  hemin  crystals  from  the  gastric  contents.     The 

test  is  not  always  successful,  but  if  successful  it  indicates  the  presence  of  blood. 

We  put  a  small  portion  of  the  suspected  gastric  contents  upon  an  object  glass 

with  a  trace  of  common  salt  and  a  few  drops  of  glacial  acetic  acid.    If  we  now 

evaporate  slowly  to  dryness  there  are  formed  small,  brown,  rhombic  hemin 

33 


518  DISEASES   OF  THE   DIGESTIVE   ORGANS 

crystals  (see  Fig.  71),  which  can  be  seen  by  the  microscope.  Of  course,  when- 
ever we  examine  the  contents  of  the  stomach  for  blood,  we  should  bear  in 
mind  that,  if  found,  the  blood  may  be  due  to  the  ingestion  of  underdone  meat, 
preparations  of  hemoglobin,  or  similar  substances. 

To  sum  up  briefly  all  that  has  been  said,  a  careful  examination  of  the 
stomach  should  proceed  in  the  following  manner :  First,  rinsing  out  of  the 
fasting  stomach  early  in  the  morning,  to  determine  whether  there  may  be 
stagnation  or  hypersecretion  (marked  HO  reaction).  We  should  also  notice 
whether  there  is  any  collection  of  mucus  in  the  stomach  when  fasting.  Sec- 
ondly, we  determine  the  position  and  size  of  the  stomach  by  inflation.  Thirdly, 
the  stomach  being  empty,  we  administer  a  test  breakfast;  an  hour  later  we 
examine  the  contents  for  hydrochloric  or  lactic  acid.  Fourthly,  at  noon  we 
give  a  test  meal,  and  seven  hours  later  wash  out  the  stomach,  to  determine 
its  motor  efficiency.  If  there  is  stagnation  of  the  gastric  contents,  we  test 
again  for  hydrochloric  and  lactic  acids.  Fifthly,  microscopic  examination  of 
the  gastric  contents.  Blood  test.  Finally,  we  scarcely  need  to  repeat  that 
in  all  important  cases  we  ought  not  to  be  satisfied  with  a  single  examination 
of  the  stomach,  but  we  should  make  certain  of  our  results  by  repeated  tests. 


CHAPTEE    II 

ACUTE  GASTRIC  CATARRH 

(Acute  Gastritis) 

iEtiology  and  Pathological  Anatomy. — The  mucous  membrane  of  the 
stomach  not  being  open  to  direct  examination,  as  is  that  of  the  mouth  and 
throat,  the  existence  of  acute  gastritis  is  mainly  a  matter  of  inference  from 
our  observations  of  other  mucous  membranes.  When  some  harmful  agency 
acts  in  a  direct  manner  upon  the  mucous  membrane  of  the  stomach,  we  shall 
usually  be  right  in  supposing  that  there  is  a  greater  or  less  degree  of  genuine 
inflammation  of  the  lining  of  the  stomach,  unless  the  organ  in  a  simply  func- 
tional way  at  once  rids  itself  of  the  irritant — for  example,  by  vomiting  when 
the  stomach  has  been  "  overloaded."  If  some  noxious  material  acts  long  and 
continuously  upon  the  mucous  membrane,  there  will  be  abnormal  changes 
not  only  in  the  blood  vessels  and  the  interstitial  tissue,  but  also  in  the  cellular 
elements  of  the  mucous  membrane  and  its  glands.  As  yet,  we  know  little 
about  the  minute  degenerative  changes  in  the  specific  secreting  cells.  The 
microscopic  inflammatory  lesions,  which  we  may  with  great  certainty  assume 
to  be  present,  are  hyperemia  and  swelling  of  the  mucous  membrane,  perhaps 
associated  with  an  increase  in  the  secretion  of  mucus,  and  with  small  hemor- 
rhages here  and  there.  If  the  irritant  is  insignificant  the  lesions  will  be  mild 
and  superficial  (mild  catarrhal  gastritis) .  If  the  noxious  agent  is  more  power- 
ful (for  example,  corrosive  poison),  it  will  give  rise  to  a  deeper  parenchyma- 
tous inflammation,  with  peeling  off  of  the  mucous  membrane  and  similar 
effects  (severe  toxic  gastritis). 

The  mild  catarrhal  forms  of  gastritis  are  caused  by  simple  chemical  and 
mechanical   influences,   and  perhaps  by  thermic  irritation.      They  are  most 


ACUTE   GASTRIC   CATARRH  519 

often  the  result  of  errors  in  diet,  such  as  the  ingestion  of  too  large  an  amount 
of  food,  or  of  food  that  is  difficult  to  digest,  unsuitable,  highly  spiced,  or  very 
acid.  In  the  same  class  belong  the  acute  indigestion  following  excess  in  alco- 
hol, and  the  frequent  derangement  of  tin.'  sioiiiach  from  taking  medicines; 
and  also  cases  due  to  the  accidental  or  willful  ingestion  of  all  sorts  of  injuri- 
ous and  poisonous  substances.  The  severe  cases  of  toxic  gastritis  are  most 
often  caused  by  the  action  of  concentrated  mineral  acids  and  alkalies.  In 
this  class  comes  poisoning  from  sulphuric  acid,  nitric  acid,  hydrochloric  acid, 
caustic  potash,  and  caustic  soda. 

A  special  importance  attaches  to  the  ingestion  of  decaying  substances. 
The  incautious  use  of  tainted  meat  or  fish  may  be  followed  by  relatively  severe 
forms  of  acute  gastric  catarrh.  The  products  of  decomposition  act  as  chem- 
ical irritants  upon  the  mucous  membrane ;  and  the  ferments  and  putrefactive 
agents  likewise  continue  in  activity  after  reaching  the  stomach,  and  thus 
contribute  to  produce  the  inflammation.  The  reason  that  this  sort  of  gastric 
catarrh  is  not  much  more  frequent  than  it  is,  is  undoubtedly  the  presence  of 
hydrochloric  acid  as  a  constituent  of  the  gastric  juice,  because  it  has  an  anti- 
septic action. 

It  is  universally  assumed  that  a  chill  of  the  outer  surface  of  the  body  may 
excite  gastric  catarrh,  but  there  seems  to  be  actual  proof  of  this  in  but  few 
cases.  On  the  other  hand,  there  can  be  no  doubt  that  many  cases  of  acute 
gastric  catarrh,  of  apparently  primary  origin,  are  referable  to  infection. 
Infectious  catarrh  of  the  stomach  may  occur  at  times,  particularly  in  sum- 
mer, with  especial  frequency.  As  to  the  precise  nature  of  the  pathogenic 
germ,  we  do  not  as  yet  possess  any  certain  knowledge. 

The  predisposition  of  certain  individuals  to  gastric  catarrh  differs  greatly. 
Some  persons  always  have  a  "weak"  stomach,  and  the  disease  is  prone  to 
attack  feeble  children,  anaemic  persons,  fever  patients,  and  convalescents  from 
severe  diseases,  as  well  as  chronic  invalids  who  are  ill-nourished.  Enfeebled 
persons  of  this  sort  sometimes  fall  sick  when  vigorous  and  healthy  individuals 
would  entirely  escape.  In  many  of  these  cases  of  unusual  predisposition  to 
gastric  disease,  we  may  surmise  that  the  secretion  of  hydrochloric  acid  is 
scanty,  and  that  there  may  be  a  diminution  in  the  motor  power  of  the  stom- 
ach. Each  of  these  factors  would,  of  course,  render  ingested  irritants  more 
harmful. 

Symptoms. — The  most  constant  subjective  symptom  is  anorexia.  In  severe 
cases  the  very  thought  of  food  excites  disgust.  What  the  patient  does  eat 
tastes  flat,  and  he  is  therefore  very  eager  for  piquant  dishes,  highly  spiced  or 
sour.     Thirst  is  often  present,  and  a  feeling  of  dryness  in  the  mouth. 

The  subjective  gastric  sensations  are  seldom  those  of  marked  pain;  but 
sometimes  there  are  attacks  of  pain  which  are  in  all  probability  due  to  cramp- 
like contractions  of  the  muscular  coat.  The  usual  complaint  is  of  constant 
pressure  and  fullness.  Sometimes  the  patient  is  conscious  of  the  peristaltic 
movements  of  the  stomach.     He  has  "  rumbling  "  in  the  abdomen. 

There  is  nausea,  and  often  vomiting.  In  severe  cases  everything  swallowed 
is  at  once  rejected.  The  vomitus  consists  for  the  most  part  of  undigested 
food  (often  ill-smelling),  with  which  mucus,  and  sometimes  bile,  is  mingled. 
Eructations  of  gas  or  liquid  are  frequent. 

Physical   external   examination  reveals   little.     The  epigastrium  may  be 


520  DISEASES  OF   THE   DIGESTIVE   ORGANS 

somewhat  prominent  as  a  whole,  and  may  be  tender  on  pressure.  The  tongue 
is  almost  always  thickly  coated  and  dry.  The  breath  is  usually  disagreeable, 
and  there  is  a  persistent  flat  or  bitter  taste  in  the  mouth.  In  ordinary  cases 
of  acute  gastritis  examination  of  the  gastric  contents  is  hardly  necessary,  but 
in  the  majority  of  the  severe  cases  we  find  a  marked  diminution  in,  or  entire 
absence  of,  the  hydrochloric-acid  reaction,  and  sometimes  distinct  delay  in 
the  motor  activity  of  the  stomach.  Sometimes  lactic  acid  and  the  fatty  acids 
are  present  in  large  amounts. 

In  severe  cases  there  is  always  considerable  constitutional  disturbance. 
The  patient  feels  languid,  and  disinclined  for  any  exertion;  the  pulse  is 
moderately  rapid,  although  it  may  exceptionally  be  slower  than  normal;  the 
urine  is  usually  somewhat  concentrated,  often  it  gives  a  marked  indican  reac- 
tion. There  may  be  no  fever,  but  not  infrequently  there  is  a  moderate  eleva- 
tion of  temperature  with  sensations  of  chilliness  or  heat.  In  rare  cases  we 
may  observe  an  approach  to  the  typhoid  condition,  with  such  nervous  symp- 
toms as  headache,  vertigo,  and  dullness.  These  cases  were  formerly  termed 
"  gastric  fever,"  and  they  are  probably  most  of  them  infectious,  but  yet  the 
constitutional  symptoms  are  probably  only  exceptionally  referable  to  coin- 
cident constitutional  infection.  It  is  more  probable  that  toxic  influences  are 
exerted  by  the  abnormal  products  of  the  fermentation  which  takes  place  in 
the  stomach.  For  example,  Senator  mentions  sulphureted  hydrogen  as  thus 
generated;  and  Litten  has  described  several  cases  in  which  at  first  there  were 
such  dyspeptic  symptoms  as  nausea,  vomiting,  flatulence,  and  a  coated  tongue, 
but  which  soon  gave  evidence,  by  restlessness,  headache,  great  muscular  weak- 
ness, and  a  gradual  lapse  into  somnolence,  of  rather  severe  nervous  disturbance 
in  addition.  The  breath  had  a  marked  "  acetone "  odor ;  and,  on  adding 
chlorid  of  iron  to  the  urine,  a  strong  reddish  color  was  developed  (Gerhardt's 
[diacetic  acid]  reaction),  so  that  it  seems  probable  that  an  autointoxication 
had  occurred  somewhat  resembling  diabetic  coma. 

Chief  among  complications  are  the  intestinal  symptoms,  which  are  fre- 
quently coincident  with  the  gastric  disorder.  Constipation  is  the  rule.  There 
may  be  diarrhea.  The  gastric  catarrh  may  by  extension  involve  the  duodenum 
and  give  rise  to  jaundice.  Sometimes  herpes  appears  upon  the  skin.  This 
fact  argues  for  the  infectious  nature  of  many  cases  of  gastric  catarrh. 

It  is  evident  from  what  has  been  said  that  acute  gastric  catarrh  is  by  no 
means  uniform  in  its  aetiology,  and  the  general  course  of  the  disease  is  also 
subject  to  great  variations.  Sometimes  there  are  mild  dyspeptic  symptoms 
which  vanish  in  the  brief  time  of  one  or  two  days,  while  in  other  cases  we 
have  a  rather  severe  disease  associated  with  considerable  constitutional  dis- 
turbance, and  lasting  three  to  ten  days.  There  is  also  great  variation  in  the 
intensity  of  the  various  symptoms,  particularly  the  vomiting.  The  progress 
of  the  case  may  be  irregular  and  there  may  be  relapses,  but  still  the  prognosis 
of  primary  acute  gastritis  is  entirely  favorable.  The  diagnosis  is  usually  easy, 
although  we  should  never  omit  to  make  an  unprejudiced  and  careful  exam- 
ination into  the  general  condition.  If  there  is  fever  we  should  bear  in  mind 
the  possibility  of  a  mild  typhoid  (see  Typhoid  Fever). 

Treatment. — If,  at  the  beginning  of  the  disease,  there  is  reason  to  suppose 
that  the  stomach  is  loaded  with  undigested  food,  an  emetic  is  indicated.  If 
it  is  desired  to  avoid  the  irritative  action  of  an  emetic  upon  the  gastric  mucous 


CHRONIC   GASTRITIS— CHRONIC   CATARRH   OF   THE   STOMACH    521 

membrane,  a  subcutaneous  injection  of  one  sixth  of  a  grain  (f-rm.  0-01  )  of 
apomorphin  may  be  given.  Still  more  efficient,  although  disagreeable  for  the 
patient,  is  a  washing  out  of  the  stomach  by  means  of  the  stomach  tube,  par- 
ticularly in  severe  cases  of  toxic  or  infectious  origin  ;  but  of  course,  when  the 
gastric  walls  may  have  been  weakened  by  corrosive  poisons,  the  stomach  tube 
is  eontraindieated. 

In  most  cases,  however,  emetics  and  lavage  may  be  dispensed  with.  The 
treatment  in  such  cases  consists  mainly  in  a  strict  regulation  of  the  diet,  allow- 
ing for  a  time  nothing  whatever,  and  then  such  food  as  thickened  soups,  iced 
milk,  and  toast.  Of  internal  remedies,  10  to  15  drops  of  dilute  hydrochloric 
acid  in  half  a  wineglass  of  water  sometimes  seems  beneficial ;  while  in  other 
cases,  in  which  there  are  sour  eructations  and  vomiting,  alkalies  are  to  be 
given.  We  may  order  as  much  bicarbonate  of  soda  or  as  much  Carlsbad  salts 
as  will  rest  on  the  point  of  a  penknife,  or  Ems  water.  The  so-called  stom- 
achics and  bitters  are  also  often  prescribed,  for  example,  compound  tincture 
of  gentian  or  tincture  of  rhubarb.  Another  favorite  remedy  is  resorcin,  of 
which  4  gr.  dissolved  in  some  aromatic  water  may  be  given  every  two  hours. 
If  the  vomiting  is  obstinate,  relief  may  be  got  from  bits  of  ice  or  sips  of  cold 
Seltzer  water.  In  severer  cases  we  must  resort  to  narcotics,  such  as  opium, 
cocain,  and  chloroform,  administered  internally. 

If  there  is  decided  constipation,  an  enema  must  be  employed,  or  such  laxa- 
tives as  calomel,  Epsom  salts,  or  rhubarb. 


CHAPTEE    III 

CHRONIC    GASTRITIS— CHRONIC    CATARRH    OF    THE    STOMACH 

iEtiology. — The  same  causes  which  excite  acute  gastric  catarrh,  if  often 
repeated,  lead  at  last  to  chronic  catarrh  of  the  stomach ;  but,  at  least  in  adults, 
infectious  influences  are  seldom  prominent  in  the  causation  of  the  disease. 
In  many  cases  it  is  due  chiefly  to  the  chemical  and  mechanical  irritation  of 
an  unsuitable  diet  long  continued.  By  far  the  most  frequent — indeed,  to 
speak  more  correctly,  the  only  frequent — form  of  chronic  gastric  catarrh  in 
adults  is  due  to  hard  drinking.  The  habitual  use  of  distilled  liquors  is  more 
influential  in  this  regard  than  excess  in  wine  or  beer.  The  harm  done  by 
alcohol  may  be  reenforced  by  other  dietetic  causes.  We  have  often  met  with 
genuine  chronic  gastritis  in  extremely  destitute  persons,  who  for  a  long  time 
had  to  eat  food  that  was  insufficient,  bad,  or  even  decayed.  It  should  also 
be  pointed  out  that  abnormal  conditions  of  the  mouth,  and,  particularly,  dirty 
or  carious  teeth,  may  occasion  dyspeptic  and  catarrhal  conditions.  Habitual 
excess  in  smoking  is  also  said  sometimes  to  occasion  chronic  gastritis;  and 
finally,  it  is  probable  that  the  bad  habit  of  rapid  eating  with  imperfect  mastica- 
tion leads  at  last  to  gastric  disturbance.  As  is  the  case  with  all  external  irri- 
tants of  this  sort,  the  results  are  influenced  by  individual  differences  in  the 
resisting  powers  of  the  affected  organ,  and  personal  predisposition  to  disease 
plays  a  certain  part  in  the  development  of  chronic  gastric  catarrh.  Often  this 
predisposition  seems,  to  a  certain  extent,  a  matter  of  family  and  heredity. 


522  DISEASES   OF  THE   DIGESTIVE   ORGANS 

Chronic  gastric  catarrh  is  not  always  a  primary  affection.  It  may  be  sec- 
ondary to  some  other  disease.  In  particular,  all  diseases  associated  with 
portal  congestion  are  apt  to  lead  to  secondary  catarrh  of  the  stomach.  This 
includes  hepatic  cirrhosis  and  hepatic  syphilis.  Again,  the  gastric  catarrh 
associated  with  chronic  cardiac,  pulmonary,  or  renal  disease  is  in  part  to  be 
regarded  as  due  to  congestion.  On  the  other  hand,  however,  we  should  al- 
ways consider  how  manifold  are  the  other  conditions,  associated  with  all 
sorts  of  chronic  diseases,  which  may  lead  to  chronic  gastric  disturbance. 
We  may  mention,  for  instance,  anaemia,  muscular  insufficiency,  and  auto- 
intoxication. 

Pathology. — The  macroscopic  changes  in  the  gastric  mucous  membrane  are 
in  most  cases  very  moderate.  Usually  it  is  thickened  and  coated  with  a  layer 
of  tough,  grayish-white  mucus,  in  which  is  suspended  a  greater  or  less 
amount  of  detached  epithelium.  The  membrane  is  brownish  red,  unless  ren- 
dered gray  by  excessive  pigmentation.  Under  the  microscope  we  find  a  well- 
marked  infiltration  of  the  interstitial  tissue  with  round  cells,  and  well-marked 
parenchymatous  changes,  particularly  extensive  degeneration  of  the  glan- 
dular cells.  All  these  changes  are  especially  marked  in  the  pyloric  portion 
of  the  stomach.  If  the  catarrh  has  lasted  a  long  time  there  may  be  still 
further  changes  in  the  mucous  membrane.  In  many  cases  it  appears  smooth 
and  atrophic.  The  glandular  layer  of  the  stomach  may  at  last  be  almost 
destroyed,  and  the  muscular  and  submucous  coats  share  in  the  atrophy,  while 
the  organ  as  a  whole  is  usually  dilated.  In  other  less  frequent  cases  there 
is  a  marked  growth  of  interstitial  connective  tissue,  with  resultant  contrac- 
tion. In  this  variety,  also,  the  glandular  layer  atrophies,  the  stomach  walls 
grow  firmer,  and  the  whole  organ  shrivels  (cirrhosis  of  the  stomach) .  Con- 
trasting with  these  forms  which  lead  to  atrophy  or  sclerosis,  there  are  others 
which  occasion  a  hyperplasia  of  the  mucous  membrane.  Its  inner  layer  is 
thickened  and  mammillated  (etat  mamelonne) ,  and  there  may  be  actual  polypi 
formed.  The  hyperplasia  in  these  cases  affects  mainly  the  gland  tubes  of  the 
mucous  membrane,  but  there  is  also  a  considerable  thickening  of  the  sub- 
mucous coat. 

Symptoms  on  the  Part  of  the  Stomach. — The  symptoms  of  chronic  gastric 
catarrh  are  the  same  dyspeptic  symptoms  which  we  meet  in  various  com- 
bination and  degree  in  all  diseases  of  the  stomach.  They  include  disturbance 
of  the  appetite;  pressure  or  pain  in  the  region  of  the  stomach;  a  bad  taste 
in  the  mouth;  abnormal  sensations  in  the  throat;  and  finally,  motor  phenom- 
ena, including  rumbling,  eructations,  and  vomiting. 

The  appetite  is  usually  impaired  in  chronic  gastric  catarrh.  There  is 
sometimes  a  moderate  appetite,  but  it  is  soon  changed  to  a  feeling  of  repletion 
upon  the  ingestion  of  even  a  slight  amount  of  food.  In  other  cases  there 
is  actual  dislike  of  any  form  of  nourishment ;  the  patient  eats  little,  and  pre- 
fers highly  spiced,  piquant  dishes.  There  is  often  a  persistent  bitter,  flat, 
disagreeable,  or  otherwise  abnormal  taste  in  the  mouth. 

Subjective  sensations  in  the  region  of  the  stomach  are  rarely  entirely 
absent.  As  a  rule,  there  is  a  feeling  of  fullness  or  pressure  and  of  dull  pain. 
These  troubles  may  either  be  constant  or  occur  after  meals.  Sometimes, 
especially  after  errors  in  diet,  there  may  be  actual  pain.  This  is  termed  car- 
dialgia  or  gastralgia,  and  is  probably  due  in  most  cases  to  cramp-like  contrac- 


CHRONIC   GASTRITIS— CHRONIC   CATARRH   OF   THE   STOMAMJ    r/S.'> 

tions  of  the  muscles;  but  in  general,  habitual  and  severe  pain  does  not  belong 
to  the  clinical  picture  of  simple  catarrh. 

A  very  frequent  and  annoying  symptom,  which  is  particularly  ap1  to  come 
on  after  eating,  is  the  eructation  of  gas,  usually  air,  but  sometimes  gi 
which  are  formed  in  the  stomach  by  the  processes  of  decomposition.  Such 
gases  have  a  disagreeable  odor.  The  eructations  may  bring  up,  also,  some  of 
the  fluid  contents  of  the  stomach.  If  there  is  a  bitter  taste  associated  with  it 
this  is  usually  occasioned  by  peptones,  but  sometimes  perhaps  by  bile  (vide 
infra).  Acid  eructations  indicate  excessive  acidity  of  the  gastric  contents, 
ordinarily  due  to  hydrochloric  acid,  but  exceptionally  to  lactic  acid  (vide 
infra),  or  to  the  fatty  acids,  which  are  recognizable  by  their  odor.  The  burn- 
ing feeling  in  the  pharynx  and  lower  down,  which  is  occasioned  by  acid  eruc- 
tations and  which  is  usually  termed  heartburn,  is  almost  always  caused  by  an 
excess  of  hydrochloric  acid  in  the  gastric  contents,  and  consequently  is  not 
a  frequent  symptom  of  genuine  chronic  gastric  catarrh  (vide  infra). 

In  many  cases  the  feeling  of  nausea  increases,  especially  after  eating,  to 
actual  vomiting,  but  in  chronic  gastric  catarrh  vomiting  is  not  very  frequent, 
and  if  it  occurs  it  is  the  result  of  some  special  cause,  such  as  errors  in  diet. 
There  is  this  exception,  that  in  the  chronic  gastric  catarrh  of  drunkards  a 
peculiar  form  of  vomiting  is  very  common.  This  is  called  morning  vomiting. 
By  this  is  understood  a  fairly  regular  occurrence  of  vomiting  in  the  morning 
before  breakfast,  with  the  ejection  of  considerable  amounts  of  watery  mucus, 
usually  alkaline.  This  vomiting  is  due  not  only  to  the  chronic  catarrh  of 
the  stomach,  but  also  to  the  chronic  catarrh  of  the  pharynx,  which  latter 
occasions  a  great  tendency  to  gagging — e.  g.,  when  rinsing  out  the  mouth. 
The  vomitus  consists  not  only  of  mucus  from  the  stomach,  but  in  large  part, 
also,  of  a  mixture  of  saliva  and  mucus  from  the  mouth  and  throat.  In  the 
other  forms  of  chronic  gastric  catarrh  the  vomitus  consists  often  of  ill-di- 
gested food  and  more  or  less  mucus.  If  there  are  vigorous  efforts  at  vomiting 
and  retching,  the  vomitus  may  contain  also  some  bile  and  small  amounts  of 
blood,  which  have  no  serious  significance. 

The  external  examination  of  a  patient  with  chronic  gastritis  shows  little 
unusual.  The  general  nutrition,  of  course,  is  often  impaired,  although  in 
drunkards  and  gourmands  an  abundant  fat  layer  persists  for  a  long  time. 
The  tongue  is  usually  coated,  especially  in  its  center,  while  its  sides  and  tip 
are  red.  A  thickly  coated  tongue  and  salivation  are  both  of  them  due  rather 
to  accompanying  stomatitis  and  pharyngitis — complications  which  are  present 
in  the  case  of  most  drunkards,  and  sometimes  also  in  excessive  smokers.  Ex- 
amination of  the  epigastrium  shows  often  a  considerable  prominence  of  the 
stomach  and  tenderness  on  pressure,  but  the  only  means  of  obtaining  an 
actual  insight  into  the  abnormal  process  is  a  careful  investigation  by  means 
of  the  stomach  tube.  This  should  not  be  omitted  in  any  case  of  chronic  gas- 
tritis of  any  severity,  especially  as  the  results  of  it  furnish  the  only  true 
guide  for  a  rational  treatment  of  the  disease.  If  we  examine  the  gastric 
juice  after  the  manner  already  described,  we  shall  find  that  free  hydrochloric 
acid  in  chronic  gastritis  is  scanty  (below  0.1  per  cent),  or  even  absent.  Its 
complete  absence  is  particularly  common  in  chronic  alcoholic  catarrh,  and 
also  in  cases  of  chronic  gastritis  in  which  there  is  atrophy  of  the  mucous 
membrane.     In  the  latter  case  pepsin,  also,  is  often  absent.     With  regard  to 


524  DISEASES   OF   THE   DIGESTIVE   ORGANS 

abnormal  acids,  we  may  find  lactic  acid,  but  seldom  in  large  amounts,  because 
in  simple  chronic  catarrh  there  is  scarcely  ever  much  stagnation  of  the  gastric 
contents.  If  there  are  abnormal  processes  of  decomposition,  we  find  acetic 
acid,  butyric  acid,  and  volatile  fatty  acids,  but  these  are  very  rarely  present. 

The  demonstration  of  an  excessive  production  of  mucus  in  the  stomach  is 
of  great  diagnostic  importance.  We  have  mentioned  that  sometimes  the 
vomitus  contains  a  distinct  admixture  of  mucus,  but  the  only  way  of  forming 
an  accurate  opinion  with  regard  to  the  amount  of  mucus  in  catarrh  of  the 
stomach  is  by  siphonage,  especially  in  cases  in  which  vomiting  is  absent  or 
infrequent.  If  we  examine  the  stomach  when  fasting  we  shall,  in  many  cases, 
find  at  every  trial  an  abundance  of  mucous  fluid  with  scarcely  any  other  in- 
gredients. In  other  cases  there  is  more  apt  to  be  an  abundance  of  mucus  after 
a  meal — either  in  a  viscid,  ropy  fluid,  or  in  separate  transparent  masses  of 
varying  size.  Excess  of  mucus  in  the  stomach  is  usually  associated  with 
anacidity,  but  there  are  a  few  exceptional  cases  in  which  it  is  associated  with 
increased  secretion  of  hydrochloric  acid  (gastritis  acida;  acid  catarrh  of  the 
stomach.  Boas,  Eiegel,  and  others).  We  must  avoid  confounding  secretion 
from  the  mouth  and  pharynx  that  has  been  swallowed  with  mucus  produced 
in  the  stomach.    The  latter  is  intimately  mixed  with  the  food,  if  there  be  any. 

The  motor  function  of  the  stomach  is  seldom  much  disturbed  in  chronic 
gastritis.  Often  it  is  surprising  how  rapidly  the  stomach  empties-  itself;  but' 
there  may  be  delay,  partly  because  digestion  is  impaired  and  partly  because 
there  is  a  gradual  development  of  weakness  and  atrophy  of  the  muscular  coat 
of  the  stomach,  analogous  to  the  weakness  of  the  muscles  of  the  vocal  cords 
in  chronic  laryngitis.  If  food  is  long  retained  in  the  stomach,  there  is  prob- 
ably some  other  disease  than  simple  catarrh.  The  size  of  the  stomach  in 
chronic  catarrh  may  be  somewhat  increased,  but  this  has  no  special  importance. 

Symptoms  on  the  Part  of  Other  Organs.  Course  of  the  Disease. — Of  the 
other  organs,  the  intestine  most  frequently  suffers  in  chronic  gastric  catarrh. 
In  almost  all  cases  of  chronic  gastric  catarrh  the  bowels  are  irregular.  Habit- 
ual constipation  is  the  rule,  but  sometimes  there  is  diarrhea.  If  much  gas 
is  generated  in  the  stomach,  the  intestinal  canal  often  becomes-  implicated,. 
and  tympanites  and  flatulence  develop. 

There  has  been  great  stress  laid,  particularly  in  recent  times,  upon  the 
frequent  occurrence  of  nervous  disturbance  in  association  with  chronic 
catarrh  of  the  stomach.  This  takes  the  form  of  hypochondriasis  and  depres- 
sion of  spirits  in  association  with  all  sorts  of  other  nervous  symptoms,  in- 
cluding pressure  in  the  head,  headache,  dullness  of  mind,  and  dizziness  (vertigo 
e  stomacho  laeso)  ;  but,  while  we  may  admit  that  the  disease  of  an  organ 
which,  for  many  human  beings,  is  the  main  source  of  happiness,  may  well  put 
the  patient  out  of  sorts,  yet  there  is  no  doubt  that  many  earlier  reports  about 
nervous  disturbances  were  due  to  a  confusion  of  chronic  gastric  catarrh  with 
nervous  dyspepsia  (vide  infra).  Genuine  chronic  catarrh  of  the  stomach, 
as  such,  has  no  peculiar  relation  to  nervous  disease,  except  in  the  rare  cases 
in  which  certain  unusual  symptoms  develop,  not  improbably  from  the  ab- 
sorption of  toxins. 

When  the  catarrh  is  of  any  duration  and  severity,  the  general  nutrition 
is  apt  to  be  seriously  impaired.  The  diminished  appetite  and  the  imperfect 
digestion  and  absorption  of  what  is  eaten  contribute  to  produce  a  gradual 


CHRONIC    GASTRITIS— CHRONIC    CATARRH    OF   THE   STOMACH    525 

and  considerable  loss  of  weight.     The  fatty  and  muscular  tissues   atrophy. 
The  skin  grows  dry  and  harsh,  and  usually  has  a  dirty  pale  color.     In  rare 
cases  of  extreme  atrophy  of  the  mucous  membrane   (probably  almost  alwi 
combined  with  atrophy  of  the  intestinal  mucous  membrane)  there  are  devel- 
oped symptoms  like  those  of  progressive  pernicious  anaemia  (q.  v.). 

Individual  cases  differ  greatly  in  tbe  combination  of  symptoms  they  pre- 
sent and  in  their  course.  The  anorexia,  gastric  oppression,  eructations,  vom- 
iting, and  other  important  disturbances  already  mentioned,  exhibit  the 
greatest  diversity  in  their  intensity  and  their  grouping.  In  the  milder  cases, 
loss  of  appetite  and  moderate  local  uneasiness  may  be  the  only  symptoms. 
Frequent  vomiting  is  confined  to  the  severer  cases.  The  disease  often  lasts 
for  years,  especially  if  the  patient  neglects  himself.  In  most  cases  there  are 
frequent  remissions  and  exacerbations,  usually  dependent  upon  external  causes. 

The  disease  is  not  intrinsically  fatal  except  in  the  above-mentioned  rare 
cases  of  complete  atrophy  of  the  mucous  membrane,  but  the  general  debility 
consequent  upon  it  may  indirectly  shorten  life. 

Diagnosis. — If  we  except  the  self-evident  cases  of  chronic  alcoholic  catarrh, 
the  only  proper  way  of  making  a  diagnosis  of  chronic  gastritis  is  by  means 
of  a  careful  examination  of  the  gastric  contents,  along  with  a  consideration 
of  the  associated  conditions.  If  a  patient  has  for  some  time  been  suffering 
from  the  ordinary  gastric  symptoms  of  anorexia,  gastric  oppression,  eructa- 
tions, and  vomiting,  we  must  first  determine  whether  we  have  to  deal  with  a 
primary  disease  of  the  stomach  or  with  a  secondary  disturbance  referable  to 
such  conditions  as  cardiac  disease,  renal  disease,  or  pulmonary  tuberculosis. 
If  the  indigestion  is  not  symptomatic  we  must  then  consider  in  order  each  of 
the  primary  diseases  of  the  stomach.  If  there  is  no  indication  of  ulcer  or 
carcinoma,  we  have  remaining  actual  gastritis,  nervous  dyspepsia  (q.  v.),  and 
a  dislocation  of  the  organ  (gastroptosis).  One  important  factor  is  the  gen- 
eral condition  of  the  patient — for  instance,  if  there  is  neurasthenia  or  the 
like.  JSTo  actual  conclusion  can  be  reached,  however,  except  by  examining  the 
contents  of  the  stomach.  We  cannot  assume  that  there  is  a  chronic  gastritis 
unless  there  are  direct  objective  changes  to  be  demonstrated,  chief  among 
which  is  an  abnormal  production  of  mucus,  associated  with  a  change  in  the 
amount  of  hydrochloric  acid  in  the  gastric  juice.  This  change  is  in  most 
cases  a  diminution,  but  exceptionally  an  increase  of  the  amount  secreted. 
We  wish,  in  this  connection,  to  emphasize  once  more  the  statement  that  genu- 
ine chronic  gastritis,  except  in  drunkards,  is  by  no  means  a  common  disease 
and  is  much  less  frequent  than  nervous  dyspepsia. 

Treatment. — If  the  disease  seems  to  be  merely  symptomatic — the  result, 
for  instance,  of  venous  stasis  due  to  chronic  cardiac,  pulmonary,  or  hepatic 
disease — our  efforts  must,  of  course,  be  directed  chiefly  to  the  relief  of  the 
original  trouble.  We  must  also  take  into  consideration  all  other  causative 
influences,  such  as  neglected  or  decayed  teeth,  improper  mode  of  life,  and  un- 
healthy occupation. 

The  direct  treatment  of  chronic  gastric  catarrh  must  always  begin  with  a 
regulation  of  the  diet.  Such  vague  injunctions  as  "  to  be  cautious  "  or  "  to 
avoid  indigestible  articles  of  food  "  are  useless.  The  patient  must  have  a 
perfectly  definite  bill  of  fare  prescribed  for  him ;  nor  can  any  universal  diet, 
suitable  for  all  cases,  be  drawn  up.    In  each  individual  instance  the  individual 


526  DISEASES  OF  THE   DIGESTIVE   ORGANS 

circumstances  must  be  considered.  The  personal  experiences  of  the  patient 
himself  are  by  no  means  to  be  disregarded.  One  man  may  be  quite  unable 
to  digest  what  is  well  borne  by  others,  and  vice  versa. 

In  the  first  place,  certain  foods  must  be  utterly  forbidden  to  such  patients 
as  do  not  themselves  avoid  whatever  disagrees  with  them.  All  articles  must 
be  prohibited  which  may  irritate  the  mucous  membrane,  either  mechanically 
or  chemically.  This  includes  all  the  coarser  sorts  of  vegetables  or  fruits 
containing  a  large  proportion  of  indigestible  cellulose,  and  all  dishes  that  are- 
very  sour,  strongly  salted,  or  highly  spiced.  Potatoes,  farinaceous  food,  and 
all  substances  composed  mainly  of  hydrocarbons  must  also  be  interdicted,  be- 
cause almost  all  the  abnormal  fermentative  processes,  the  evil  consequences 
■of  which  have  already  been  considered,  are  promoted  by  the  hydrocarbons. 
Pat  is  also  harmful.  It  impedes  digestion  by  protecting  the  contents  of  the 
stomach  from  the  action  of  the  gastric  juice  in  a  purely  mechanical  way,  and 
then,  being  changed  into  the  fat  acids,  it  causes  sour  eructations  and  pyrosis. 
Yet  we  must  not  go  too  far  in  forbidding  starches  and  fats.  Particularly  if 
the  patient  is  emaciated  it  is  advisable  to  give  such  fatty  substances  as  good 
butter  and  cream  in  cautious  amounts,  and  often  the  result  is  satisfactory. 
In  general,  we  should  not  forget  that  with  regard  to  diet  the  skill  of  the 
physician  often  lies  more  in  what  he  permits  than  in  what  he  forbids.  The 
limitation  or  withholding  of  alcoholic  beverages  is  an  important  point.  As 
we  have  already  mentioned,  the  great  majority  of  cases  of  chronic  catarrh  are 
the  direct  result  of  excess  in  alcohol — the  most  important  factors  being  chem- 
ical irritation  and  mechanical  distention  of  the  mucous  membrane.  More- 
over, the  experiments  of  Fleischer  and  others  have  shown  that  alcohol  pro- 
longs and  hinders  the  process  of  digestion.  In  every  severe  case  it  is  better 
to  forbid  alcoholic  beverages  entirely,  and  ordinarily  such  an  injunction  is 
much  better  obeyed  than  advice  to  use  them  sparingly.  In  mild  cases  we 
admit  that  small  portions  of  beer  and  wine  may  be  permitted  unhesitatingly, 
especially  if  the  patient  himself  experiences  no  feeling  of  discomfort  from 
them,  but  rather  an  improvement  in  his  appetite. 

In  determining  what  the  patient  may  be  allowed  to  eat,  we  are  to  consider, 
as  already  mentioned,  his  own  personal  experience  as  well  as  our  more  general 
knowledge.  An  intelligent  patient  will  often  be  himself  the  best  judge  of  what 
agrees  or  disagrees  with  him.  The  following  foods  are  very  easy  to  digest: 
milk,  soft-boiled  or  raw  eggs,  broths  (especially  veal  and  chicken  broths),  and 
certain  artificial  preparations,  chief  among  which  stand  meat  juices,  peptones, 
sanatogen,  somatose,  and  many  others.  It  must  be  confessed  that  patients 
soon  tire  of  these  articles.  The  brain  and  sweetbread  of  calves  are  easily 
digestible;  also  birds,  such  as  pigeons,  chickens,  and  partridges,  thin  shavings 
of  raw  beef  or  raw  ham,  rice,  potato  puree,  etc.  Gradually  we  may  proceed 
to  somewhat  heartier  food — veal,  game,  roast  beef,  trout,  and  light  farinaceous 
•dishes.  The  worse  the  symptoms  are  in  any  case,  the  more  strict  must  we  be 
in  regard  to  diet.  For  drink,  besides  water  or  Seltzer  water,  very  weak  tea, 
cocoa,  chocolate,  and  water  reddened  with  claret  are  allowable. — Shall  we  per- 
mit coffee  ?  This  is  a  question  which  must  be  answered  according  to  the  indi- 
vidual experience  of  the  patient.  Coarse  bread  is  to  be  forbidden.  Ordinary 
white  bread,  toasted,  if  it  seems  desirable,  may  be  allowed  in  moderate  amount, 
also  rusks. 


CHRONIC   GASTRITIS— CHRONIC   CATARRH   OF   THE   STOMACH   527 

Solid  articles  of  diet  must  be  finely  out  up  and  well  chewed  before  being 
swallowed.  The  food  must  not  be  very  hot  or  very  cold.  It  i-  sometimes  ad- 
vantageous to  take  more  than  three  meals  a  day,  each  one  being  proportionally 
smaller.  Other  patients  relish  their  food  better  if  the  intervals  between  eating 
are  prolonged.  It  should  be  added  that  excessive  smoking  is  harmful  in 
chronic  dyspepsia. 

There  are  other  special  indications  to  be  met.  In  all  severe  cases  by  far  the 
most  efficient  mode  of  treatment  consists  in  methodical  washing  out  of  the 
stomach.  This  is  especially  true  when  there  is  excessive  jn-oiliicii.ni  of  mucus, 
or  a  tendency  to  decomposition  of  food  in  the  stomach.  In  this  way  we  pre- 
vent the  accumulation  of  any  great  amount  of  undigested  food.  We  remove 
the  excreted  mucus  and  the  products  of  abnormal  fermentation  and  decompo- 
sition, and,  moreover,  we  may  perhaps  exert  a  direct  and  favorable  influence 
upon  the  mucous  membrane.  In  such  cases  we  are  accustomed  to  rinse  out  the 
stomach  daily,  and  the  best  time  for  this  is  in  the  morning  before  the  patient 
has  had  breakfast.  Fresh  fluid  must  be  poured  in  and  emptied  out  rapidly. 
until  the  stomach  is  freed  from  all  foreign  material,  especially  mucus.  We 
use  for  the  rinsing  fluid  a  weak  solution  of  hydrochloric  acid  (one  to  two  per 
mille),  or  a  one-per-cent  solution  of  either  common  salt  or  bicarbonate  of 
soda ;  and,  if  there  is  much  mucus,  a  favorite  remedy  is  very  dilute  limewater, 
two  to  four  tablespoonfuls  of  liquor  calcis  to  a  liter  (quart)  of  water.  If  fer- 
mentation is  going  on,  we  employ  weak  solutions  of  hydrochloric,  boric,  or 
salicylic  acids,  or  resorcin.  It  has  also  been  recommended  to  spray  or  douche 
the  mucous  membrane  of  the  stomach,  for  which  purpose  stomach  tubes  are 
employed  with  numerous  small  openings,  and  such  fluids  are  chosen  as  weak 
solutions  of  alum,  tannin,  and  condurango. 

If  we  now  turn  to  a  consideration  of  the  internal  remedies  used  in  chronic 
gastric  catarrh,  it  is  possible  to  decide  with  regard  to  their  employment  in  a 
much  more  intelligent  fashion  than  heretofore,  because  in  all  severer  cases  we 
make  a  more  accurate  investigation  of  the  digestive  process.  If  the  examina- 
tion of  the  gastric  juice  shows  a  diminution  of  hydrochloric  acid,  this  may  be 
artificially  supplied.  We  prescribe  thirty  to  sixty  minutes  after  each  meal, 
10  to  15  drops  of  dilute  hydrochloric  acid  in  half  a  glass  of  water.  The  benefit 
to  be  thus  derived  must  not  be  overestimated.  In  appropriate  cases,  however, 
its  influence  is  favorable.  If  there  is  no  pepsin  in  the  gastric  juice  we  may 
prescribe  pepsin  as  well  as  hydrochloric  acid.  Pancreatin  and  papain  are  also 
recommended,  but  their  usefulness  is  very  doubtful.  Pankreon  seems  to  me 
more  active.  The  popular  wines  of  pepsin  are  not  to  be  recommended,  because 
■of  the  alcohol  in  them. 

Alkalies  have  long  been  employed  as  well  as  hydrochloric  acid,  and  often 
with  good  results,  although  the  most  common  form  of  chronic  gastric  catarrh 
has  a  less  than  normal  secretion  of  hydrochloric  acid,  and  consequently  the  use 
of  alkalies  would  seem  to  be  contraindicated ;  yet  experience  shows  them  to  be 
useful.  Probably  their  beneficial  effect  is  that  they  neutralize  the  abnormal 
acids,  promote  the  emptying  of  the  stomach  into  the  duodenum,  dissolve  the 
mucus,  and  finally  stimulate  the  secretion  of  the  gastric  juice.  This  has  been 
•experimentally  demonstrated  with  regard  to  carbonate  of  soda,  common  salt, 
and  carbonic  acid.  Prom  what  has  been  said  it  is  evident  that  in  chronic 
gastric  catarrh  alkalies  are  not  usually  given  during  digestion,  but  when  the 


528  DISEASES  OF  THE   DIGESTIVE   ORGANS 

stomach  is  empty  and  before  meals.  As  is  well  known,  the  alkalies  are  pre- 
scribed more  especially  in  the  form  of  alkaline  mineral  waters,  which  the 
patient  drinks  at  home,  or  at  the  various  health  resorts.  The  springs  of  Carls- 
bad possess  the  greatest  reputation.  Those  at  Ems,  Kissingen,  Tarasp,  and 
Vichy  also  deserve  to  be  mentioned  as  health  resorts  for  patients  with  gastric 
trouble.  A  good  portion  of  the  benefit  at  these  places  is,  to  be  sure,  dependent 
upon  the  fact  that  many  patients  are  much  more  apt  to  follow  a  strict  regimen, 
when  they  make  use  of  a  particular  "  cure  "  than  when  they  remain  at  home. 
It  is  self-evident  that  large  doses  of  bicarbonate  of  soda  are  indicated  in  that 
form  of  chronic  gastritis  which  is  associated  with  hypersecretion. 

If  the  character  of  the  vomitus,  or  gastric  contents  obtained  by  rinsing, 
indicates  abnormal  fermentation,  we  may  not  only  wash  out  the  stomach  (vide 
supra),  but  also  try  certain  antifermentative  remedies.  First  among  these  i& 
hydrochloric  acid  in  rather  large  doses,  and  we  also  give  salicylic  acid  (in 
powders,  containing  8  gr.  [gm.  0.5] )  ;  creosote  (two  or  three  0.5-gr.  pills  daily 
[gm.  0.03])  ;  benzine  (20  drops  in  capsules  or  in  milk),  and  similar  drugs. 
As  a  rule,  however,  the  last-named  remedies  are  seldom  employed. 

The  best  drugs  to  stimulate  the  secretion  of  gastric  juice  are  the  bitters. 
It  is  this  property  which  has  earned  them  the  name  of  stomachic  tonics.  Com- 
pound tincture  of  gentian,  tincture  of  nux  vomica,  tinctura  amara,  and  tine 
tura  calami,  P.  G.,  quassia  and  columbo — these  are  much  employed.  In  gen- 
eral, however,  they  are  not  very  efficient.  An  excellent  tonic  in  many  of  these 
cases  is  condurango  bark.  A  decoction  may  be  made  (15  parts  to  200  of 
water)  ;  or  we  may  employ  the  fluid  extract,  giving  a  teaspoonful  in  water 
two  or  three  times  a  day. 

A  few  remedies  remain  to  be  mentioned,  which  are  said  to  exert  a  direct 
beneficial  influence  upon  the  catarrh,  and  which  many  physicians  extol  highly. 
Their  efficacy,  however,  is  somewhat  problematical.  We  refer  chiefly  to  sub- 
nitrate  of  bismuth,  sulphate  of  zinc,  and  nitrate  of  silver.  (See  prescriptions 
in  the  Appendix.) 

Certain  symptoms  may  demand  especial  treatment,  such  as  vomiting.  It 
will  usually  yield  to  regular  and  persistent  washing  out  of  the  stomach.  Other 
remedies  are  small  bits  of  ice  and  minute  doses  of  opium  or  chloral.  Potas- 
sium bromid  and  chloroform,  internally  administered,  may  also  be  tried. 

Violent  gastralgia  requires  narcotics,  such  as  morphin  and  opium.  The 
best  external  applications  are  poultices  or  wet  compresses.  "  Sour  stomach  " 
may  be  relieved  by  a  pinch  of  bicarbonate  of  soda,  or  of  calcined  magnesia- 
Persistent  anorexia  may  yield  to  the  bitters  mentioned  above,  or  to  small 
doses  of  quinin  or  compound  tincture  of  cinchona.  If  the  bad  taste  in  the 
mouth  is  annoying,  the  mouth  should  be  frequently  rinsed  out  with  Seltzer 
water,  a  one-per-cent  solution  of  carbolic  acid,  or  five  drops  of  tincture  of 
myrrh  to  a  glass  of  water.  For  habitual  constipation,  enemata,  or  the  various 
mineral  waters,  are  good;  also  Carlsbad  salts.  In  obstinate  cases  pills  of 
rhubarb  or  aloes  may  be  employed.  Still,  we  ought  never  to  forget  that  the 
infrequency  of  the  stools  is  often  merely  a  natural  consequence  of  the  scanty 
diet,  and  that  it  is  therefore  possible  to  do  harm  with  our  purgatives.  Iron  is 
often  prescribed  for  the  concomitant  anaemia;  but  it  should  be  employed, 
cautiously,  for  it  is  often  ill  borne  in  gastric  disease. 


GASTRIC  ULCER  529 


CHAPTER    IV 


PHLEGMONOUS   GASTRITIS 
(Purulent  Inflammation  of  the  Stomach) 

Purulent  inflammation  of  the  stomach  is  very  rare,  and  little  is  yet 
known  about  it.  In  most  cases  no  special  causes  for  it  have  been  ascertain- 
able. It  is  occasionally  one  of  the  symptoms  of  grave  pyaemic  or  puerperal 
inflammation.  We  have  seen  one  case  in  which  suppuration  of  the  pharynx 
led  to  an  acute  phlegmonous  inflammation  of  the  submucous  coat  of  the 
oesophagus,  also  involving  a  large  portion  of  the  stomach,  with  a  fatal  ter- 
mination. 

Two  forms  are  distinguished — a  diffuse  and  a  limited  variety.  The  latter 
is  equivalent  to  gastric  abscess.  The  submucous  layer  is  almost  invariably  the 
chief  seat  of  suppuration.  From  this  starting  point  the  process  invades  the 
muscular  and  serous  coats  on  the  one  hand,  and  the  mucous  membrane  itself 
on  the  other — the  usual  result  being  multiple  sieve-like  perforations  inward 
or  outward. 

The  usual  symptoms  are  violent  gastric  derangement,  with  pain  and  vomit- 
ing, high  fever,  and  the  indications  of  constitutional  infection,  namely,  head- 
ache, delirium,  and  general  prostration.  Sometimes  the  disease  is  quickly 
fatal,  sometimes  it  runs  a  more  chronic  course.  The  few  cases  in  which  re- 
covery has  been  reported  are  somewhat  obscure. 

The  disease  can  never  be  diagnosticated  with  absolute  certainty.  Treat- 
ment must  be  purely  symptomatic.  Ice,  both  internally  and  externally,  and 
the  narcotics,  are  chiefly  employed. 


CHAPTER.   V 


GASTRIC   ULCER 

(Simple  or  Round  Ulcer  of  the  Stomach) 

iEtiology. — Since  Cruveilhier  gave  the  first  accurate  description  of  gastric 
ulcer,  numerous  explanations  of  its  occurrence  have  been  propounded.  Even 
yet  there  is  no  universally  accepted  view.  We  may,  in  general,  hold  to  the 
assertion  that  the  development  of  an  ulcer  is  preceded  by  a  local  disturbance 
of  nutrition,  or  necrosis  of  the  gastric  mucous  membrane,  and  that  then  the 
enfeebled  or  necrotic  tissue  is  dissolved  by  the  gastric  juice — i.  e.,  digested 
("peptic  ulcer").  But  it  is  not  known  what  are  the  special  causes  which 
occasion  the  primary  damage  to  the  tissue,  nor  why  the  loss  of  substance 
when  it  occurs  is  not  at  once  healed,  but  extends  in  width  and  depth.  There 
is,  indeed,  no  lack  of  theories  to  solve  these  questions,  and  pathologists  have 
made  many  experiments  with  regard  to  the  pathogenesis  of  gastric  ulcer. 

The  explanation  of  the  fact  that  the  normal  gastric  mucous  membrane  is 
not  attacked  by  gastric  juice  lies  probably  not  so  much  in  the  presence  of 
the  alkaline  blood  flowing  through  the  membrane  as  in  the  intrinsic  vital 


530  DISEASES   OF   THE   DIGESTIVE   ORGANS 

resisting  powers  of  the  normal  living  cells.  If  the  cells  are  in  any  way  dam- 
aged there  occurs  at  once  an  autodigestion  at  that  spot.  Damage  of  this  sort 
may  be  produced  experimentally  in  different  ways ;  for  example,  by  artificially 
produced  embolism  of  the  smaller  arteries  of  the  stomach,  and  by  wounds, 
including  bruising,  burning,  and  cauterization  of  limited  portions  of  the 
mucous  membrane.  In  all  such  cases  a  peptic  ulcer  is  formed,  but  almost 
invariably  this  promptly  heals,  or,  at  any  rate,  it  shows  no  tendency  at  all  to 
extension.  If,  as  a  symptom  of  severe  gastritis  or  portal  congestion,  there 
are  small  hemorrhages  into  the  mucous  membrane,  they  result  in  so-called 
hemorrhagic  erosions ;  but  these  again  are  limited  to  the  small  spot  destroyed 
by  the  hemorrhage. 

Virchow  assumed  that  ordinary  round  ulcer  of  the  stomach  in  man  is,  in 
most  cases,  the  result  of  the  plugging  of  the  small  vessels  with  a  thrombus 
or  embolus,  because  of  various  diseased  conditions  of  their  walls,  but  this  sup- 
position remains  entirely  without  proof.  One  fact  that  tends  to  contradict 
this  view  is  the  appearance  of  ulcer  in  young  individuals  without  any  signs 
of  cardiac  or  vascular  disease.  Only  in  exceptional  cases  does  a  gastric  ulcer 
develop  in  older  persons  apparently  on  an  arteriosclerotic  basis.  Other  in- 
vestigators thought  of  the  possibility  of  accidental  injuries,  and,  perhaps  in 
some  few  cases,  even,  of  external  trauma  (burns,  etc.).  Such  suppositions 
may  be  correct,  although  they,  again,  in  most  cases  are  incapable  of  demon- 
stration. Then  we  have  still  to  meet  the  second  above-mentioned  question: 
Why,  in  all  such  cases,  the  little  erosions,  if  they  are  formed,  do  not  immedi- 
ately heal,  as  the  experimentally  produced  ulcers  almost  invariably  do.  Lately 
the  attempt  has  been  made  to  settle  this  difficulty  by  pointing  out  that  in 
ulcer  of  the  stomach  the  acidity  of  the  gastric  juice  is  shown  to  be  abnormally 
great.  This  hyperacidity  is  assumed  to  exist  even  before  the  development 
of  the  ulcer,  and  in  a  certain  degree  to  cause  a  predisposition  for  its  develop- 
ment, as  well  as  to  explain  the  unwillingness  of  the  ulcer  to  heal  and  its 
proneness  in  many  cases  to  extend  farther,  to  spread.  If  a  gastric  ulcer  is 
artificially  produced,  the  process  of  healing  may  be  considerably  delayed  by 
introducing  solutions  of  hydrochloric  acid  into  the  stomach.  It  is  very  pos- 
sible that  hyperacidity  of  the  gastric  juice  is  a  factor  in  the  aetiology  of  ulcer, 
but  the  whole  matter  is  by  no  means  easily  intelligible.  We  remain  uncertain 
as  to  what  is  the  primary  cause  of  the  ulcer,  and  it  has  not  yet  been  proved 
that  hypersecretion  and  hyperacidity  exist  before  the  formation  of  the  ulcer. 
We  might  also  believe  that  the  excessive  acidity  is  secondary  to  the  sensory 
irritation  occasioned  by  the  raw  spot.  In  a  word,  our  present  knowledge  of 
the  development  and  extension  of  gastric  ulcer  is  vague. 

Gastric  ulcer  occurs  but  seldom  in'  childhood.  It  is  most  often  seen  be- 
tween the  ages  of  eighteen  and  thirty.  The  cicatricial  stenosis  of  the  pylorus 
and  other  sequela?  are  often  seen  in  still  older  individuals,  between  thirty  and 
forty-five  years;  but  in  most  of  these  cases  the  disease  probably  originated 
much  earlier.  In  still  later  life  gastric  ulcer  is  rare.  In  general,  the  disease 
seems  to  be  more  frequent  in  the  female  sex  than  in  the  male ;  but  if  we  count 
only  the  absolutely  demonstrated  cases,  the  difference  is  not  a  very  great  one. 
The  view  that  ulcer  of  the  stomach  attacks  by  preference  anaemic  and  chlorotic 
girls  is  very  general,  but  to  the  author  seems  much  exaggerated.  The  prob- 
able explanation  is  that  gastric  disturbances  in  chlorotic  persons  are  often 


GASTRIC   ULCER  531 

ascribed  to  gastric  ulcer  without  sufficient  reason.  Taking  into  consideration 
only  the  absolutely  certain  cases,  the  author's  experience  does  not  show  any 
especially  close  connection  between  chlorosis  and  gastric  ulcer.  Yet  it  must, 
of  course,  be  confessed  that  indubitable  cases  ol'  gnstric  ulcer  occur  in  cblorotie 
girls. 

Pathological  Anatomy. — The  ulcer  is  usually  approximately  round  or  oval. 
Its  borders  are  sharp ;  the  walls  often  slope  inward,  giving  the  ulcer  the  form 
of  a  shallow  funnel.  The  base  of  the  ulcer  is  almost  always  perfectly  clean, 
so  that  in  microscopic  sections  we  see  the  ends  of  the  gland  tubes  remaining 
unchanged,  and  reaching  out  into  the  surface  of  the  ulcer.  After  an  ulcer 
has  lasted  some  time,  a  reactive  inflammation  develops  around  the  necrotic 
area,  leading  to  the  formation  of  connective  tissue  and  cicatrization.  If 
superficial,  the  ulcer  does  not  extend  farther  than  to  the  muscular  coat,  but 
it  may  be  deep  enough  to  expose  the  serous  membrane,  or  even  to  perforate  it 
(vide  infra).  The  size  varies  greatly.  Some  are  hardly  as  large  as  a  pea; 
others  may  measure  10  to  15  cm.  in  their  greatest  diameter.  As  to  position, 
most  of  them  are  found  near  the  pylorus.  They  attack  the  posterior  wall  of 
the  stomach,  particularly  the  neighborhood  of  the  lesser  curvature,  far  more 
frequently  than  the  anterior  wall,  but  the  greater  curvature  is  not  infre- 
quently the  seat  of  an  ulcer.  As  a  rule,  we  find  but  a  single  ulcer,  although 
exceptions  to  this  statement  are  not  very  rare. 

If  an  ulcer  of  any  size  heals,  a  scar  is  formed,  with  radiating  lines  and 
often  of  considerable  size;  smaller  superficial  ulcers  heal  with  a  smooth  scar. 
Cicatricial  contraction  may  alter  the  shape  of  the  stomach  considerably.  If 
a  deep  constriction  is  formed  around  the  middle  of  the  stomach,  we  have  what 
is  called  the  hour-glass  shape.  Scars  of  pyloric  ulcers  are  of  the  greatest 
clinical  importance,  because  they  lead  to  cicatricial  stricture  of  the  pylorus, 
with  resultant  dilatation  of  the  stomach. 

If  the  gastric  ulcer  extends  to  the  serous  membrane,  the  final  result  may 
be  perforation  into  the  abdominal  cavity  and  general  peritonitis,  unless  the 
stomach  previously  becomes  attached  at  the  point  threatened  to  some  neigh- 
boring organ,  because  of  adhesive  inflammation.  The  ulcers  being  usually 
on  the  posterior  wall  of  the  stomach,  it  is  oftenest  the  pancreas  to  which  the 
stomach  becomes  adherent.  In  other  instances  it  is  the  liver,  transverse 
colon,  diaphragm,  or  spleen.  If  adhesions  are  formed  before  the  perforation 
of  a  gastric  ulcer,  there  may  be  circumscribed  peritoneal  abscesses.  These  are 
situated  with  comparative  frequency  between  the  upper  surface  of  the  liver 
and  the  diaphragm,  or  between  the  stomach  and  the  diaphragm  (subphrenic 
abscess).  Again,  after  such  adhesions  there  may  be  perforation  into  the. 
pleural  cavity,  the  transverse  colon,  the  pericardium,  or  the  lungs. 

The  ulcer  may  cause  erosion  of  a  blood  vessel,  and  thus  give  rise  to  one 
of  the  most  important  symptoms  of  the  disease,  namely,  gastric  hemorrhage. 

Clinical  History. — There  may  be  absolutely  no  symptoms.  It  is  not  a  rare 
thing  to  find  at  autopsies  a  still  active  ulcer  of  the  stomach,  or  the  cicatrix 
left  by  one,  in  subjects  who  never  had  during  life  any  gastric  disturbances 
whatever.  Nor  is  it  very  exceptional  for  a  person  suddenly  to  exhibit  grave 
symptoms,  such  as  gastric  hemorrhage,  or  peritonitis  due  to  perforation,  when 
there  has  been  no  reason  previously  to  apprehend  the  existence  of  an  ulcer. 

In  other  instances  the  ulcer  does,  indeed,  give  rise  to  symptoms,  but  they 


532  DISEASES  OF  THE  DIGESTIVE   ORGANS 

are  not  sufficiently  characteristic  to  point  to  the  correct  diagnosis.  TJsually 
the  gastric  symptoms  are  long  continued,  but  comparatively  slight.  They 
consist,  for  instance,  of  a  sense  of  oppression  or  slight  pain  in  the  epigastrium, 
■eructations,  and  occasional  vomiting.  In  these  cases,  also,  grave  symptoms 
consequent  upon  the  ulceration  may  suddenly  arise. 

In  a  third  class  of  cases  there  are  symptoms  which  are,  to  a  certain  extent, 
•characteristic,  and  lead  with  more  or  less  definiteness  to  the  true  diagnosis. 
These  "  symptoms  of  ulcer  "  are  chiefly  a  peculiar  epigastric  pain,  which  is 
usually  intermittent,  and  vomiting,  or,  what  is  yet  more  distinctive,  the 
vomiting  of  blood,  or  hematemesis;  also  the  signs  of  an  increased  secretion  of 
hydrochloric  acid  in  the  gastric  juice  (hyperchlorhydria  and  hypersecretion). 
These  symptoms  and  their  diagnostic  value  we  must  now  consider  in  detail. 

Pain  in  the  stomach  is  one  of  the  most  frequent  symptoms  of  round  ulcer. 
Its  forms  are  very  diverse.  Often  the  patient  complains  only  of  a  diffuse, 
painful  sensation  of  pressure  referred  to  the  entire  region  of  the  stomach. 
This  may  be  uninterrupted,  or  it  may  occur  only  after  meals,  or  after  ex- 
cessive exertion,  or  as  the  result  of  some  other  special  cause.  This  sort  of 
pain  is  the  least  diagnostic  of  any,  inasmuch  as  exactly  similar  sensations 
may  be  caused  by  other  chronic  disorders  of  the  stomach.  More  characteristic 
■of  ulcer  is  a  decided  cardialgia,  or,  more  correctly,  gastralgia — that  is,  a  very 
violent  pain,  coming  on  at  intervals  like  neuralgia.  It  is  described  as  "  cut- 
ting/' "  tearing,"  "  boring,"  and  the  like.  These  attacks  of  pain  occur  at 
various  times,  but  oftenest  after  eating,  and  particularly  after  the  ingestion 
•of  a  large  amount  of  food,  or  of  food  of  a  rather  coarse  sort.  Often  they 
•occur  with  tolerable  regularity  a  definite  time  after  eating,  say  half  an  hour 
or  an  hour.  This  is  partly  to  be  explained  by  the  beginning  of  the  expulsion 
of  food  through  the  pylorus,  and  partly  by  the  acme  of  the  secretion  of  acid 
being  due  at  this  time.  The  pain  is  felt  chiefly  in  the  epigastrium,  but  not 
infrequently  it  extends  toward  the  umbilicus,  backward  toward  the  vertebras, 
into  the  thorax,  or  even  into  the  upper  extremities.  In  many  instances  a 
marked  sensation  of  thoracic  oppression  accompanies  it.  A  change  of  posi- 
tion may  sometimes  affect  the  severity  of  the  pain.  It  is  sometimes  observed 
that  the  patient,  when  lying  upon  his  right  side,  feels  violent  pain,  which 
is  at  once  relieved  by  changing  to  the  left  side,  probably  because  the  ulcer  is 
located  near  the  pylorus.  An  attack  of  cardialgia  may  last  for  a  few  minutes 
or  for  several  hours.  A  third  variety  of  pain  may  be  observed  in  gastric  ulcer. 
The  suffering  may  be  localized  in  a  very  limited  area.  Such  pain  is  thought 
to  be  due  to  irritation  of  the  floor  of  the  ulcer  by  food,  or  to  its  edges  being 
pulled  upon  during  the  movements  of  the  organ.  It  generally  comes  on  after 
eating,  and  ceases  if  the  stomach  is  perfectly  quiet.  In  position  this  pain  is 
generally  epigastric,  but  sometimes  it  is  umbilical,  or  even,  now  and  then, 
more  toward  the  back.  In  many  cases  of  gastric  ulcer  there  is  also  tenderness 
on  pressure  in  a  quite  sharply  defined  area  and  at  one  particular  spot.  Most 
authors  regard  the  accurately  localized  pain  as  the  most  nearly  pathognomonic ; 
but  it  must  be  said  that  it  is  decidedly  the  least  frequently  exhibited  of  any. 
Transitional  forms  and  combinations  of  the  various  kinds  of  pain  are  often 
observed.  Two  things  may  be  said  to  be  characteristic  in  all  the  sorts  of  pain 
•connected  with  ulcer  of  the  stomach:  the  localization  of  the  pain  each  time 
in  the  same  spot,  and  the  relation  of  the  pain  to  the  ingestion  of  food.     Com- 


GASTRIC   ULCER  533 

ploto  bodily  rest  is  beneficial;  external  pressure  upon  the  epigastrium  usually 
increases  the  pain. 

Vomiting  is  a  frequent  symptom  in  gastric  ulcer,  although  it  may  excep- 
tionally be  absent  or  nearly  so.  Ordinarily,  vomiting  occurs,  like  the  cardial- 
gic  attacks,  after  eating,  and  particularly  after  partaking  of  indigestible 
dishes.  The  vomitus  in  such  cases  consists  mainly  of  partially  digested  food. 
It  usually  has  a  strongly  acid  reaction.  If  there  is  hypersecretion  there  may 
sometimes  occur  vomiting  of  a  strongly  acid  fluid,  not  containing  much  that 
has  been  swallowed.  If  the  ulcer  has  led  to  stenosis  of  the  pylorus,  the  way 
in  which  the  vomiting  occurs  is  very  characteristic.  We  shall  describe  this 
form  of  vomiting  later,  in  detail.  Vomiting  is  of  the  greatest  diagnostic  im- 
portance when  blood  appears.  This  may  be  intermixed  in  greater  or  less 
amount  with  the  other  contents  of  the  stomach,  or  it  may  be  vomited  as  pure 
blood  (hematemesis).  A  gastric  hemorrhage  demonstrated  by  the  vomiting 
of  blood  is  the  most  valuable  diagnostic  sign  of  gastric  ulcer.  If  there  is  no 
hemorrhage  at  all,  the  recognition  of  gastric  ulcer  is  almost  always  rather 
difficult  and  uncertain. 

Hematemesis  is  frequently  the  symptom  which  first  leads  the  patient  to 
apply  to  a  physician.  Up  to  this  time  he  may  have  felt  perfectly  well,  or, 
although  there  may  have  been  some  gastric  derangement,  he  has  not  thought 
anything  of  it.  The  patient  suddenly  becomes  faint,  perhaps  while  he  is  pur- 
suing his  regular  occupation,  or  it  may  be  at  night.  He  feels  dizzy,  and 
everything  looks  black.  Then  he  has  nausea,  and  finally  is  obliged  to  vomit. 
The  vomitus  is  either  pure  blood,  or  a  mixture  of  blood  and  food.  It  is  partly 
coagulated,  and  often  has  a  rather  dark  or  blackish  color,  like  tar.  This 
change  in  color,  as  well  as  the  coagulation,  is  due  to  the  action  of  the  gastric 
juice.  The  hemoglobin  is  transformed  by  the  action  of  the  hydrochloric  acid 
into  hematin.  If  the  blood,  before  it  is  vomited,  has  remained  for  some  time 
in  the  stomach,  the  vomitus  has  the  appearance  of  "  coffee  grounds,"  and  no 
longer  contains  unchanged  red  blood  corpuscles  (for  the  chemical  demonstra- 
tion of  blood,  vide  supra,  page  517).  The  amount  varies  greatly  in  different 
cases :  there  may  be  a  quart  or  more.  Sometimes  there  is  a  single  hemorrhage, 
but  not  infrequently  blood  is  repeatedly  vomited  either  at  short  intervals  or 
on  successive  days.  Part  of  the  blood  escapes  through  the  pylorus,  so  that, 
after  a  profuse  gastric  hemorrhage,  blood  is  sure  to  be  found  in  the  stools. 
In  them  it  is  black  and  tarry.  Exceptionally  it  happens  that  all  the  blood, 
beyond  what  is  absorbed  from  the  intestinal  canal,  passes  off  per  anum,  so 
that  none  whatever  is  vomited.  In  such  cases  it  is  often  a  difficult  matter  to 
locate  the  hemorrhage.  If  there  is  a  sudden  faintness  with  pallor,  and  with- 
out vomiting,  but  followed  by  black  fecal  discharges,  we  should  always  think 
of  the  possibility  of  a  gastric  hemorrhage.  Sometimes  the  diagnosis  of  a 
gastric  ulcer  becomes  probable  if  small  quantities  of  blood  can  be  demon- 
strated chemically  in  the  stools,  when  the  patient  has  been  on  a  diet  free  from 
hemoglobin   (so-called  occult  gastric  hemorrhage). 

The  consequences  of  gastric  hemorrhage  depend,  of  course,  chiefly  on  the 
amount  of  blood  lost.  Sometimes,  although  fortunately  rarely,  a  large  blood 
vessel  is  eroded  and  the  patient  dies.  This  event  may  be  sudden,  or  it  may 
occur  more  gradually  under  the  influence  of  repeated  hemorrhages  and  after 
a  few  days,  during  which  all  the  symptoms  of  acute  anaemia  are  exhibited.  On 
34 


534  DISEASES  OF  THE  DIGESTIVE  ORGANS 

the  other  hand,  the  loss  of  blood  may  be  so  insignificant  as  to  produce  no 
especial  symptoms.  In  most  instances  life  is  not  actually  threatened,  but  yet 
the  signs  and  results  of  a  more  or  less  marked  general  anaemia  are  clearly 
visible. 

In  such  cases  the  patient  feels  extremely  exhausted,  and  at  once  takes  to 
his  bed.  He  has  also  all  the  subjective  symptoms  of  cerebral  anaemia.  There 
are  vertigo,  tinnitus  aurium,  specks  before  the  eyes,  frequent  gaping,  and 
sometimes  headache.  To  assume  an  erect  posture  aggravates  the  disturbance. 
There  is  usually  excessive  thirst.  Now  and  then  a  temporary  amaurosis  has 
followed  an  excessive  hemorrhage. 

Objectively,  we  notice  at  once  the  excessive  pallor  of  the  skin,  particularly 
of  the  face.  The  lips  and  conjunctiva?  are  also  blanched.  The  pulse  is  rapid, 
and  often  ill  sustained.  For  some  days  there  may  be  anaemic  murmurs  over 
the  heart,  and  there  is  a  distinct  sound  to  be  heard  in  the  femoral  arteries. 
A  moderate  rise  of  temperature  is  very  common,  probably  due  to  the  absorp- 
tion of  the  blood  decomposing  in  the  intestines.  This  is  known  as  anaemic 
fever.  The  urine  is  pale,  and  usually  rather  abundant.  Its  specific  gravity 
is  not  infrequently  relatively  high,  namely,  1.015  to  1.020.  All  these  symp- 
toms are  directly  referable  to  the  loss  of  blood,  and  they  will  be  discussed 
with  greater  detail  in  the  section  on  anaemia. 

If  the  hemorrhage  is  not  repeated,  the  patient  gradually  regains  his 
strength.  To  be  sure,  the  pallor  usually  persists  for  a  long  time,  but  the 
disagreeable  symptoms  gradually  abate.  When  gastric  discomfort  has  existed 
previously  to  the  hemorrhage,  it  often  disappears  entirely  after  it — a  circum- 
stance which  is  probably  due  in  part  to  the  excessive  caution  of  the  patient 
thereafter.  At  the  end  of  a  few  weeks  the  patient  often  feels  perfectly  well 
again :  and,  indeed,  recovery  is  not  infrequently  complete  and  permanent.  In 
other  cases,  however,  the  symptoms  of  ulcer  return,  sooner  or  later. 

The  third  group  of  symptoms  in  ulcer  of  the  stomach  is  furnished  by  an 
examination  of  the  gastric  contents  with  the  aid  of  the  stomach  tube.  These 
are  of  extreme  importance.  Earlier,  when  the  soft  tube  now  universally 
employed  was  not  in  use,  we  feared  to  introduce  a  tube  into  the  stomach  in 
case  of  ulcer,  and  even  now  we  should  not  do  it,  in  case  of  hematemesis,  if  it 
can  be  avoided,  until  some  weeks  have  elapsed;  but  with  this  exception  abun- 
dant experience  has  shown  that  we  do  not  need  to  be  at  all  timid  about  the 
introduction  of  the  stomach  tube;  and  particularly  if  there  is  doubt  about 
diagnosis  we  should  never  fail  to  avail  ourselves  of  it.  The  most  important 
fact  which  the  investigations  of  the  gastric  contents  in  patients  with  ulcer 
has  taught  us  is  that  there  are  almost  invariably  present  hyperacidity  and 
hypersecretion  of  the  gastric  juice.  If  the  stomach  is  examined  when  fasting, 
we  shall  find  a  fluid  containing  a  large  amount  of  hydrochloric  acid,  and  if 
we'  examine  it  an  hour  after  a  test  breakfast,  we  shall  find  an  excessively  high 
amount  of  acid  (see  page  513).  This  fact  was  discovered  by  Eiegel,  and  we 
have  found  it  true  in  all  uncomplicated  cases  of  ulcer  of  the  stomach ;  indeed, 
it  seems  to  be  so  much  the  rule  that  if  anacidity  were  found  it  would  render 
any  previous  suspicion  of  ulcer  extremely  improbable.  If,  however,  the  ulcer 
has  led  to  stenosis  of  the  pylorus,  and  so  to  extreme  stagnation  of  the  gastric 
contents,  there  may  be  temporary  subacidity  or  anacidity  (vide  infra).  Like- 
wise— and  this  is  a  point  of  great  practical  importance — hydrochloric  acid 


GASTRIC   ULCER  535 

may  bo  absent  if  a  gastric  carcinoma  lias  developed  on  the  base  of  a  former 
gastric  ulcer  (vide  infra).  Lactic  acid  is  invariably  absent  when  there  is 
hyperacidity  from  hydrochloric  acid;  or,  at  most,  if  there  is  great  stagnation 
of  the  gastric  contents,  there  may  be  a  moderate  formation  of  lactic  acid.  It 
is  also  very  important  in  cases  in  which  there  is  no  vomiting  at  all,  to  examine 
the  gastric  contents  obtained  by  rinsing  out  the  stomach,  with  regard  to  the 
possible  presence  of  blood.  Not  only  considerable  quantities,  but  particularly 
also  smaller  admixtures  of  blood,  which  are  not  recognized  maeroscopically 
(the  so-called  occult  gastric  hemorrhages),  are  of  great  diagnostic  importance, 
as  in  association  with  hyperacidity  they  are  strong  evidence  of  gastric  ulcer. 

The  motor  efficiency  of  the  stomach  in  ulcer  is  at  first  normal  or  even 
somewhat  exaggerated,  because  the  digestion  of  albumen  is  very  energetic 
owing  to  the  excess  of  hydrochloric  acid  in  the  stomach.  But  if  the  ulcer  is 
located  in  the  pyloric  region  and  leads  to  a  cicatricial  stenosis,  the  emptying 
of  the  stomach  is  delayed  and  a  greater  or  less  amount  of  food  will  be  found 
seven  or  eight  hours  after  the  test  meal.  We  shall  later  describe  the  symp- 
toms of  well-marked  obstruction  of  the  pylorus.  If  there  is  suspicion  of  an 
ulcer,  the  stomach  is  usually  not  inflated  at  all,  or  if  so  only  by  means  of  the 
condom  (see  page  516).  If,  however,  there  is  a  cicatricial  stenosis  of  the 
pylorus,  or  an  hour-glass  contraction  of  the  stomach,  our  best  means  of  deter- 
mining the  form  and  size  of  the  organ  is  by  the  X-ray  examination  of  the 
stomach  filled  with  bismuth  paste. 

There  are  no  other  symptoms  in  gastric  ulcer  so  important  as  those  already 
described.  The  appetite  in  many  cases  is  well  maintained,  and  if  the  patient 
takes  little  food  it  is  only  because  he  dreads  the  ensuing  pain.  Eructations 
may  be  absent  or  there  may  be  sour  eructations  and  heartburn,  symptoms 
referable  to  the  existence  of  hypersecretion  and  hyperacidity.  The  tongue  is 
seldom  coated,  being  usually  smooth  and  red;  the  bowels  are  apt  to  be  some- 
what constipated;  the  urine  is  often  only  very  faintly  acid,  so  that  there  is  a 
tendency  to  a  deposit  of  phosphates. 

The  general  nutrition  of  the  patient  often  remains  good,  but  there  may  be 
marked  emaciation  if  there  is  a  long-continued  diminution  in  the  amount  of 
food  taken,  or  if  there  is  obstinate  vomiting.  Sometimes,  but  by  no  means 
invariably,  the  patients  display  great  anaemia.  This  may  precede  the  ulcer 
(vide  supra,  aetiology),  or  it  may  develop  in  association  with  the  symptoms 
of  ulcer,  and  even  without  any  severe  hemorrhage  to  explain  it;  but  that  after 
severe  hematemesis  there  should  be  a  severe  anaemia  is  a  matter  of  course,  and 
has  already  been  alluded  to. 

An  event  which  has  been  already  mentioned  under  pathology — namely, 
perforation  due  to  the  ulcer — is  of  great  clinical  importance.  The  two  most 
frequent  varieties  of  perforation  are  (1)  into  the  peritoneal  cavity,  causing 
peritonitis,  and  (2)  into  the  left  pleura  or  left  lung. 

Perforation  into  the  peritoneal  cavity  leads  almost  invariably  to  a  quickly 
fatal  peritonitis.  When  the  ulcer  has  previously  caused  few  symptoms,  if  any, 
the  excruciating  abdominal  pain,  tympanites,  vomiting,  collapse,  and  sudden 
death  from  peritonitis  may  abruptly  supervene  upon  a  state  of  apparently  per- 
fect health.  In  other  cases  in  which  there  has  been  a  previous  formation  of  ad- 
hesions, we  have  an  encapsulated  abscess,  either  subphrenic,  between  the  stom- 
ach and  the  diaphragm,  or  elsewhere  in  the  abdomen.    The  subphrenic  abscess 


536  DISEASES   OF   THE   DIGESTIVE   ORGANS 

may  contain  air  as  well  as  pus,  and  is  then  termed  pyopneumothorax  sub- 
phrenicus.  In  making  a  diagnosis  of  any  subphrenic  abscess,  we  should  con- 
sider the  direct  and  constitutional  symptoms,  and  also  the  thoracic  signs,  for 
the  respiration  and  the  inspiratory  expansion  of  the  lungs  should  be  normal. 
If  there  is  perforation  outward  or  into  a  coil  of  intestine,  recovery  may  result. 
More  often,  however,  the  termination  is  fatal,  unless  surgical  intervention  is 
successful. 

Perforation  into  the  left  pleural  cavity  we  have  observed  repeatedly.  It 
causes  a  purulent  or  septic  pleurisy  on  that  side,  and  pulmonary  gangrene 
may  develop  at  the  same  time  or  later,  as  a  result  of  perforation  into  the  lung. 
Whenever  we  meet  a  case  of  apparently  spontaneous,  left-sided  empyema,  we 
should  at  any  rate  always  think  of  the  possibility  of  gastric  ulcer. 

A  third  possibility,  which  although  rare  should  nevertheless  be  mentioned, 
is  perforation  into  the  transverse  colon  with  the  formation  of  a  gastro-colic 
fistula.  This  condition  may  occasionally  be  recognized  by  the  alternating 
discharge  of  gastric  contents  from  the  intestine  (slightly  altered  food  rem- 
nants and  hydrochloric  acid)  and  of  fecal  intestinal  contents  from  the  stom- 
ach either  through  vomiting  or  through  gastric  lavage. 

In  some  cases  of  ulcer  we  observe  signs  of  threatening  perforation — that 
is,  localized  pain  due  to  peritonitis,  vomiting,  and  similar  symptoms,  and  yet 
the  case  finally  clears  up.  Probably  in  most  such  instances  there  is  a  limited 
peritonitis  resulting  in  adhesions.  In  certain  rare  instances  such  chronic 
peritonitic  adhesions  in  the  neighborhood  of  the  stomach  are  the  cause  of 
constant  symptoms,  especially  pain.  Surgical  measures  may  be  indicated  for 
their  relief. 

The  general  course  of  round  ulcer  of  the  stomach  varies  greatly,  as  we  can 
see,  in  different  cases.  Complete  recovery  is  by  no  means  rare.  In  other  cases 
the  symptoms  persist  for  years  with  varying  intensity.  We  have  already 
spoken  of  the  hemorrhage  and  perforation  which  may  suddenly  intervene,  and 
of  their  significance.  Eelapses  are  not  infrequent,  even  after  apparent  recov- 
ery. If  the  ulcer  cicatrizes,  the  scar  itself  may  give  rise  to  persistent  dis- 
turbances :  there  may  be  obstinate  cardialgia,  or,  if  the  scar  is  at  the  pylorus, 
the  symptoms  of  pyloric  stenosis  may  gradually  be  developed.  This  extremely 
important  sequel  of  gastric  ulcer  deserves  special  consideration. 

The  cicatrization  and  contraction  of  a  gastric  ulcer  which  result  in  stenosis 
of  the  pylorus  may  be  complete,  but  it  is  by  no  means  exceptional  for  the 
ulcerative  process  to  persist  in  other  places  while  there  is  a  scar  at  the  pylorus, 
so  that  we  may  have  the  symptoms  of  stenosis  combined  with  all  the  other 
symptoms  of  ulcer,  such  as  pain,  hyperacidity,  hemorrhage,  and  perforation. 
The  narrowing  of  the  outlet  of  the  stomach  is  partly  due  to  the  contraction 
of  the  scar,  and  partly  to  the  callous,  fibrous  thickening  of  the  stomach  wall 
at  the  edge  of  the  ulcer.  Many  physicians  lay  great  stress  upon  a  simultane- 
ous pylorospasm — i.  e.,  a  tonic  cramp-like  closure  of  the  pylorus  due  to  irrita- 
tion of  the  surface  of  the  ulcer  or  to  hypersecretion.  The  assumption  does  not 
seem  to  me  to  be  proved.  At  any  rate,  in  my  opinion,  the  mechanical  and 
anatomical  conditions  play  a  much  more  important  role  than  this  assumed 
pyloric  cramp.  To  the  mechanical  effect  of  a  pyloric  stenosis  is  added  some- 
times, perhaps,  a  disturbance  of  the  expulsive  power  of  the  stomach  in  so  far 
as  deep-seated  ulcers  may  destroy  a  part  of  the  muscular  coat  of  the  stomach. 


GASTRIC   ULCER  537 

The  first  and  most  important  result  of  pyloric  stenosis  is  prolonged  reten- 
tion of  the  gastric  contents.  So  long  as  the  muscular  coal  of  the  stomach 
is  able  by  increased  effort  to  overcome  the  increased  resistance,  there  is  do 
disturbance  to  be  noticed.  It  is  proper  to  speak  of  a  compensated  pyloric 
stenosis,  just  as  we  speak  of  a  compensated  valvular  disease  of  the  heart ;  but 
if  the  stenosis  becomes  greater,  so  that  even  the  hypertrophied  muscular  coat 
ceases  to  be  able  to  discharge  the  chyme  into  the  intestine,  there  is  a  gradually 
increasing  collection  of  food  in  the  stomach,  and  the  only  way  for  the  organ 
to  relieve  itself  is  by  vomiting.  The  vomiting,  in  case  of  pyloric  stenosis,  is 
somewhat  characteristic.  It  occurs  from  time  to  time,  perhaps  at  intervals 
of  two  or  three  days,  and  is  very  profuse.  Then,  the  stomach  being  partially 
emptied,  new  collections  may  form  until  their  large  amount  leads  to  vomiting 
again.  The  vomitus  in  cases  of  stenosis  due  to  ulcer  is  usually  very  acid  and 
contains  much  free  hydrochloric  acid,  and  sometimes  blood.  The  stomach 
itself  becomes  gradually  and  increasingly  dilated,  because  of  the  stagnation 
of  its  contents.  Usually  this  secondary  dilatation  of  the  stomach  may  be 
recognized  by  mere  external  examination.  We  can  feel  the  stomach  as  a  great 
limp,  flabby  bag;  and  from  time  to  time  we  can  see  its  walls  bulge  out  from 
muscular  contraction.  We  can  often  distinctly  recognize  the  peristaltic  waves 
passing  from  the  fundus  to  the  pylorus.  In  the  region  of  the  pylorus  we  may 
sometimes,  though  by  no  means  invariably,  make  out  a  distinct  resistance  on 
palpation,  suggesting  a  tumor  and  corresponding  to  the  thickening  of  the 
gastric  walls  from  scar  formation.  In  such  cases  it  is  often  especially  difficult 
to  distinguish  between  the  scar  of  an  ulcer  and  a  carcinoma.  Even  if  we  can 
feel  no  tumor,  visible  contractions  of  the  stomach  with  distinct  peristalsis 
are  almost  invariably  pathognomonic  of  pyloric  stenosis.  In  such  cases  there 
is  usually  a  cramp-like,  painful  sensation,  associated  with  very  marked  con- 
traction of  the  muscular  coat.  During  these  contractions  of  the  stomach  its 
contour  is  often  so  evident  that  we  can  obtain  a  perfectly  distinct  idea  of  its 
size,  extent  (often  reaching  below  the  navel),  and  position.  But  we  must 
especially  emphasize  the  fact  that  the  size  of  the  stomach,  its  dilatation,  is  not 
the  essential  point.  The  main  thing  is  the  stenosis  of  the  pylorus,  and,  above 
all,  the  degree  of  consequent  motor  inefficiency.  With  regard  to  the  latter, 
we  can  reach  no  complete  conclusions  without  using  the  stomach  tube.  With 
its  aid  we  can  determine  the  amount  the  stomach  contains,  and  recover  in- 
gesta,  such  as  cranberries  and  green-colored  vegetables,  which  had  been  eaten 
many  days  before.  If  we  empty  the  stomach  completely  and  give  a  test  meal, 
we  can  gauge  more  accurately  the  degree  of  motor  insufficiency.  We  may  also 
determine  precisely  the  position,  form,  and  size  of  the  stomach  when  emptied, 
by  means  of  inflation.  In  exceptional  cases  there  is  a  large  amount  of  bile 
mingled  with  the  gastric  contents.  The  author  surmises  that  in  such  cases  the 
cicatricial  process  has  changed  the  pylorus  into  a  rigid,  though  narrow,  tube, 
which  can  neither  be  opened  nor  closed.  Thus  we  have  an  "  insufficiency  " 
associated  with  the  stenosis  of  the  pylorus,  so  that  no  obstacle  is  opposed  to  the 
entrance  of  bile  into  the  stomach. 

When  there  is  a  well-marked,  uncompensated  stenosis  of  the  pylorus,  there 
is  always  a  decided  impairment  of  the  general  health.  Nutrition  grows  more 
and  more  imperfect  because  of  the  persistent  vomiting,  and  there  may  he 
extreme  emaciation.     Still,  many  patients  with   stenosis  due  to  ulcer  may 


538  DISEASES  OF  THE  DIGESTIVE  ORGANS 

maintain  a  tolerable  condition  of  health  for  many  years,  if  they  take  proper 
care  of  themselves  by  regular  washing  of  the  stomach  and  by  eating  proper 
food  (vide  infra)  ;  but  finally,  even  in  such  individuals,  the  symptoms  grow 
worse,  or  a  new  trouble  develops,  one  of  which  there  is  always  danger  in  any 
case  of  stenosis  due  to  ulcer.  We  refer  to  the  secondary  development  of  car- 
cinoma at  the  seat  of  the  former  ulcer.  This  happens  not  infrequently,  and 
is  to  be  considered  at  length  in  the  next  chapter.  There  remain  to  be  men- 
tioned some  special  symptoms,  associated  with  ulcers  of  the  pylorus  when  they 
lead  to  stenosis.  There  is  usually  a  decided  tendency  to  constipation;  the 
urine  is  faintly  acid  and  often  has  an  abundant  deposit  of  phosphates;  the 
pulse  is  often  remarkably  infrequent;  and,  finally,  there  are  sometimes  attacks 
of  tetany. 

Diagnosis. — The  diagnosis  can  be  made  only  when  the  above-mentioned 
characteristic  symptoms  are  present.  Of  these,  hematemesis  is  by  far  the  most 
significant,  for  it  is  with  very  few  exceptions  the  result  of  gastric  ulcer.  Par- 
ticularly is  this  true  of  individuals  under  middle  age.- — But  how  shall  we  de- 
termine whether  the  blood  ejected  did  not  come  from  the  nose  or  the  lungs, 
rather  than  the  stomach?  The  answer  is  not  always  easy.  If  an  epistaxis 
occurs  at  night,  a  part  of  the  blood  often  flows  back  into  the  nasopharynx, 
and,  being  swallowed,  excites  vomiting,  so  that  a  gastric  hemorrhage  is  sug- 
gested. 

In  doubtful  cases  we  must,  therefore,  make  an  accurate  examination  of  the 
nose.  It  is  also  very  important  for  the  physician  to  remember  that  blood  may 
be  "  vomited  "  in  hysterical  cases.  If  there  is  also  nervous  cardialgia,  one 
might  easily  be  misled  to  assume  the  existence  of  a  gastric  ulcer.  Usually, 
however,  we  can  make  sure  of  the  diagnosis  by  means  of  the  other  symptoms 
of  hysteria  (see  the  chapter  on  Hysteria),  and  by  examining  the  "vomited" 
blood.  The  latter  does  not  come  from  the  stomach  at  all,  but  from  the  gums, 
the  pharynx,  or  the  nasopharynx,  and  consequently  it  is  almost  always  com- 
paratively bright-red,  rather  fluid,  and  mixed  with  mucus  and  saliva;  and  on 
microscopic  examination  it  shows  pavement  epithelium  and  microorganisms 
from  the  mouth. 

The  diagnosis  between  gastric  and  pulmonary  hemorrhage  in  doubtful  cases 
depends  on  the  following  factors :  1.  The  previous  condition  of  the  patient— 
whether  he  has  had  cough,  expectoration,  and  other  pulmonary  symptoms,  or, 
on  the  other  hand,  gastric  pain  and  vomiting.  2.  On  the  character  of  the 
hemorrhage,  whether  accompanied  by  vomiting  or  by  cough.  But  there  may 
have  been  both.  Violent  vomiting  may  excite  a  cough;  and,  on  the  other 
hand,  blood  which  has  been  coughed  up  may  be  in  part  swallowed  and  induce 
vomiting.  3.  On  the  character  of  the  blood:  if  from  the  lungs,  it  is  usually 
bright-red  and  frothy,  containing  bubbles  of  air,  with  few  clots,  and  of  alkaline 
reaction.  In  gastric  hemorrhage  it  is  usually  dark,  mixed  with  food,  partly 
clotted,  and  acid  in  reaction  from  admixture  with  the  gastric  juice.  4.  On 
the  results  of  physical  examination.  In  this,  of  course,  we  must  be  extremely 
cautious  after  a  hemorrhage,  lest  the  movements  of  the  patient  excite  fresh 
bleeding ;  and  yet  we  may  be  able  to  perceive  from  the  general  condition  of  the 
patient,  or  from  dullness  at  the  apices,  or  moist  rales,  that  pulmonary  disease 
is  probable.  If  the  blood  comes  from  the  stomach,  we  usually  detect  nothing 
but  the  signs  of  anaemia.    5.  The  subsequent  symptoms.    In  cases  of  pulmonary 


GASTRIC   ULCER  539 

hemorrhage  there  is  almost  sure  to  be  an  expectoration  for  the  nexl  few  da 
cither  of  pure  blood  or  of  matter  stained  with  blood;  and,  in  gastric  hemor- 
rhage, the  next  dejection  will  almost  certainly  be  black,  from  the  presence 
of  decomposed  blood.  In  doubtful  cases  the  appearance  of  blood  in  the  -tools 
almost  invariably  settles  the  question  in  favor  of  gastric  hemorrhage.  The 
best  way  of  testing  for  blood  in  the  feces  is  by  means  of  guaiac  and  turpentine 
(vide  supra). 

If  no  gastric  hemorrhage  has  ever  occurred  in  the  course  of  the  disease,  vio- 
lent and  persistent  gastralgia  of  the  peculiar  character  above  described  is  that 
symptom  which  would  first  arouse  suspicion  of  an  ulcer,  particularly  if  the  pain 
is  from  time  to  time  associated  with  vomiting.  If  hyperacidity  or  hypersecre- 
tion has  been  demonstrated,  this  condition  in  association  with  other  symptoms 
may  greatly  strengthen  the  diagnosis.  Severe  gastric  pain,  combined  with 
hypersecretion,  makes  the  diagnosis  of  gastric  ulcer  very  probable.  To  make 
an  absolutely  certain  distinction  between  ulcer  and  nervous  hypersecretion 
(q.  v.)  is  impossible,  if  there  is  no  hematemesis.  In  general,  we  must  remem- 
ber that  it  is  often  possible  to  observe  more  or  less  distinct  "  symptoms  of 
ulcer,"  without  being  absolutely  certain  that  an  ulcer  exists.  Often  we  are 
obliged  to  await  the  further  course  of  the  disease,  and  particularly  the  results 
of  treatment,  in  order  to  settle  our  doubts. 

The  two  diseases  which  it  is  most  difficult  to  distinguish  from  ulcer  are 
nervous  dyspepsia  with  nervous  gastralgia,  and  carcinoma.  When  we  consider 
these  diseases  we  shall  discuss  at  greater  length  the  differential  diagnosis  be- 
tween them  and  ulcer  of  the  stomach.  Cholelithiasis,  especially  if  this  has 
produced  chronic  cholecystitis  and  pericholecystitis  with  adhesions,  may  also 
be  confused  with  gastric  ulcer.  This  is  true,  too,  of  certain  cases  of  chronic 
appendicitis.  We  shall  discuss  this  matter  later.  Finally,  chlorotic  patients 
often  have  gastric  symptoms  (see  the  chapter  on  Chlorosis)  which  excite  sus- 
picion of  an  ulcer,  especially  as  hypersecretion  of  the  gastric  juice  is  often 
associated  with  chlorosis.  Frequently  it  is  impossible  to  make  an  absolute 
diagnosis  in  these  cases,  but  the  results  of  treatment  may  be  decisive.  Prepa- 
rations of  iron,  particularly  Blaud's  pills,  are  ill  borne  in  ulcer,  while  in  case 
of  genuine  chlorosis  they  usually  cause  rapid  improvement  in  the  gastric 
symptoms,  as  well  as  in  the  general  condition. 

Prognosis. — The  chief  dangers  in  ulcer  of  the  stomach,  hemorrhage  and 
perforation,  have  already  been  spoken  of.  Whether  these  complications  will 
actually  occur  in  any  individual  case,  and  when,  we  cannot  determine. 

There  can  be  no  doubt  that  a  large  number  of  ulcers  heal  perfectly;  but, 
as  we  have  already  said,  even  the  resulting  scar  may  cause  trouble.  We  must 
remember  the  possibility  of  persistent  gastric  disturbance,  particularly  car- 
dialgia,  and  also  the  development  of  a  cicatricial  stenosis  with  its  conse- 
quences. Finally,  we  have  the  danger,  already  mentioned,  of  the  eventual 
development  of  carcinoma  in  the  scar  of  an  old  ulcer. 

Treatment. — If  the  diagnosis  of  gastric  ulcer  is  evident,  or  if  the  symp- 
toms are  of  such  a  nature  that  there  is  a  justifiable  suspicion  of  an  ulcer,  the 
patient  should  be  urgently  advised  to  submit  himself  to  careful  and  method- 
ical treatment,  for  it  is  only  by  means  of  a  sufficiently  persistent  and  properly 
conducted  treatment  that  we  can  hope  for  good  therapeutic  results  in  ulcer 
of  the  stomach. 


540  DISEASES  OF  THE   DIGESTIVE  ORGANS 

One  essential  condition  is  that  the  patient  should  keep  his  bed  for  the 
first  part  of  the  treatment  at  least  for  three  or  four  weeks.  Complete  bodily- 
rest  is  certainly  important  in  promoting  healing  of  the  ulcer.  The  patient 
should  also  have  moist  compresses,  or,  still  better,  as  Leube  has  advised,  warm 
poultices  applied  all  day  long  to  the  epigastrium.  These  applications  are 
very  good  for  the  pain,  and  they  also  have  a  certain  psychological  importance, 
for  they  reconcile  the  patient  to  keeping  quiet  in  bed.  Thirdly,  and  this  is 
probably  the  most  important  point,  the  patient  must  keep  strictly  to  a  pre- 
scribed diet.  This  diet  we  are  about  to  describe  at  length.  The  main  consid- 
eration in  determining  the  patient's  diet  is  that  all  mechanical  and  chemical 
irritation  of  the  floor  of  the  ulcer  must  be  avoided.  Fourthly,  we  should  have 
regard  to  the  almost  invariable  existence  of  hyperacidity  of  the  gastric  juice. 
We  therefore  give  to  patients  alkaline  carbonates,  either  in  the  form  of 
Carlsbad  water  (on  waking  a  large  glassful  of  the  Miihlbrunnen  warmed  to 
about  98.6°  F.  [37°  C]  ;  then  in  the  forenoon,  between  ten  and  eleven,  as 
much  more),  or,  what  we  consider  in  many  ways  still  better,  bicarbonate  of 
soda  (either  alone  or  combined  with  subnitrate  of  bismuth).  Of  the  soda 
we  should  give  as  much  as  is  held  upon  the  point  of  a  knife  every  hour,  so  as 
to  keep  the  gastric  juice  constantly  neutralized.  With  regard  to  the  dietetic 
treatment  of  gastric  ulcer,  the  best  way  is  to  follow  Leube's  example,  and  have 
four  diet  lists.  Beginning  with  the  first,  we  gradually  go  on  at. definite  in- 
tervals of  time  to  the  second,  third,  and  fourth.  For  the  first  ten  days  of 
treatment  the  patient  follows  the  first  diet  list.  This  contains  boiled  milk, 
broth,  unsweetened  rusks,  softened  by  soaking;  to  this  we  may  add  various 
artificial  food  preparations,  such  as  sanatogen,  somatose,  hygiama  and  bioson, 
and  meat  juices.  Then  during  the  next  week  we  have  the  second  diet  list, 
comprising  gruel,  soft-boiled  rice  and  oatmeal,  eggs,  boiled  calf's  brain  and 
sweetbread,  boiled  pigeon  and  chicken.  From  the  eighteenth  to  the  twenty- 
fourth  clay  of  treatment  we  have,  in  addition,  the  third  diet,  with  scrapings  of 
raw  beef  and  beefsteak,  potato  puree,  boiled  calf's  feet,  and  for  beverage  some 
tea  or  weak  coffee.  From  the  twenty-fourth  to  the  thirtieth  day  the  patient 
has  the  fourth  diet  list — that  is,  broiled  fowl  or  pigeon,  partridge,  venison, 
roast  beef,  tenderloin,  finely  chopped  macaroni,  and  bread.  It  is  understood 
that  with  each  advance  in  diet  the  previous  diet  lists  are  also  permitted.  In 
general,  the  patient  has  about  five  meals  a  day,  the  amount  of  each  being  de- 
termined by  the  appetite  and  symptoms  of  the  patient.  If  everything  goes 
favorably,  the  gastric  pain  will  wholly  cease  after  a  few  days  of  this  diet, 
under  the  other  regulations  above  enumerated.  The  patient  then  proceeds 
toward  recovery  without  any  discomfort,  except,  possibly,  hunger.  If  the 
transition  to  a  more  advanced  diet  causes  pain,  we  must  resort  for  a  few 
days  to  the  simpler  foods.  The  above  suggestions,  however,  must  be  regarded 
as  an  outline  from  which  certain  variations  may  be  made  to  suit  the  indi- 
vidual case.  Thus,  Lenhartz  particularly  has  lately  called  attention  to  the 
fact  that  some  ulcer  patients,  even  after  a  severe  gastric  hemorrhage,  tolerate 
a  diet  of  milk,  scraped  meat,  soft-boiled  eggs,  ham,  and  butter  well,  and  re- 
cover more  quickly  than  under  the  former  stricter  regime.  Such  a  plan,  how- 
ever, cannot  be  applied  generally.  We  must  ever  be  guided  in  each  case  by 
the  appetite  and  the  symptoms.  In  some  cases  the  administration  of  pure 
olive  oil,  which  may  be  combined  with  oil  of  peppermint,  has  been  very  use- 


GASTRIC   ULCER  541 

ful.  Two  and  a  half  to  three  ounces  (gm.  75  to  100)  are  given  daily.  The  high 
nutritive  value  of  the  oil  and  its  occasional  evident  analgesic  effect  are  indi- 
cations for  its  use.  Many  patients  take  the  remedy  without  any  aversion. 
In  general,  we  may  be  well  assured  that  the  result-  are  I  idler  and  more 
certain  the  more  strict  and  methodical  the  treatment  is.  If  the  patient  has 
borne  the  articles  of  the  fourth  diet  list  for  about  a  week  without  any  discom- 
fort he  may  go  on  by  slow  degrees  to  other  simple  dishes,  such  as  veal,  pike, 
trout,  porridge,  vegetables,  and  other  similar  articles,  and  so  to  an  ordinary 
diet.     Of  course  caution  in  eating  and  drinking  is  necessary  for  a  long  time. 

With  the  mode  of  treatment  just  descrihed  we  shall  in  most  cases  accom- 
plish as  much  as  possible;  but  if,  despite  this  regimen,  the  symptoms  do  not 
cease,  there  are  two  other  remedies  which  deserve  to  be  tried — viz.,  subnitrate 
of  bismuth  and  nitrate  of  silver.  These  are  specially  employed,  also,  in  treat- 
ing poor  persons  whose  circumstances  often  render  it  impossible  to  carry  out 
strict  dietary  rules.  The  subnitrate  of  bismuth  is  almost  always  given  in 
combination  with  bicarbonate  of  soda;  of  a  mixture  containing  3  to  5  parts 
of  bismuth  and  30  parts  of  soda  and  5  of  the  oleosaccharate  of  peppermint, 
we  give  several  times  a  day  a  generous  "  knife-point  full "  before  meals.  In 
severe  and  obstinate  cases  of  ulcer,  we  can  from  our  own  experience  recom- 
mend also  "injections"  of  bismuth  (Fleiner).  The  patient's  stomach  is 
washed  out  in  the  morning  before  breakfast,  and  then  5  iv  to  v  (gm.  15  to  20) 
of  the  subnitrate  of  bismuth  suspended  in  a  glass  of  warm  water  is  poured 
slowly  into  the  stomach  tube;  the  patient  should  at  the  same  time  lie  on  his 
right  side,  and  so  remain  for  at  least  half  an  hour.  The  heavy  bismuth  powder 
is  expected  to  deposit  itself  upon  the  surface  of  the  ulcer  (which  is  probably 
in  the  pyloric  portion  of  the  stomach),  and  thus  in  a  mechanical  way  protect 
it  from  irritation  and  promote  its  healing.  The  symptomatic  results  of  this 
method  are  sometimes  excellent.  Often,  also,  favorable  results  are  obtained 
from  nitrate  of  silver.  This  may  be  partly  explained  by  its  neutralization  of 
the  hydrochloric  acid  and  the  formation  of  chlorid  of  silver.  The  drug  is 
prescribed  in  a  solution  of  6  gr.  to  4  ounces  of  water  (gm.  0.3  to  120),  to  be 
kept  in  opaque  glass,  and  of  this  a  teaspoonful  should  be  given  three  or  four 
times  a  day  before  meals. 

If,  in  spite  of  a  continuous,  methodical,  medical  treatment,  we  obtain 
no  marked  result,  then  there  usually  exist  special  anatomical  conditions,  such 
as  cicatricial  stenoses  and  deformities  of  the  stomach,  hour-glass  stomach,  or 
chronic  adhesions  with  neighboring  organs,  etc.,  which-  cannot  be  influenced 
by  the  treatment.  In  such  cases  we  are  justified,  provided  the  symptoms  are 
severe  and  continuous,  to  advise  surgical  intervention  (gastro-enterostomy, 
separation  of  adhesions,  extirpation  of  the  cicatrix,  etc.). 

Sometimes  the  violent  pain  does  not  abate  under  the  ordinary  treatment, 
and  demands  symptomatic  remedies.  Of  course,  morphin  is  the  most  efficient, 
given  internally  or  subcutaneously.  Chloroform  may  also  be  tried:  we  give 
a  tablespoonful  of  a  mixture  containing  1  part  to  120  of  water.  I  have  occa- 
sionally seen  excellent  results  from  orthoform,  15  gr.  (gm.  1.0)  several  times 
a  day,  and  more  frequently  from  ansesthesin,  5  to  10  gr.  (gm.  0.3  to  0.5)  in 
powder  form,  several  times  daily.  Gerhardt  recommends  for  the  gastric  pain 
3  or  4  drops  of  the  solution  of  perchlorid  of  iron  in  a  wineglass  of  water. 

Excessive  vomiting  and  persistent  nausea  are  likewise  to  be  combated  by 


542  DISEASES  OF  THE  DIGESTIVE   ORGANS 

the  narcotics.  Opium  is  the  best;  morphin,  cocain,  chloral,  and  bromid  of 
potassium  may  also  be  tried.  At  the  first  appearance  of  blood  in  the  vomitus 
the  greatest  bodily  quiet  and  most  careful  dieting  is  absolutely  indispensable. 
For  the  first  day  or  two  it  is  best  to  allow  nothing  except  ice-cold  milk  and 
bits  of  ice  in  the  mouth  to  appease  the  burning  thirst.  In  severe  cases  we 
may  try  giving  water  and  milk  by  the  rectum,  so  as  to  afford  the  stomach 
complete  rest.  The  patient  must  lie  as  quietly  as  he  can.  A  flat  ice  bag,  not 
too  heavy,  should  be  placed  on  the  epigastrium.  In  case  of  persistent  nausea 
or  eructations,  small  doses  of  opium  or  morphin  are  to  be  prescribed.  If  the 
hemorrhage  is  obstinate  we  may  try  the  subcutaneous  injection  of  ergo  tin  or 
cornutin,  or,  by  mouth,  acetate  of  lead  or  chlorid  of  iron.  Gelatin  injections 
(see  page  33)  may  also  be  tried.  In  severe  cases,  finally,  surgical  measures 
(gastro-enterostomy,  jejunostomy)  have  repeatedly  been  tried. 

We  must  wait  four  or  five  days  after  a  hemorrhage  before  we  can  give  a 
little  more  food  by  the  mouth,  and  this  must  be  allowed  cautiously  and  in  a 
liquid  form.  [If  in  persistent  hemorrhage  or  obstinate  irritability  of  the 
stomach  we  wish  to  give  the  organ  complete  rest,  we  may  try  to  supply  food 
by  rectal  injection  and  moisture  by  normal  saline  infusions  under  the  skin, 
1  or  2  pints  twice  a  day.  Morphin  (-^  gr.)  may  be  given  every  four  hours  to 
lessen  hunger.] 

If  peritonitis  appears  as  the  result  of  perforation,  the  best  means  to  try 
are  the  outward  application  of  ice  to  the  epigastrium  and  the  internal  use 
of  opium  in  large  amounts — that  is,  half  a  grain  to  a  grain  (gm.  0.03  to  0.05) 
every  two  or  three  hours,  or  20  to  30  drops  of  laudanum.  Unfortunately, 
however,  the  cases  are  exceptional  in  which  the  peritonitis  does  not  become 
general.  The  only  remaining  hope  lies  in  surgical  interference,  although  the 
results  even  of  laparotomy  are  dubious.  The  earlier  the  laparotomy  is  per- 
formed in  cases  of  perforation,  the  better  are  the  chances  of  success. 

If  the  s}anptoms  of  pyloric  stenosis  are  growing  more  and  more  distinct — 
that  is,  if  the  hypertrophied  muscular  coat  of  the  stomach  is  no  longer  vigor- 
ous enough  to  prevent  the  stagnation  of  food,  with  consequent  dilatation  of 
the  stomach  and  vomiting,  we  can  perhaps  restore  the  patient  to  a  comfortable 
condition  by  means  of  regular  washing  out  of  the  stomach,  combined  with  a 
suitable  diet.  This  irrigation  prevents  any  great  and  burdensome  accumu- 
lation of  food  in  the  stomach.  Moreover,  it  rids  the  patient,  for  a  time  at 
least,  of  the  large  amount  of  strongly  acid  gastric  juice  which  is  usually  pres- 
ent. These  beneficial  and  agreeable  effects  are  soon  so  noticeable  that  often 
the  patient  learns  to  rinse  out  his  stomach  himself,  or  even,  by  bending  over 
and  pressing,  to  empty  out  the  gastric  contents  through  the  tube.  As  a  rule, 
in  cases  of  gastrectasia  resulting  from  pyloric  stenosis,  we  wash  out  the 
stomach  every  morning  before  breakfast.  Ordinary  lukewarm  water  suffices, 
but  if  there  is  an  excessive  secretion  of  hydrochloric  acid  it  is  satisfactory  to 
employ  one-  to  two-per-cent  solutions  of  bicarbonate  or  borate  of  sodium.  In 
severe  cases  the  operation  may  be  repeated  in  the  evening  before  supper. 

The  diet  in  stenosis  following  ulcer  should  consist  of  such  articles  of  food 
only  as  can  pass  with  comparative  ease  through  the  narrow  pylorus,  being  at 
the  same  time  highly  nutritious.  Most  suitable  are  milk,  eggs,  soups  with 
the  addition  of  meat  juice,  somatose,  oatmeal,  rice,  or  flour;  gruel  made  from 
rice,  oatmeal,  or  preparations  like  Mellin's  food;  and,  finally,  finely  chopped 


CANCER  OF  THE  STOMACH  543 

meat  of  all  sorts.  The  meals  should  not  be  too  large,  but  should  rather  be 
frequently  repealed — a  little  Food  often. 

In  this  way  it  is  ol'len  possible  to  give  the  patieni  considerable  relief  for 
many  years,  and  even  to  make  him  gain  weight.  Other  methods  of  treatment 
— by  applying  electricity  to  the  stomach,  by  cautious  massage  of  the  organ, 
or  by  the  administration  of  strychnin — may  be  employed  now  and  then  in 
practice,  but  they  have  no  special  value  in  actual  stenosis. 

It  may  well  be  questioned  whether  the  existence  of  such  patients,  who  are 
preserved  from  excessive  discomfort  only  by  means  of  daily  lavage  and  a  monot- 
onous and  limited  diet,  is  really  bearable;  and,  still  further,  what  are  we  to 
do  when,  in  spite  of  the  most  skillful  treatment  by  the  method  described,  the 
symptoms  persist  and  the  nutrition  and  strength  of  the  patient  grow  gradually 
more  and  more  impaired?  For  such  there  is  still  the  possibility  of  actual  and 
complete  recovery.  We  refer  to  surgical  intervention.  In  no  other  severe 
disease  of  the  stomach  do  operative  procedures  offer  so  great  a  prospect  of  fa- 
vorable result  as  in  stenosis  of  the  pylorus  following  ulcer,  and  therefore  it 
has  been  our  rule  for  a  series  of  years,  in  every  severe  case  of  this  sort,  to  urge 
the  patient  strongly  to  an  operation.  Moreover,  we  should  not  delay  too  long,  if 
the  patient  is  already  enfeebled,  or  if  there  is  reason  to  suspect  that  carcinoma 
is  developing.  The  operation  is  usually  gastroenterostomy,  or  more  rarely 
pyloroplasty;  but  we  cannot  enter  here  into  particulars.  Certainly  we  ought 
not  to  conceal  from  the  patient  that  we  have  to  do  with  a  serious  operation, 
which  is  not  absolutely  without  danger;  yet  in  the  great  majority  of  cases 
the  results  of  treatment  are  excellent.  After  a  successful  operation  the  pa- 
tient is  freed  from  all  discomfort,  he  regains  the  appearance  of  health,  and 
sometimes  even  the  dilatation  of  the  stomach  completely  disappears.  It  is 
true  that  later,  perhaps  years  later,  relapses  may  occur,  whether  because  of 
special  mechanical  conditions  or  from  the  development  of  secondary  car- 
cinoma; but  even  then  perhaps  assistance  will  be  given  by  a  second  operation. 


CHAPTEE   YI 
CANCER   OF   THE   STOMACH 

iEtiology. — We  cannot  here  discuss  the  aetiology  of  carcinoma  in  general, 
and  we  shall  therefore  merely  enumerate  the  factors  which  experience  has 
shown  to  favor  the  development  of  cancer  in  the  stomach. 

Age  has  a  remarkable  influence.  Gastric  cancer  is  decidedly  most  fre- 
quent late  in  life,  between  the  fortieth  and  sixtieth  year.  Still,  it  is  not  very 
rarely  seen  in  younger  persons.  We  have  ourselves  seen  several  cases  in 
persons  between  twenty-two  and  twenty-five  years  of  age. 

Sex  is  of  no  importance. 

Heredity  has  a  slight  but  undeniable  influence.  The  more  closely  we 
search,  the  more  frequently  shall  we  be  able  to  demonstrate  an  hereditary  pre- 
disposition to  cancer.  The  most  famous  example  of  the  transmission  of  can- 
cer is  presented  by  the  family  of  Napoleon. 

The  relations  of  gastric  cancer  to  previous  disease  of  the  stomach  is  very 


544  DISEASES  OF  THE  DIGESTIVE  ORGANS 

important.  It  is  not  probable  that  the  tendency  to  cancer  is  increased  by 
frequent  errors  in  diet,  indulgence  in  alcohol,  or  similar  causes.  Most  of 
those  who  are  attacked  by  gastric  cancer  have  previously  lived  in  a  perfectly 
temperate  manner,  and  report  that  they  have  thus  far  always  enjoyed  a  good, 
digestion.  The  exception  is  to  discover  that  there  has  been  any  special  injury 
or  trauma,  such  as  scalding  or  corrosive  poisoning,  and  if  there  is  a  history 
of  them  they  are  to  be  regarded  as  merely  contributory  causes.  Far  more 
important,  however,  is  the  fact  which  the  investigations  of  Hauser  have  lately 
confirmed,  that  gastric  carcinoma  is  not  infrequently  developed  in  the  cica- 
trized edges  of  a  previous  gastric  ulcer.  We  have  ourselves  had  a  consider- 
able number  of  cases  in  which  both  the  clinical  course  of  the  disease  and  the 
results  of  the  autopsy  illustrated  this  mode  of  development.  We  shall  later 
discuss  in  greater  detail  certain  important  clinical  peculiarities  of  this  "  ulcer 
carcinoma." 

Pathology. — The  stomach  is  a  favorite  seat  for  cancer.  About  a  third  of 
all  cases  of  cancer  are  gastric.  The  parts  of  the  organ  most  often  attacked 
are  the  pyloric  end  and  the  lesser  curvature.  Less  frequently  the  cardiac  end 
and  the  fundus  suffer. 

The  new  growth  takes  the  form  either  of  a  circumscribed  tumor  or  of  a 
diffuse  infiltration,  thickening  the  walls.  The  disease  invariably  originates 
in  the  mucous  layer,  extending  thence  after  perforating  the  muscularis 
mucosae  into  the  submucous,  muscular,  and  serous  coats.  Often  the  cancer 
extends  by  way  of  the  lymph-channels,  or  sometimes  the  veins.  The  lymph- 
glands  and  the  omentum  are  frequently  attacked  by  the  new  growth.  More- 
over, we  find  metastases  in  the  peritoneum,  and  also  with  particular  frequency 
and  abundance  in  the  liver,  whither  cancerous  cells  are  carried  by  the  branches 
of  the  portal  vein.  The  connective  and  muscular  tissues  in  the  neighborhood 
of  the  cancer  are  quite  often  considerably  hypertrophied. 

Histologically,  gastric  cancer  is  of  the  cylindrical-cell  variety,  starting 
from  the  glandular  epithelium.  The  soft  tumors  are  termed  medullary;  the 
firm  and  hard,  scirrhous  or  fibroid.  The  medullary  cancers  are  particularly 
apt  to  be  quite  extensively  broken  down  on  their  exposed  internal  surface,  thus 
forming  what  are  known  as  cancerous  ulcers.  This  seems  to  be  mainly  the 
result  of  the  gastric  juice  acting  on  the  superficial  and  insufficiently  vascu- 
larized portion  of  the  tumor.  The  base  of  these  ulcers  is  therefore  usually 
clean.  Not  infrequently,  however,  the  base  has  a  necrotic  and  gangrenous 
character  and  parts  of  the  tumor  may  slough  off.  In  many  cases  affecting 
rather  young  subjects,  and  sometimes  in  others,  we  find  colloid  cancer.  This 
form  also  may  appear  either  in  nodules  or  as  a  diffuse  growth,  infiltrating  the 
tissues.  It  is  peculiarly  apt  to  involve  the  peritoneum  extensively,  with  con- 
sequent ascites. 

Clinical  History. — Most  cases  of  gastric  cancer  exhibit  a  combination  of 
grave  digestive  disturbances  with  a  relatively  rapid  loss  of  flesh  and  strength. 
Now  and  then  the  gastric  symptoms  assume  less  prominence.  The  chief  sign 
of  disease  is  a  constantly  progressive  marasmus  or  anaemia,  the  true  cause  of 
which  is  either  entirely  latent  or  not  unmistakably  recognizable  till  late  in 
the  illness. 

Some  of  the  gastric  symptoms  are  not  very  characteristic.  They  merely 
show  that  digestion  is  disordered.     The  tongue  is  usually  thickly  coated  and 


CANCER  OF  THE   STOMA*  II  545 

dry.  There  is  loss  of  appetite,  often  a  special  aversion  to  meat,  and  distn 
after  meals.  The  patient  complains  of  a  disagreeable  sensation  of  pressure 
in  the  epigastrium,  increased  by  food.  Sometimes  this  amounts  to  actual 
cardialgia.  A  constant  painful  sensation  in  the  gastric  region  and  also  burn- 
ing pains  in  the  back  are  frecpiently  observed.  Some  patients  are  annoyed  by 
eructations.  Occasionally  vomiting  is  troublesome;  in  other  instances  there 
is  scarcely  any.  The  constant  recurrence  of  vomiting  is  an  almost  sure  sign 
that  the  cancer  is  situated  in  the  pyloric  region  and  obstructs  the  orifice.  The 
vomitus  may  contain  nothing  but  mucus  and  ingesta ;  or  it  may  assume,  from 
the  admixture  of  blood,  a  very  characteristic  and  somewhat  pathognomonic 
appearance. 

Free  gastric  hemorrhage  and  consequent  hematemesis  is  exceptional,  or  at 
least  it  is  much  less  frequent  than  in  ulcer  of  the  stomach;  but  the  vomitus 
often  contains  decomposed  blood,  and  in  many  cases  this  will  be  for  a  time 
almost  a  constant  appearance.  Most  of  the  ulcerated  cancers  bleed  frequently, 
a  little  at  a  time.  When  it  reaches  the  stomach  the  blood  is  decomposed  and 
gives  that  well-known  "  coffee-grounds  "  or  "  chocolate-colored  "  appearance 
to  the  vomitus,  or  to  the  gastric  contents  obtained  by  means  of  a  stomach 
tube,  which  is  so  important  a  symptom  for  the  diagnosis  of  cancer  of  the 
stomach.  In  such  cases  the  best  means  for  demonstrating  the  presence  of 
blood,  in  the  brownish  or  blackish  fluid,  is  the  guaiac-turpentine  test  (vide 
supra,  page  517).  This  gives  an  extremely  distinct  reaction  in  the  case  of 
carcinoma  of  the  stomach,  because  lactic  acid  also  is  usually  present.  We 
should  mention  that  in  the  case  of  ulcerating  carcinoma  ventriculi  the  vomitus 
may  have  so  foul  an  odor  that  it  may  even  be  regarded  as  stercoraceous. 

Immediate  microscopic  examination  of  the  vomitus  may  reveal  red  blood 
globules.  Further,  the  vomitus  consists  of  partially  digested  food,  and  also 
contains  an  abundance  of  microorganisms.  Sarcinge  are  found  much  less 
often  in  carcinoma  than  in  ulcer  of  the  stomach,  but  we  frequently  see  under 
the  microscope  an  abundance  of  yeast  cells,  and  of  long  threadlike  bacilli 
which  have  a  relation  to  lactic-acid  fermentation  (vide  infra).  It  is  extremely 
rare  to  find  in  the  vomitus  characteristic  particles  of  cancer.  It  is  somewhat 
less  unusual  to  find  little  pieces  of  the  growth  attached  to  the  stomach  tube 
when  the  carcinoma  is  at  the  cardiac  end  or  in  the  fundus  of  the  stomach. 
These,  if  obtained,  are,  of  course,  to  be  submitted  to  microscopic  examination. 

External  objective  examination.  Sometimes  we  can  clearly  recognize  by 
mere  inspection  the  position  and  size  of  the  organ,  any  peristaltic  motions  (vide 
infra)  that  there  may  be,  and  even  in  some  cases  the  presence  of  a  tumor. 

Palpation  must  be  practiced  with  especial  care  in  every  doubtful  case.  It 
is  carried  out  with  the  patient  in  a  completely  horizontal  dorsal  position,  or 
occasionally,  under  special  circumstances,  in  a  lateral  position.  We  must  try 
to  obtain  the  greatest  possible  relaxation,  and,  if  necessary,  we  should  palpate 
while  the  patient  is  in  a  warm  bath.  We  palpate  alternately  with  gentle  and 
with  deep  respiration  to  determine  the  mobility  of  any  existing  tumor.  It  is 
often  useful  to  exert  counter  pressure  on  the  soft  parts  by  placing  the  left 
hand  under  the  patient's  back.  We  must  always  begin  with  very  gentle  pal- 
pation and  then  gradually  use  deeper  pressure.  In  a  great  many  cases  the 
new  growth  can  be  felt  with  distinctness  through  the  abdominal  wall  as  a  hard 
irregular  tumor.     It  is  often  useful  to  hold  the  fingers  quiet  and  press  lightly 


546  DISEASES  OF  THE  DIGESTIVE  ORGANS 

on  the  abdominal  wall  while  the  patient  breathes  deeply.  We  then  occasion- 
ally feel  the  tumor  gliding  downward  under  the  fingers.  The  situation  of  the 
tumor  is,  in  a  majority  of  cases,  the  epigastrium.  Carcinoma  of  the  pylorus, 
which  is  the  most  common,  is  usually  felt  in  the  middle  or  in  the  right  half 
of  the  epigastrium;  carcinoma  of  the  greater  curvature  somewhere  in  the 
level  of  the  navel.  But  it  should  be  considered  that  the  position  of  the  stom- 
ach may  be  considerably  altered  by  the  presence  of  a  growth — for  example, 
we  have  seen  a  case  of  pyloric  cancer  with  secondary  dilatation  of  the  stomach, 
in  which  the  pylorus  had  sunk  so  low  that  the  tumor  could  be  felt  about  a 
hand's  breadth  above  the  symphysis.  In  some  cases  the  tumor  varies  its  posi- 
tion (vide  infra)  according  to  the  degree  of  distention  of  the  stomach.  The 
influence  of  respiration  upon  the  tumor  is  various.  The  majority  of  gastric 
cancers,  particularly  cancers  of  the  lesser  and  greater  curvatures,  move  with 
respiration.  When  displaced  downward  by  inspiration  they  may  be-  held  in 
that  position  with  the  hand,  returning  to  their  ordinary  location  when  the 
hand  is  removed.  Tumors  of  the  liver  and  cancers  of  the  stomach  which  are 
adherent  to  the  liver  cannot  be  thus  held  down.  When  the  carcinoma  is  situ- 
ated high  up,  in  the  lesser  curvature  or  near  the  oesophagus,  it  may  not  be  felt 
at  all  except  during  inspiration. 

In  a  minority  of  the  cases  no  tumor  can  be  felt  at  any  time.  The  tumor 
is  undiscoverable,  first,  in  most  cases  of  diffuse  cancerous  infiltration  of  the 
stomach  walls.  We  may,  indeed,  notice  an  increased  sense  of  resistance  and 
hardness  in  the  epigastrium,  but  we  cannot  refer  this  condition  with  certainty 
to  a  new  growth.  Secondly,  the  new  growth  may  extend  chiefly  inward,  toward 
the  cavity  of  the  organ,  and  may  thus  escape  detection.  And,  finally,  the  tumor 
may  be  so  concealed  by  the  liver  or  the  edge  of  the  ribs  that  it  is  inaccessible 
to  the  touch.  Such  cancers  as  attack  the  cardiac  extremity,  the  posterior  wall, 
or  the  lesser  curvature  of  the  stomach,  are  particularly  apt  to  be  out  of  reach 
of  palpation. 

Percussion  of  the  cancer  rarely  gives  flatness,  but  instead  a  muffled  tym- 
panitic resonance.  This  is  sometimes  an  influential  factor  in  the  differential 
diagnosis  from  cancer  of  the  liver.  In  a  few  cases,  upon  auscultation  in  the 
neighborhood  of  the  tumor,  we  may  hear  a  soft  systolic  murmur,  probably  due 
to  compression  of  a  rather  large  artery. 

Examination  of  the  gastric  contents.  While  introducing  the  stomach  tube, 
or  perhaps,  if  need  be,  a  less  flexible  instrument,  we  should  notice  whether  the 
tube  enters  the  stomach  with  ease.  Carcinoma  at  the  cardia  is  not  infrequently 
the  cause  of  a  sensible  resistance  to  the  tube  when  it  passes  the  lower  end  of 
the  oesophagus.  With  regard  to  the  examination  of  the  gastric  contents,  the 
chief  point  is  about  free  hydrochloric  acid.  Von  der  Velden  first  pointed  out 
what  numerous  investigations  have  since  confirmed,  that  in  almost  all  cases 
of  gastric  carcinoma  there  is  no  free  hydrochloric  acid,  so  that  the  phloro- 
glucin-vanillin  reaction  an  hour  after  the  test  breakfast  is  negative.  Asso- 
ciated with  other  symptoms  this  is  an  extremely  important  diagnostic  sign 
(vide  infra).  The  cause  of  this  almost  invariable  absence  of  free  hydrochloric 
acid  in  carcinoma  of  the  stomach  has  not  yet  been  determined,  especially  as 
this  symptom  has  often  been  observed  very  early  in  the  course  of  the  disease. 
The  associated  catarrh  of  the  gastric  mucous  membrane  and  its  secondary 
atrophy  may  have  some  influence,  but  probably  there  are  also  other  unknown 


CANCER  OF  THE  STOMACH  547 

causes  at  work.  An  examination  for  pepsin  may  be  omitted  in  practice;  it  also 
often  turns  out  negative.  Far  greater  importance  attaches  to  the  fact  thai  the 
gastric  contents  in  carcinoma  are  very  apt  to  show  a  surprising  amount  of  laci  ic 
acid.  This  is  almost  invariably  so  when  the  carcinoma  obstructs  the  pylorus. 
The  explanation  of  this  is  very  simple.  There  is  no  hydrochloric  acid  to 
exert  an  antiseptic  action,  and  the  food  is  stagnant  in  the  stomach,  so  that 
there  is  an  especially  favorable  opportunity  for  the  development  of  a  vigorous 
lactic-acid  fermentation.  There  is,  then,  nothing  specific  about  the  presence 
of  lactic  acid  in  the  gastric  contents  in  cases  of  carcinoma,  only  it  is  a  very 
frequent  and  therefore  important  symptom. 

The  producers  of  lactic-acid  fermentation  in  the  stomach  contents  are  the 
lactic-acid  bacilli  [Oppler-Boas  bacilli]  which  are  usually  readily  demonstrated 
microscopically  whenever  the  gastric  contents  contains  lactic  acid.  They  are 
distinguished  by  their  growth  into  long  threads.  The  microscopic  demonstra- 
tion in  the  gastric  juice  of  the  "long  bacilli"  (vide  Fig.  72),  which  may  also 
be  easily  grown  in  pure  culture,  has  therefore  no  slight  diagnostic  significance 
in  the  recognition  of  carcinoma  of  the  stomach. 

The  motor  efficiency  of  the  stomach  is  impaired  in  most  cases  of  carci- 
noma, except  in  cancer  affecting  the  cardia,  or  in  small  cancers  on  the  fundus. 
Whenever  there  is  an  extensive  development  of  carcinoma  of  the  stomach,  the 
muscular  coat  of  the  organ  is  sufficiently  damaged  to  embarrass  its  motor  activ- 
ity ;  but  of  course  the  hindrance  to  the  discharge  of  its  contents  is  greatest  when 
the  new  growth  is  at  the  pylorus.  In  this  case,  besides  the  direct  destruction  of 
the  muscular  tissue,  we  have  the  purely  mechanical  stenosis,  and  this  may 
at  last  become  extreme.  For  this  reason,  if  we  find  a  marked  stagnation  of  the 
ingesta  we  can  usually  infer  that  the  seat  of  the  carcinoma  is  the  pylorus  (vide 
infra).  We  should  not  omit  to  inflate  the  stomach  when  it  is  possible.  We 
can  thus  determine  not  only  the  size  and  position  of  the  stomach,  but  also  its 
relations  to  any  tumor  that  may  be  felt ;  and  finally,  it  should  be  added  that  a 
test  for  blood  (vide  infra)  should  be  made  with  the  fluid  obtained  by  washing 
out  the  stomach. 

Certain  peculiarities  in  the  clinical  picture  of  gastric  carcinoma  are  occa- 
sioned by  its  special  location ;  if  at  the  cardia,  the  symptoms  are  similar  to  those 
of  cancer  of  the  oesophagus.  As  soon  as  the  cardia  is  narrowed,  the  patient  him- 
self feels  that  it  is  difficult  for  food  to  enter  the  stomach,  and  speedily  there 
appears  vomiting,  or,  more  accurately,  regurgitation  of  food,  so  that  the  patient 
can  take  nothing  but  liquid  nourishment.  The  diagnosis  of  carcinoma  at  the 
cardia  is  usually  easy.  We  feel  the  resistance  at  the  cardia  with  the  stomach 
tube  some  16  to  18  inches  (40  to  45  cm.)  from  the  front  teeth.  Externally 
the  growth  cannot  be  felt  until  it  invades  the  lesser  curvature  of  the  stomach. 
Then  we  often  feel  the  tumor  in  the  epigastric  angle,  especially  on  deep  inspira- 
tion. In  carcinoma  of  the  fundus  the  symptoms  may  be  indefinite  for  a  long 
time.  The  pylorus  remaining  permeable,  there  may  be  no  vomiting  at  all.  In 
late  stages  the  tumor  which  may  be  felt  is  often  very  large,  particularly  if  there 
is  involvement  of  the  omentum,  which  changes  it  into  a  great  cancer  mass. 

When  cancer  at  the  pylorus  leads  to  stenosis,  the  clinical  picture  is  especially 
important  as  well  as  very  common  and  very  characteristic.  As  soon  as  there  is 
a  hindrance  to  the  emptying  of  the  stomach,  whether  because  the  muscular  coat 
is  impaired  by  infiltration  with  carcinoma  or  because  there  is  the  direct  mechan- 


548  DISEASES  OF  THE  DIGESTIVE  ORGANS 

ical  obstacle  of  stenosis,  there  result  retention  and  accumulation  of  food  in  the 
stomach,  with  exaggerated  peristalsis,  and  finally  gastric  dilatation.  The  cir- 
cumstances are  precisely  similar  to  those  depicted  in  the  preceding  chapter  when 
speaking  of  cicatricial  stenosis  (cf.  page  536).  In  advanced  cases  the  contours 
of  the  dilated  organ  are  clearly  seen  through  the  emaciated  and  collapsed  ab- 
dominal walls.  From  time  to  time  a  contraction  occurs,  and  we  see  the  peristal- 
tic wave  slowly  travel  toward  the  pylorus.  Very  often  the  carcinomatous  growth 
near  the  pylorus  is  distinctly  palpable,  and  even  visible.  Often  it  moves  with 
respiration.  Washing  out  the  stomach  will  demonstrate  the  stagnation  of  its 
contents,  and  by  inflation  we  determine  its  size  and  position.  If  the  stomach 
is  not  emptied  artificially,  from  time  to  time  very  large  amounts  are  vomited, 
the  vomitus  being  invariably  devoid  of  hydrochloric  acid  but  containing  much 
lactic  acid,  and  sometimes  also  showing  fermentation  (vide  supra,  page  510). 

In  addition  to  the  symptoms  of  gastric  cancer,  referable  to  the  stomach 
itself,  the  greatest  attention  should  also  be  paid  to  the  general  disturbance  of 
nutrition  occasioned  by  this  gastric  disease.  Loss  of  flesh  is  not  rarely  the 
very  first  symptom  which  calls  the  patient's  attention  to  his  disease.  This 
wasting  is  observed  earliest  in  cases  which  are  attended  with  anorexia  and 
vomiting.  The  patient  also  gradually  takes  on  that  familiar  sallow  cachectic 
look  which  is  characteristic  of  most  cases  of  cancer.  This  abnormal  color  of  the 
face  is  all  the  more  striking  because  patients  with  gastric  cancer  comparatively 
rarely  have  marked  gray  hair.  As  my  teacher,  Wunderlich,  always  empha- 
sized in  his  clinic,  and  as  I  can  confirm  from  my  own  experience,  it  is  cer- 
tainly remarkable  how  frequently  even  elderly  patients  with  gastric  cancer 
(over  fifty  years  of  age)  have  hair  that  is  scarcely  tinged  with  gray.  Some 
patients  become  excessively  anasmic.  The  skin  acquires  a  waxy  pallor,  and  there 
are  all  the  symptoms  which  result  from  great  anaemia,  such  as  cerebral  dis- 
turbances and  functional  cardiac  murmurs.  Sometimes  the  blood  itself  pre- 
sents decided  peculiarities  in  such  cases.  Thus  we  may  find  microcytes  and 
poikilocytes  in  it.  Gastric  cancer  and  pernicious  anaemia  (q.  v.)  have  been 
repeatedly  confounded.  In  one  such  case  we  made  the  interesting  discovery 
of  extremely  abundant  metastatic  cancer  in  the  bones.  As  the  bone  marrow 
is  known  to  have  something  to  do  with  the  production  of  the  blood,  it  may  be 
that  the  anaemia  was  due  to  this  abnormal  condition.  At  any  rate,  the  grave 
anaemia  which  results  from  cancer  cannot  be  regarded  in  just  the  same  light 
as  the  loss  of  flesh  and  the  cachexia.  We  often  find  extreme  anaemia  in  patients 
who  are  tolerably  well  nourished,  while,  on  the  other  hand,  many  patients  with 
carcinoma,  though  emaciated  to  a  skeleton,  do  not  display  this  peculiar  anaemic 
pallor.  The  anaemia  must,  therefore,  depend  upon  some  special  circumstances, 
and  I  have  no  doubt  that  it  is  most  frequently  caused  by  continued  though 
small  hemorrhages,  due  to  ulceration  of  the  new  growth.  In  other  cases, 
however,  it  would  seem  that  the  blood  is  also  affected  by  specific  harmful  influ- 
ences. 

Special  derangements  of  other  organs  are  relatively  infrequent.  Metastatic 
cancer  is  of  importance.  It  attacks  the  liver  chiefly.  If  the  hepatic  new  growth 
is  considerable,  it  may  quite  overshadow  the  primary  cancer — there  being  jaun- 
dice and  a  greatly  enlarged,  nodular,  and  tender  liver.  Secondary  carcinosis 
of  the  peritoneum  is  also  apt  to  cause  marked  symptoms,  such  as  ascites  and 
abdominal  pain.     Extensive  carcinoma  of  the  omentum  often  produces  large 


CANCER   OF  THE   STOMACH  549 

tumors  which  may  be  felt  even  during  life,  and  which  are  difficult  to  differ- 
entiate from  the  actual  stomach  tumor.  Large  tumors,  lying  transversely 
across  the  epigastrium,  are  frequently  found  at  autopsy  to  be  a  carcinomatous 

degenerated  and  shrunken  omentum.  The  fact  is  very  important  that  we  not 
infrequently  can  demonstrate  peritoneal  metastases  in  the  true  pelvis  by  rectal 
or  vaginal  examination.  Secondary  cancer  may  also  involve  the  mesenteric 
and  retroperitoneal  lymph-glands,  the  lungs,  and  other  organs,  but  it  does  not 
usually  give  rise  to  striking  symptoms  when  so  situated,  although  the  discov- 
ery of  even  small  metastases  by  palpation  may  have  great  diagnostic  signifi- 
cance. Metastatic  lymph-gland  enlargement  in  the  left  supraclavicular  fossa 
(so-called  Virchow's  gland)  is  not  common,  though  I  have  repeatedly  observed 
it  in  characteristic  form.  Swelling  of  the  inguinal  glands  is  also  important. 
We  have  seen  small  metastases  in  them  several  times.  Finally,  we  would  like 
to  call  special  attention  to  the  appearance  of  small  secondary  nodules  at  the 
navel,  a  fact  which  I  have  repeatedly  noticed.  The  discovery  of  such  a  growth 
is  of  great  diagnostic  value  when  no  primary  tumor  can  be  made  out  by  palpa- 
tion. Occasionally  a  rounded,  hard  strand  can  be  felt  running  from  the  umbili- 
cus downward  along  the  linea  alba — a  carcinomatous  lymphatic  vessel  (?). 

Direct  extension  of  the  new  growth  into  neighboring  organs  is  not  very  fre- 
quent. We  will  venture  to  mention  one  case  which  we  saw,  on  account  of  its 
great  rarity.  The  new  growth  caused  adhesion  of  the  anterior  wall  of  the  stom- 
ach to  the  abdominal  walls,  and  then,  penetrating  through  them  and  the  skin  of 
the  epigastrium,  finally  appeared  as  a  tumor,  of  about  the  size  of  one's  first,  pro- 
jecting outward.  If  a  cancer  ulcerates,  it  may  destroy  all  the  layers  of  the 
stomach,  and  result  in  perforation  and  secondary  peritonitis;  or,  if  previous 
adhesions  have  been  formed,  the  perforation  may  open  up  an  abnormal  commu- 
nication between  the  stomach  and  some  neighboring  part  of  the  intestine.  The 
transverse  colon  is  the  part  usually  perforated;  less  often  the  small  intestine. 
With  perforation  into  the  colon  a  temporary  communication  may  form  between 
this  organ  and  the  stomach.  Then,  as  we  have  had  occasion  to  observe  in  one 
case,  feculent  masses  may  be  vomited,  and  the  stool  present  the  appearance  of 
gastric  contents. 

As  to  the  bowels,  constipation  is  the  rule.  Diarrhea  is  rare.  A  dark  appear- 
ance of  the  stool  due  to  admixture  of  blood  may  be  of  diagnostic  significance. 
The  urine  is  usually  pale  and  but  slightly  acid.  Its  amount  is  diminished,  as 
we  should  expect  from  the  slight  amount  of  nourishment  taken,  and  from  the 
vomiting.  Over  the  heart  we  may  sometimes  hear  soft  anaemic  murmurs.  The 
pulse  is  usually  accelerated,  although,  if  there  be  extreme  marasmus,  it  may  be 
slow.  The  blood  shows  the  microscopic  changes  of  anaemia  (vide  supra)  and 
a  slight  leucocytosis,  which  latter  fact  may,  under  certain  conditions,  be  used 
in  the  differential  diagnosis  from  pernicious  anaemia. 

The  temperature  is  often  normal.  If  the  patient  is  greatly  emaciated  it  is 
not  infrequently  subnormal,  but,  on  the  other  hand,  if  the  thermometer  is  care- 
fully used  we  shall  very  often  find  occasional  irregular  elevations  of  tempera- 
ture, 100.5°  to  102°  F.  (38°  to  39°  C),  or  even  a  persistent  or  intermittent 
fever.  The  cause  of  these  elevations,  exclusive  of  complications,  is  probably,  in 
most  cases,  the  absorption  of  septic  material  from  the  ulcerated  surface  of  the 
carcinoma.  If  there  are  hemorrhages,  another  factor  may  be  the  absorption  of 
the  decomposed  blood  (fibrin  ferment).  Not  infrequently,  in  advanced  stages 
35 


550  DISEASES  OF  THE  DIGESTIVE  ORGANS 

of  the  disease  there  is  more  or  less  oedema  of  the  ankles,  hands,  and  other  parts. 
The  explanation  of  this  is  the  same  as  in  most  cases  of  oedema  in  cachectic  and 
anaemic  patients — viz.,  the  impaired  nutrition  of  the  vascular  walls,  the 
hydremia,  and  the  associated  cardiac  weakness.  Sometimes  there  also  occur 
marked  pains  in  the  arms  and  legs.  The  temperature  is  normal,  or  even  sub- 
normal. If  there  is  some  inflammatory  complication,  or  if  the  anaemia  is  ex- 
treme, fever  may  occur. 

The  entire  duration  of  the  disease  may  be  one  or  two  years.  It  is  excep- 
tional for  it  to  last  longer,  except  when  the  cancer  develops  in  the  floor  of  a  pre- 
existing ulcer.  In  this  case  the  symptoms  of  gastric  ulcer  pass  into  those  of 
carcinoma.  The  change  may  be  gradual,  but  there  may  be  an  intervening  period 
of  apparent  health.  We  have  by  careful  questioning  repeatedly  been  able  to 
make  the  diagnosis  of  this  transformation  during  the  life  of  the  patient,  in  cases 
later  confirmed  by  autopsy.  In  individual  instances  the  disease,  of  course,  ex- 
hibits many  variations  and  departures  from  the  typical  course.  Sometimes  the 
constitutional  symptoms  of  weakness  and  emaciation  are  more  prominent,  and 
sometimes  the  distinctively  gastric  disturbances. 

The  fatal  termination  is  usually  preceded  by  the  s}rmptoms  of  constantly 
increasing  weakness.  It  may  be  hastened  by  complications,  such  as  perforative 
peritonitis.  Now  and  then  grave  nervous  symptoms  appear,  often  quite  sud- 
denly. The  patient  falls  into  a  condition  resembling  that  of  diabetic  coma 
(q.  v.),  he  is  somnolent,  and  has  a  peculiar  dyspnoea,  with  deep  and  labored  res- 
pirations. Such  an  attack  is  probably  due  to  autointoxication,  and  almost 
always  ends  fatally.     Recovery  from  cancer  of  the  stomach  is  unknown. 

Diagnosis. — Gastric  cancer  is  a  comparatively  frequent  disease,  and  in 
every  case  in  which  there  are  well-marked  gastric  symptoms,  particularly  in  an 
elderly  person,  the  physician  should  think  of  the  possibility  of  this  grave  disease. 
The  suspicion  is  all  the  more  justified  when  the  symptoms  occur  in  a  previ- 
ously healthy  individual  without  known  cause,  and  if  they  are  associated  from 
the  start  with  a  cachectic  look  and  a  feeling  of  weakness  and  languor,  as  well  as 
with  marked  emaciation.  If  now,  having  such  suspicions,  we  wish  to  reach  a 
diagnosis,  the  first  requirement  is  a  thorough  investigation  of  the  stomach. 
External  examination  should  be  particularly  directed  to  the  discovery  of  a  pal- 
pable tumor,  if  any  exists.  We  should  examine  while  the  patient  is  lying  on  his 
back  or  on  his  side.  If  possible,  the  stomach  should  be  empty  and  we  should 
palpate  while  the  patient  is  breathing  quietly,  and  also  while  he  is  taking  deep 
inspirations.  If  a  tumor  can  be  felt,  the  next  question  is  whether  it  actually 
arises  from  the  stomach  or  from  some  other  organ.  In  most  cases  the  other 
clinical  symptoms,  such  as  vomiting,  have  already  indicated  the  stomach  as  the 
seat  of  the  disease,  and  thus  we  know  the  origin  of  the  tumor.  On  the  other 
hand,  however,  there  may  be  great  obscurity,  and  many  cases  of  gastric  tumor 
have  been  confounded  with  carcinoma  of  the  left  lobe  of  the  liver,  the  pancreas, 
the  omentum,  the  transverse  colon,  and  other  parts.  It  is  difficult  to  lay  down 
special  rules  for  diagnosis,  because  the  difficult  cases  almost  invariably  have 
their  own  special  peculiarities.  Of  importance  in  every  case  are  an  accurate 
local  examination,  a  mapping  out  of  the  neighboring  organs,  inflation  of  the 
stomach  and  perhaps  also  of  the  colon,  determining  whether  the  mass  moves 
with  respiration,  and  a  consideration  of  all  the  other  factors.  Among  these  last 
the  most  important  is  the  result  of  an  examination  with  the  stomach  tube.    The 


CANCER  OF   THE   STOMACH 


551 


main  question  in  every  case  is  the  presence  or  absence  of  free  hydrochloric  acid 
in  the  gastric;  juice.  If  it. is  absent  on  repealed  examination  our  suspicion  of 
carcinoma  is  confirmed,  provided  the  other  symptom-  poinl  in  the  same  direc- 
tion; but  if  they  do  not,  the  absence  of  free  hydrochloric  acid  is  by  no  means 
so  grave  a  matter,  for  it  is  absent  often  enough  under  other  circumstanci 
is,  however,  a  fact  of  great  practical  importance  that  when  Free  hydrochloric 
acid  has  been  distinctly  and  repeatedly  demonstrated  in  the  gastric  juice, 
gastric  cancer  is  quite  unlikely,  even  if  other  symptoms  poinl  to  it. 

In  those  cases  alone,  where  a  carcinoma  has  developed  on  the  basis  of  an 
old  gastric  ulcer,  the  gastric  contents  may,  at  least  in  the  beginning,  still  show 
a  greater  or  lesser  amount  of  free  hydrochloric  acid.  It  is  often  impossible  to 
make  the  diagnosis  of  a  cancer  just  developing  when  it  is  certain  that  there  is 
pyloric  stenosis  due  to  ulcer.  If  there  is  no  free  hydrochloric  acid,  but  lactic 
acid,  and  also  impaired  motor  efficiency,  the  circumstances  are  different.  The 
diagnosis  of  pyloric  cancer  is  then  almost  certain.  The  demonstration  of  im- 
paired motor  efficiency  is  therefore  at  least  as  important  as  the  examination 
for  free  hydrochloric  acid.  In  case  of  stasis  with  simultaneous  absence  of 
hydrochloric  acid,  even  if  no  tumor  can  be  felt,  there  is  great  probability  of  a 
gastric  carcinoma,  probably  involving  the  pylorus. 

Very  important,  also,  are  the  other  characteristics  of  the  gastric  contents, 
the  defective  digestion  of  food,  the  putrid  odor,  and  above  all  the  demon- 
stration of  blood  in  the  gastric  contents  (vide  supra,  page  517).  If  we  have 
distinct  "  coffee-ground  "  vomitus,  and  at  the  same  time  achlorhydria,  these 
factors  alone  almost  establish  the  diagnosis,  but  even  smaller  amounts  of  blood, 
only  chemically  demonstrable,  are  important.  Finally,  we  should  bear  in 
mind  that  when  no  gastric  tumor  is  made  out  there  may  be  metastatic  growths 
which  can  be  felt — for  ex- 
ample, in  the  lymph-glands — 
and  thus  a  diagnosis  of  can- 
cer confirmed. 

In  case  of  symptoms  which 
indicate  stenosis  of  the  py- 
lorus, with  subsequent  gas- 
trectasia,  it  is  of  great  prac- 
tical importance  to  determine 
whether  they  are  due  to  can- 
cer or  to  the  scar  of  an  ulcer. 
In  this  instance,  even  if  we 
feel  a  tumor,  that  fact  is  not 
decisive,  for  the  cicatricial 
hyperplasia  of  gastric  ulcer 
may  cause  a  distinct  tumor, 
although  a  comparatively 
small  one;  but,  as  a  rule,  it 
is  not  difficult  to  reach  a  de- 
cision.      Suggesting     a     scar 

from  ulcer  would  be :  long  duration  of  the  disease  (two  years,  sometimes  four 
or  five  years,  and  longer)  ;  youth  of  the  patient;  comparatively  healthy  appear- 
ance; distinct  history  of  ulcer;  cardialgia;  profuse  hematemesis;  and  finally, 


j__  /<!)#$/  / 


Fig.  72. — Gastric  Contents  in  Cancer  of  the  Pylorus. 
a.  Long  (Oppler-Boas)  bacilli,  b.  Yeast  cells,  c. 
Fat  droplet,  d.  Fatty-acid  crystals,  e.  Starch  gran- 
ules.   /.  Detritus,     g.  Leucocyte,     h.  Erythrocytes. 


552 


DISEASES   OF  THE   DIGESTIVE   ORGANS 


Fig.  73. — Gastric  contents  in  benign  stenosis,  a.  Sarcinas.  b. 
Yeast  cells,  c.  Fat  droplet,  d.  Fatty  acid  crystals,  e.  Starch 
granules.    /.  Detritus,     g.  Muscle  fiber. 


as  a  decisive  factor,  the  demonstration  of  an  abundance  of  hydrochloric  acid 
and  hypersecretion  in  the  stomach.  Under  these  circumstances  the  differen- 
tiation of  stenosis  from  ulcer  is  absolutely  certain.     On  the  other  hand,  there 

is  complete  certainty  of  a 
cancerous  stenosis  if  the 
disease  has  developed  in  a 
comparatively  brief  time 
— in  one  or  two  years;  if 
it  has  attacked  an  elderly 
person;  if  there  is  dis- 
tinct cachexia;  and,  most 
important  of  all,  if  hy- 
drochloric acid  is  never 
demonstrable  in  the  gas- 
tric contents,  while  there 
is  an  abundance  of  lactic 
acid.  Other  cases  occur 
which  are  not  typical  nor 
of  easy  diagnosis.  Age, 
duration  of  the  disease, 
and  previous  symptoms 
may  suggest  a  stenosis 
due  to  ulcer,  and  yet  on  washing  out  the  stomach  we  find  no  hydrochloric  acid 
at  all,  or,  at  most  a  faint  trace.  In  these  cases  we  are  usually  justified  in 
assuming  that  carcinoma  has  developed  secondarily  on  the  floor  of  a  former 
ulcer.  It  must  be  confessed  that  in  simple  stenosis  following  ulcer,  when 
there  is  an  excessive  stagnation  of  the  gastric  contents,  there  may  be  tem- 
porarily a  complete  combination  of  all  the  hydrochloric  acid  with  albumen, 
and  consequently  no  reaction  for  free  hydrochloric  acid;  but  if  the  stomach 
is  washed  out  a  few  times  we  soon  find  an  abundance  of  free  hydrochloric 
acid.  On  the  other  hand,  when'  a  stenosis  due  to  ulcer  has  lasted  for  a  long 
time,  our  suspicions  should  be  aroused  if  the  reaction  for  hydrochloric  acid 
is  persistently  feeble  or  at  times  absent,  and  in  its  place  or  along  with  it  lactic 
acid  appears  in  the  gastric  contents.  We  have  ourselves  repeatedly  seen  this 
gradual  transition  of  simple  stenosis,  due  to  ulcer  with  hypersecretion,  into 
carcinomatous  stenosis  with  achlorhydria.  Finally,  it  should  be  remarked  that 
there  is  also  a  stenosis  of  the  pylorus  due  to  simple  hypertrophy  of  its  walls, 
without  any  ulcer  or  carcinoma.  We  have  ourselves  seen  a  few  cases  of  this 
sort  which  presented  the  ordinary  symptoms  of  pyloric  stenosis  with  great 
dilatation,  and  ended  fatally.  The  pathogenesis  of  this  rare  condition  has  not 
yet  been  explained.  We  venture  to  suggest  that  perhaps  it  may  be  due  to 
congenital  anomalies,  more  especially  as  this  type  of  pyloric  stenosis  has 
also  been  repeatedly  observed  even  in  suckling  infants.  Of  late,  these  cases 
have  also  been  frequently  termed  pylorospasm,  though  the  assumption  of 
an  habitual  cramp-like  condition  at  the  pylorus  is  still  purely  hypothetical. 
As  yet,  unfortunately,  no  particulars  are  known  as  to  the  constituents  of 
the  gastric  juice  in  these  cases,  and  for  the  present  it  is  scarcely  possible 
to  make  a  diagnosis  of  them  with  certainty,  except  in  pyloric  stenosis  of 
infants. 


CANCER  OF  THE  STOMACH  553 

Treatment. — If  once  the  diagnosis  of  gastric  carcinoma  has  heen  settled, 
the  question  arises  whether  there  is  any  definite  prosped  of  success  from 
surgical  treatment.     II'  not,  our  treatment  can  he  merely  symptomatic  with 

the  ohject  of  alleviating  the  patient's  suffering,  and  preserving   bis  strength 
as  long  as  possible. 

The  first  point  in  symptomatic  treatment  is  a  regulation  of  the  diet.  In 
general,  we  advise  mainly  liquids  and  soft  foods,  including  milk,  gruel,  rice, 
sago,  delicate  vegetables,  potato  puree,  softened  zwieback,  toast,  or  crackers, 
and  delicate  puddings.  We  may  also  permit  finely  chopped  or  scraped  meat, 
or,  still  better,  fowl;  and  fish,  such  as  trout,  pike,  and  perch-pike.  Such 
artificial  foods  as  somatose,  neutrose,  beef  peptone  and  beef  juice,  and  infants' 
foods,  do  good  service  for  a  time.  If  the  appetite  fails  we  order  stomachics — 
for  example,  compound  tincture  of  cinchona.  The  fluid  extract  of  condurango 
deserves  a  special  mention,  and  has  been  a  favorite  prescription  in  gastric 
carcinoma  since  condurango  bark  was  recommended  by  Friedreich.  We  usually 
prescribe  hydrochloric  acid  after  meals  (15  to  20  drops  of  the  dilute  acid  in 
water)  in  the  hope  of  making  up  for  the  achlorhydria.  Pain  is  alleviated  by 
narcotics,  such  as  morphin,  opium,  codein,  belladonna,  chloroform,  and  anaes- 
thesin,  and  by  moist  warm  or  cold  applications.  Warm  poultices  on  the 
epigastrium  for  several  hours  a  day  are  usually  beneficial.  In  some  cases  I 
have  noticed  a  striking  analgesic  effect  from  repeated  exposure  of  the  gastric 
region  to  the  Eontgen  ray. 

To  combat  obstinate  vomiting  we  may  give  the  narcotics  just  named  or 
bits  of  ice,  but  the  best  remedy  is  rinsing  out  the  stomach,  provided  the 
patient  is  not  too  feeble.  If  there  are  sour  or  offensive  eructations,  we  pre- 
scribe bicarbonate  of  soda,  magnesia,  or  powdered  charcoal.  If  the  pyloric 
cancer  is  leading  to  stenosis  with  stagnation  of  food  in  the  stomach,  the  daily 
washing  out  of  that  organ  is  an  excellent  means  of  relieving  the  patient  for 
a  time,  at  least,  of  a  great  part  of  his  discomfort.  If  this  is  practiced  regu- 
larly with  either  pure  water  or  a  one-  or  two-per-cent  solution  of  hydrochloric 
acid,  and  if  the  diet  is  suitable,  there  may  be  a  great  temporary  improvement 
in  the  condition  and  even  a  not  inconsiderable  gain  in  weight.  But,  despite 
all  our  efforts,  the  symptoms  may  become  worse  and  worse  till,  finally,  the 
subcutaneous  injection  of  morphin  may  be  indispensable.  Then  our  whole 
object  is  to  alleviate  the  patient's  sufferings,  and  to  give  him  moral  support 
and  encouragement. 

When  the  vigor  of  the  patient  is  such  as  to  permit  the  consideration  of 
surgical  interference,  the  more  promptly  the  operation  is  undertaken  the  more 
chance  is  there  of  eradicating  the  disease  and  obtaining  permanent  recovery. 
It  is,  therefore,  permissible  when  there  is  incipient  disease  and  the  diagnosis 
is  not  yet  fully  established,  although  somewhat  probable,  to  propose  to  the 
patient  an  exploratory  laparotomy,  to  be  immediately  followed  by  a  regular 
operation,  provided  the  case  turns  out  to  be  a  suitable  one.  The  results  of 
operations  on  carcinoma  of  the  stomach  have  not  been  very  brilliant.  Still, 
in  many  cases  the  surgeon  is  fully  justified  in  endeavoring  to  combat  an 
otherwise  absolutely  hopeless  disease,  since  there  is  some  prospect  of  recovery. 
Although  there  have  been  many  failures,  surgeons  have  obtained  a  number  of 
extremely  satisfactory  recoveries  under  these  circumstances.  If  there  is  a 
stenosis  of  the  pylorus  and  yet  it  is  no  longer  possible,  or  at  least  no  longer 


554  DISEASES  OF  THE  DIGESTIVE  ORGANS 

wise,  to  extirpate  the  tumor,  gastro-enterostomy  may  give  very  great  relief. 
If  the  patient  survives  the  operation,  the  suffering  is  much  diminished  and 
nutrition  may  decidedly  improve.  Many  cancer  patients  enjoy  a  compara- 
tively comfortable  existence  for  one  to  one  and  a  half  years  after  a  successful 
gastro-enterostomy.     For  the  particulars  we  refer  to  surgical  treatises. 


CHAPTER    VII 

ANOMALIES    OF    THE    SECRETION   OF   GASTRIC   JUICE 

(Achylia  Gastrica  and  Hypersecretion  of  the  Gastric  Juice) 

In  the  present  chapter  are  to  be  considered  those  dyspeptic  conditions 
which  are  associated  with  a  change — that  is,  either  a  diminution  or  an  in- 
crease— in  the  secretion  of  the  gastric  juice,  independently,  at  least  in  most 
cases,  of  any  definite  anatomical  lesion.  We  have  here  to  consider,  therefore, 
no  marked  catarrhal  condition  or  new  growth  of  the  stomach,  nor  gastric 
ulcer  with  hypersecretion.  The  cause  of  the  change  in  secretion  in  the  cases 
here  considered  must  rather  be  sought  in  the  disturbances  of  the  activity  of 
the  cells,  the  special  occasion  of  which  is  as  yet  almost  entirely  unknown. 
Many  clinical  observations,  it  is  true,  indicate  that  abnormal  nervous  influ- 
ences are  important  in  this  connection,  but,  on  the  other  hand,  it  is  possible 
that  the  explanation  lies  in  primary  changes  in  the  minute  structure  and 
chemistry  of  the  secreting  cells  themselves.  Besides  this  uncertainty  of  83tiol- 
ogy,  there  is  also  an  absolute  lack  of  thorough  anatomical  investigations  in 
this  regard,  so  that  it  is  at  present  a  very  difficult  matter  to  map  out  and 
depict  accurately  these  abnormal  conditions.  We  must,  therefore,  limit  our- 
selves preliminarily  to  a  simple  statement  of  the  clinical  facts  thus  far  known, 
and  present,  as  well  as  we  can,  the  leading  points  of  view  for  the  interpretation 
and  treatment  of  these  groups  of  symptoms. 

1.    ANACIDITY  OF  THE  STOMACH  (ACHLORHYDRIA).— ACHYLIA 

GASTRICA 

Fenwick  was  the  first  to  observe  that  there  are  cases  of  chronic  and  com- 
plete absence  of  any  demonstrable  secretion  of  gastric  juice,  independently  of 
chronic  gastritis  or  gastric  carcinoma,  but  associated  with  an  almost  complete 
atrophy  of  the  glandular  apparatus  of  the  gastric  mucous  membrane.  The 
clinical  picture  in  these  cases  displayed  scarcely  any  marked  gastric  symptoms. 
Anorexia  and  moderate  oppression  after  eating  were  almost  the  only  indica- 
tions of  dyspepsia ;  but  there  were  observed  gradually  progressive  anamiia  and 
emaciation,  so  that  finally  the  general  weakness,  independent  of  any  other 
local  symptoms,  resulted  in  death.  Since  then  we  have  learned,  particularly 
from  the  investigations  of  Martius,  that  the  grave  symptoms  of  these  cases 
cannot  possibly  be  caused  by  an  atrophy  and  cessation  of  function  of  the 
gastric  glands  alone,  but  occur  only  when  there  is  also  present  an  atrophy  of 
the  intestinal  mucous  membrane. 

It  has  been  shown,  and  we  have  ourselves  repeatedly  found,  that  it  is  pos- 


ANOMALIES  OF  THE  SECRETION   OF  GASTRIC  JUICE  555 

gible  to  have  an  achylia  gastrica — that  is,  persistent  absence  of  hydrochloric 
acid  (and  pepsin,  vide  infra),  without  any  noticeable  disturbance  of  nutrition, 
and  with  only  slight  and  fugitive  dyspeptic  symptoms,  or  even  with  no  gastric 
symptoms  whatever.    In  all  these  cases  it  is  wholly  probable  that  the  digestion 

and  absorption  by  the  intestines  are  perfectly  normal,  and  completely  replace 
the  digestive  function  of  the  stomach.  It  is  only  requisite  that  the  intestines 
should  preserve  their  normal  function,  and  that  the  motor  power  of  the  stom- 
ach should  be  unimpaired.  In  such  cases  the  stomach  serves  to  a  certain 
degree  merely  as  a  reservoir  for  the  ingested  food,  which  it  duly  passes  on 
to  the  intestines;  in  them  are  present  in  abundance  all  the  reagents,  bile,  pan- 
creatic juice,  and  intestinal  juice,  requisite  for  the  further  absorption  of  the 
ingesta.  There  is  only  one  defect  in  these  persons  with  achylia  gastrica :  there 
is  no  disinfection  of  the  gastric  contents  by  means  of  the  hydrochloric  acid 
of  the  gastric  juice.  Ordinarily  this  lack  is  unimportant,  but  if  any  hurtful 
material  reaches  the  stomach  it  is  more  likely  to  lead  to  disturbance  than 
under  normal  conditions.  This  explains  why  persons  with  achylia  gastrica 
have  a  "  sensitive  "  stomach  and  are  prone  to  suffer  from  temporary  dyspepsia. 
They  very  often  also  have  a  striking  tendency  to  diarrhea.  But  if  such  indi- 
viduals live  cautiously  and  are  not  exposed  to  any  especial  injurious  influ- 
ences, they  feel  perfectly  well  and  may  be  extremely  well  nourished. 

Is  there  an  atrophy  of  the  gastric  mucous  membrane  as  a  foundation  for 
these  benign  cases  of  achylia  gastrica?  It  is  possible,  and  in  many  cases  even 
probable,  that  there  is ;  but  it  is  not  certain.  This  is  certain :  that  sometimes 
a  long  persistent  absence  of  hydrochloric  acid  has  been  observed  clinically,  and 
later  an  autopsy  has  shown  no  anatomical  explanation  of  the  condition.  Thus, 
for  example,  a  short  time  ago  the  author  had  a  patient  under  observation  in 
his  wards  for  a  considerable  time  with  diabetes  mellitus,  in  whose  gastric  juice 
no  trace  of  hydrochloric  acid  could  be  demonstrated,  although  repeated  examina- 
tions were  made.  The  patient  died,  comatose,  and  the  stomach  seemed  to  be  per- 
fectly normal,  even  upon  microscopic  examination.  Here  there  may  perhaps 
have  been  some  toxic  inhibition  of  the  secretion.  At  any  rate,  observations  like 
this  prove  that  when  there  is  no  gastric  juice  secreted,  we  cannot  assert  that 
any  marked  anatomical  change  will  be  found  in  the  gastric  mucous  membrane. 

From  what  has  been  said  it  follows  that,  according  to  the  present  state  of 
our  knowledge,  we  must  distinguish  several  forms  of  achylia  gastrica  (or  of 
long  persistent  gastric  anacidity).  We  should  mention  incidentally  that  in  a 
strict  sense  the  name  achylia  should  be  employed  only  for  that  condition  in 
which  there  is  a  constant  absence  not  only  of  hydrochloric  acid,  but  also  of 
pepsin,  indicating  a  complete  drying  up  of  the  secretion  of  gastric  juice.- 
Those  cases  in  which  free  hydrochloric  acid  is  never  demonstrable  but  pepsin 
is  found  should,  in  strictness,  be  termed  anacidity,  or,  better,  aclorhydria. 
In  practice  it  is  true  that  we  cannot  always  make  these  fine  distinctions,  and 
that  even  such  cases  as  present  not  an  absolute  absence  but  a  slight  or  occa- 
sional trace  of  hydrochloric  acid  are  classed  in  this  latter  category.  We  dis- 
tinguish the  three  following  forms  of  achylia: 

1.  Achylia  or  achlorhydria  may  appear  as  a  symptom  in  certain  other  dis- 
eases of  the  stomach,  particularly,  as  we  have  already  seen,  in  severe  acute  and 
chronic  gastritis  (when  there  is  genuine  catarrh  of  the  stomach),  and  also  in 
cancer  of  the  stomach.    These  cases  are  to  be  termed  "  symptomatic  achylia." 


556  DISEASES  OF  THE   DIGESTIVE   ORGANS 

2.  Achylia  or  achlorhydria  may  appear  as  a  necessary  result  of  marked 
atrophy  ("  anadenia  ")  of  the  gastric  mucous  membrane.  Here  the  further 
point  is  to  determine  the  causes  of  this  distinctly  characterized  anatomical 
change  in  the  gastric  mucous  membrane.  Sometimes  it  seems  to  be  the  result 
of  a  previous  catarrhal  inflammation  (atrophic  catarrh,  analogous  to  similar 
conditions  of  other  mucous  membranes — vide  supra,  page  492).  How  far 
this  assumption  agrees  with  the  facts  must  be  determined  by  further  careful 
investigation.  Apart  from  this  secondary  or  inflammatory  atrophy  there  is 
also  a  simple  primary  atrophy  of  the  mucous  membrane.  The  cause  of  this 
condition  is  most  likely  to  be  found  in  congenital  peculiarities,  of  which  we 
as  yet  possess  no  intimate  knowledge.  We  might  see  a  certain  analogy  in 
progressive  muscular  atrophy.  In  these  cases  of  atrophy  of  the  gastric  mucous 
membrane  there  is  no  demonstrable  secretion  of  hydrochloric  acid,  nor  of 
pepsin.  The  gastric  contents  obtained  in  the  ordinary  way  are  absolutely 
devoid  of  peptic  activity,  but  at  the  same  time  the  muscular  efficiency  of  the 
stomach  is  in  many  cases  perfectly  normal,  and  this  explains  why,  although 
there  is  no  secretion  of  gastric  juice,  there  are  no  marked  symptoms  of  gastric 
discomfort.  In  many  cases,  however,  the  atrophy  of  the  gastric  mucous  mem- 
brane is  coincident  with  an  atrophy,  or  at  least  with  marked  changes  of  the 
intestinal  mucous  membrane.  Then  it  is  inevitable  that  severe  disturbances 
of  nutrition  should  gradually  develop,  for  the  food  cannot  be  sufficiently 
digested  and  absorbed.  Such  patients  grow  progressively  thin  and  feeble. 
Often  they  suffer  from  marked  intestinal  symptoms,  having  persistent  diar- 
rhea, alternating  with  constipation.  By  suitable  treatment  and  nursing  such 
patients  may  improve,  or  at  least  their  symptoms  may  be  checked.  In  a  few 
rare  cases  death  finally  occurs.  The  clinical  picture  of  pernicious  anaemia 
(q.  v.)  has  been  repeatedly  presented  in  association  with  this  sort  of  atrophy 
of  the  stomach  and  intestines.  In  our  opinion,  however,  the  nature  of  these 
cases  is  still  unsettled,  since  the  atrophy  of  the  intestinal  mucous  membrane 
of  itself  might  well  lead  to  extreme  inanition,  but  not  to  a  specific  anaemia. 
For  this  there  must  be  present  some  special  circumstances  with  which  we  are 
as  yet  unacquainted. 

3.  The  third  form  is  simple  functional  achylia.  Here  belong  the  not  in- 
frequent cases  in  which  the  symptoms  are  not  usually  particularly  severe,  con- 
sisting of  anorexia,  gastric  oppression,  nausea,  and  rarely  vomiting.  The 
complaint  may  have  been  of  recent  origin.  On  careful  examination  of  the 
gastric  contents,  we  find  complete  absence  of  hydrochloric  acid,  while  pepsin 
may  be  present,  or,  again,  in  other  cases  entirely  absent.  The  motility  of  the 
stomach  is  normal,  as  a  rule,  but  it  may  be  somewhat  impaired,  probably  be- 
cause of  a  coincident  weakness  of  the  muscular  coat  (see  the  following  chap- 
ter). With  suitable  treatment  the  symptoms  diminish  or  vanish,  but  there 
is  no  change  with  regard  to  the  absence,  or  approach  to  absence,  of  hydro- 
chloric acid  and  pepsin.  It  cannot  be  determined  how  long  this  condition 
has  existed.  Sometimes  such  patients  say,  as  we  have  already  mentioned, 
that  they  have  been  rather  subject  to  mild  dyspepsia  or  to  temporary  attacks 
of  diarrhea.  Often,  however,  their  previous  health  has  been  good.  Whether 
we  should  invariably  assume  that  there  is  a  marked  atrophy  of  the  gastric 
mucous  membrane  in  all  such  cases  is  very  questionable.  Probably  we  have 
rather  to  do  with  an  impairment  of  the  secretory  capacity  of  the  individual 


ANOMALIES  OF  THE   SECRETION   OF  GASTRIC   JUICE  557 

stomach  from  causes  not  at  present  accurately  determinable.  Apparently 
there  are  not  a  few  persons  with  achylia  of  this  sort.  Inasmuch  as  the  con- 
dition runs  along  without  any  special  symptoms,  it  is  not  diagnosticated  hy 
the  physician,  and  the  patient  is  not  subjected  to  an  accurate  examination 
until  digestive  disturbance  arises  because  of  some  special  cause  (vide  supra), 
and  then  the  anomaly  is  detected.  If  such  patients  do  suffer  from  persistent 
dyspepsia  there  will  usually  he  found  some  special  reason  for  it,  such  ae  motor 
incapacity,  possibly  dislocation  of  the  stomach,  ors  genuine  "  nervous  "  dys- 
pepsia, meaning  by  that  term  dyspepsia  of  psychical  origin.  It  would  be  an 
interesting  question  to  investigate  whether  individuals  with  persistent  achylia 
do  not  perhaps  have  a  predisposition  to  the  development  of  carcinoma.  I 
would  like  also  to  remark  here  that  I  have  seen  several  accident  ca 
with  complaint  of  persistent  and  severe  dyspeptic  symptoms  (pain,  anorexia, 
etc.).  These  arose  after  a  severe  blow  in  the  gastric  region,  and  the  exam- 
ination of  the  gastric  contents  always  showed  an  absence  of  free  hydrochloric 
acid. 

Diagnosis. — The  diagnosis  of  achylia,  whether  essential  or  secondary,  can 
always  be  easily  made  by  means  of  a  careful  examination  of  the  gastric  con- 
tents (see  the  first  chapter  of  this  section).  Of  course,  the  diagnosis  is  not 
established  until  repeated  and  painstaking  examinations  nave  been  made  at 
various  times  and  under  various  circumstances,  and  have  invariably  given 
the  same  negative  result.  If  achylia  is  demonstrated,  the  next  question  is 
whether  it  is  merely  symptomatic  or  essential.  The  presence  of  chronic  gas- 
tritis is  excluded  by  the  absence  of  all  setiological  factors  and  of  excessive 
mucous  secretion,  and  by  the  general  course  of  the  disease.  The  suspicion  of 
cancer  will  often  likewise  be  rendered  untenable  by  the  general  course  of  the 
disease  and  the  absence  of  a  tumor.  In  cases  of  atrophy  of  the  gastric  and 
intestinal  mucous  membrane,  with  consequent  emaciation  there  may  be  very 
great  difficulty  in  excluding  cancer.  On  the  whole,  however,  the  course  of 
gastro-intestinal  atrophy  is  much  slower  than  that  of  carcinoma.  Accompany- 
ing signs  of  pyloric  stenosis  invariably  indicate  the  presence  of  carcinoma; 
and  if  we  are  enabled  by  the  absence  of  any  severe  disturbance  of  nutrition 
to  exclude  any  marked  atrophy  of  the  gastric  and  intestinal  mucous  mem- 
brane, we  reach  at  last  a  diagnosis  of  simple  functional  achylia  by  exclusion. 
Whether  in  such  cases  there  is  a  demonstrable  anatomical  change  in  the  gastric 
mucous  membrane,  the  present  state  of  our  knowledge  does  not  enable  us  to 
determine. 

Treatment. — We  do  not  need  to  enter  upon  a  special  discussion  of  the 
treatment  of  symptomatic  achylia.  The  severe  cases  which  occasion  extreme 
disturbance  of  nutrition  need  the  most  careful  dietetic  management.  They 
should  have  such  food  as  milk,  soups,  eggs,  and  meat  peptones.  Practical 
experience  will  usually  be  a  better  guide  than  any  theoretical  considerations. 
Internally  we  may  try  hydrochloric  acid  and  preparations  of  pepsin  and  pan- 
creatine also  all  sorts  of  stomachics,  including  nux  vomica  and  condurango. 
The  stomach  may  be  rinsed  out  with  a  0.2-per-cent  solution  of  hydrochloric 
acid,  and  galvanic  electricity  may  be  employed.  It  is  self-evident  that  when 
there  is  actual  atrophy  of  the  mucous  membrane,  the  results  of  treatment  must 
be  very  limited.  The  milder  cases  of  achylia  do  not  need  treatment  except 
when  special  dyspeptic  symptoms  appear,  or  when  there  is  intestinal  disturb- 


558  DISEASES  OF  THE  DIGESTIVE  ORGANS 

ance,  such  as  diarrhea;  then  the  treatment  is  the  same  as  in  ordinary  dis- 
turbances of  the  stomach  or  bowels,  including  a  suitable  diet,  hydrochloric 
acid,  perhaps  rinsing  out  the  stomach  a  few  times,  and,  in  case  of  diarrhea, 
opium.  If  the  symptoms  subside,  and  we  now  find  there  is  a  persistent 
achylia,  of  course  we  must*  earnestly  recommend  such  individuals  to  exercise 
a  certain  caution  with  regard  to  diet.  They  should  not  take  too  great  a  quan- 
tity of  food  at  one  time,  and  in  general  should  choose  a  largely  vegetable  diet 
— i.  e.,  one  containing  an  abundance  of  starches.  There  is  this  exception,  that 
if  the  achylia  is  associated  with  a  dread  of  eating  and  a  tendency  to  hypochon- 
driasis, we  must  encourage  the  patient  to  take  a  rather  abundant  amount  of 
nourishment  and  employ  hydrotherapy  and  other  general  tonics. 

2.     HYPERSECRETION  AND  HYPERACIDITY   OF  THE  GASTRIC 
JUICE  (ACID   DYSPEPSIA) 

We  have  seen  in  the  first  chapter  of  this  section  that  it  may  be  regarded 
as  a  rule  that,  when  fasting,  the  stomach  is  almost  completely  empty,  and  that 
an  hour  after  a  test  breakfast  (vide  supra,  page  513)  the  acidity  of  the  gastric 
contents  is  about  55  to  65.  The  investigations  of  late  years  have  shown,  how- 
ever, that  this  rule  has  numerous  individual  exceptions  not  necessarily  patho- 
logical. There  are  many  persons  who  secrete  scarcely  any  hydrochloric  acid 
(vide  supra),  and  also  there  are  apparently  still  more  who  always  have  hydro- 
chloric acid  in  the  stomach  even  when  fasting,  and  whose  hydrochloric-acid 
index  after  a  test  breakfast  is  as  high  as  80  to  100,  or  even  higher.  Many 
such  individuals  have  no  dyspeptic  disturbances  whatever,  so  that  the  unusual 
abundance  of  hydrochloric  acid  can  be  regarded  only  as  an  individual  peculiar- 
ity of  secretion,  and  not  due  to  disease.  In  other  such  cases,  however,  there 
are  decided  gastric  symptoms,  and  these  symptoms  are  such  as  to  indicate 
very  strongly  their  direct  dependence  upon  the  increased  production  of  acid. 
This  state  is  termed  acid  dyspepsia,  by  which,  as  already  stated  (page  525), 
we  mean  the  abnormal  excess  of  hydrochloric  acid  at  the  time  of  digestion — 
that  is,  hyperacidity  as  distinguished  from  hypersecretion,  which  latter  term 
is  applied  to  the  continuous  secretion  of  gastric  juice  even  when  digestion  is 
not  taking  place,  the  stomach  having  received  no'  food,  or  having  discharged 
its  contents  into  the  pylorus.  Hypersecretion  is  probably  almost  always  asso- 
ciated with  hyperacidity,  but  not  vice  versa.  However,  we  cannot  maintain  a 
strict  clinical  distinction  between  the  two  in  practice. 

Essential,  acid  dyspepsia  should  be  sharply  distinguished  from  symptom- 
atic hyperacidity  and  hypersecretion,  such  as  occur  perhaps  in  certain  forms 
of  gastritis  (page  523),  and  almost  invariably  in  ulcer  of  the  stomach.  This 
distinction  is  very  important,  even  from  a  practical  point  of  view.  It  must 
be  confessed  that  it  may  be  scarcely  possible  to  make  a  differential  diagnosis, 
as  we  shall  soon  see,  between  ulcer  and  hypersecretion;  but  we  can,  at  any 
rate,  hold  fast  to  the  important  theoretical  distinction  between  the  two  con- 
ditions. The  term  "  essential "  hypersecretion  ought  to  be  applied  only  to 
cases  in  which  there  is  an  increase  in  the  secretion  of  hydrochloric  acid,  with- 
out any  ulcer  formation.  If  we  regard  hypersecretion  as  a  possible  cause  of 
ulcer  (vide  supra,  page  530),  then  ulcer  can  be  termed  merely  a  complication 
of  hypersecretion. 


ANOMALIES  OF  THE  SECRETION  OF  GASTRIC  JUICE  559 

As  to  the  causes  of  simple  hyperacidity  and  hypersecretion  we  have  as  yet, 
unfortunately,  scarcely  any  knowledge.  Very  few  histological  examinations 
of  the  mucous  membrane  in  characteristic  cases  have  thus  far  been  made.  It 
is,  therefore,  at  present  customary  to  assume  thai  hypersecretion  is  a  "neuro- 
sis," and  this  view  is  apparently  confirmed  by  the  frequenl  combination  of 
hypersecretion  with  other  nervous  conditions.  We  must  later  discuss  this 
point  more  fully.  On  the  other  hand,  however,  it  is  no!  impossible  that  func- 
tional disturbances  of  cellular  activity  may  lead  to  increase  in  the  secretion. 
We  are  ourselves  inclined  to  class  many  cases  of  hypersecretion  along  with  the 
well-known  cases  of  increase  in  the  secretion  of  sweat  (hyperidrosis  of  the 
hands  and  feet),  of  saliva,  and  of  similar  products.  For  such  it  is  not  at  all 
essential  that  there  should  he  abnormal  nervous  conditions. 

Having  such  imperfect  insight  into  the  true  nature  of  these  processes,  we 
must  provisionally  take  a  purely  clinical  standpoint,  and  describe  the  phe- 
nomena seen  in  practice.  It  should  be  added  that  some  of  the  conditions  are 
by  no  means  infrequent,  but  it  is  often  difficult  to  interpret  accurately  what 
we  observe.  One  important  question  is  how  far  the  symptoms  which  are 
present  are  actually  referable  to  the  hypersecretion  as  such,  and  how  far  they 
are  due  to  the  other  anomalies  which  often  accompany  the  hypersecretion, 
such  as  general  nervousness,  gastroptosis,  and  chlorosis.  In  order  to  get  a 
better  comprehension  of  the  subject  we  shall  distinguish  in  what  follows  sev- 
eral forms  of  acid  dyspepsia,  but  we  wish  to  repeat  that  a  perfect  differentia- 
tion is  impossible,  particularly  between  hyperacidity  and  hypersecretion. 

1.  Dyspepsia  with  Hyperacidity  (Hyperchlorhydria). — The  conditions 
which  belong  in  this  category  are  most  often  found  in  young  females.  They 
are  very  often  conjoined  with  symptoms  of  chlorosis,  general  nervousness,  etc. 
Certain  errors  in  diet  may  also  excite  hyperchlorhydria,  such  as  hot  or  highly 
spiced  food,  and  particularly  too  strong  coffee;  and  dyspeptic  conditions  with 
hyperchlorhydria  are  frequently  observed  in  excessive  smokers. 

The  symptoms  are  tolerably  characteristic.  They  occur  especially  after 
eating,  and  sometimes  only  after  certain  kinds  of  food,  and  consist  first  of  a 
sense  of  oppression  in  the  stomach,  often  increasing  to  genuine  cardialgia. 
Usually  the  pain  does  not  appear  until  two  or  three  hours  after  eating — i.  e., 
at  a  time  when  the  stomach  is  already  empty,  although  the  excessive  secretion 
of  acid  is  still  going  on.  Many  patients  have  noticed  that  if  they  then  take 
some  more  food  or  drink  their  pain  will  abate.  This  is  easy  to  understand. 
Often  there  will  be  acid  eructations  at  the  time  of  the  excessive  formation  of 
acid,  and  a  distinct  feeling  of  heartburn.  The  acid  gastric  contents  may  be 
vomited,  but  this  is  not  especially  frequent.  When  the  stomach  is  completely 
empty,  the  patient  feels  perfectly  well  again.  Inasmuch  as  the  appetite  is 
usually  unimpaired,  nutrition  remains  fairly  good.  The  general  course  of  the 
disease  is  chronic,  with  marked  variations.  At  many  times  the  symptoms  are 
aggravated,  particularly  under  the  influence  of  psychical  disturbances,  such 
as  anger  or  excitement,  or  because  of  an  unsuitable  mode  of  life.  At  other 
times  the  symptoms  may  entirely  vanish. 

The  diagnosis  of  hyperchlorhydria  may  be  suggested  by  the  symptoms  just 
described,  but  it  cannot  be  established  except  by  means  of  the  stomach  tube. 
External  examination  of  the  stomach  shows  nothing  special  except  that  there 
may  be  a  moderate  diffuse  tenderness  on  pressure.     It  is  not  surprising  that 


560  DISEASES  OF  THE  DIGESTIVE  ORGANS 

often  there  is  gastroptosis.  If  we  examine  the  stomach  when  fasting,  it  is 
empty  or  almost  empty,  provided  the  case  is  one  of  pure  hyperchlorhydria. 
The  acid  index  after  a  test  breakfast  is  very  high,  70  to  100  or  over.  The 
digestive  power  of  the  gastric  juice  is  greater  than  normal.  It  is  therefore 
natural  to  find,  as  we  do  find,  that  the  stomach  is  entirely  empty,  as  a  rule,  as 
soon  as  three  or  four  hours  after  a  test  meal,  which  indicates  also  a  good  degree 
of  motor  power.  At  that  time  hydrochloric  acid  is  still  present.  On  the 
other  hand,  digestion  of  starch  in  the  stomach  is  impeded  by  the  abundance 
of  hydrochloric  acid. 

If  we  find  things  as  above  depicted,  the  diagnosis  of  hyperchlorhydria  as 
such  is  established.  But  a  difficult  question  remains  to  be  answered — whether 
the  case  is  one  of  simple  functional  increase  of  the  secretion,  or  whether  the 
hyperacidity  is  symptomatic  of  an  ulcer.  If  there  are  no  characteristic  symp- 
toms of  ulcer,  such  as  gastric  hemorrhage  and  localized  tenderness,  it  is  often 
impossible  to  answer  this  question  with  more  than  a  certain  degree  of  proba- 
bility. It  is  characteristic  of  simple  hyperchlorhydria  that  the  pain  is  often 
improved  upon  taking  food,  while  in  ulcer  the  pain  is  aggravated.  If  there 
are  well-marked  symptoms  present  of  general  nervousness,  this  is  usually  de- 
cidedly in  favor  of  "  nervous  hyperacidity."  Finally,  the  results  of  treatment 
may  aid  us  in  diagnosis  (vide  infra). 

The  mode  of  treatment  will  be  considered  with  that  of  hypersecretion. 

2.  Dyspepsia  with  Hypersecretion  of  the  Gastric  Juice  ("  Continuous  Flow 
of  Gastric  Juice"). — Here  belong  those  cases  of  dyspepsia  in  which  the  ex- 
amination of  the  stomach  shows  the  presence,  even  when  fasting,  of  consider- 
able amounts  of  fluid  containing  an  excess  of  hydrochloric  acid,  and  in  which 
this  hypersecretion  cannot  be  regarded  as  the  result  of  an  ulcer. 

The  disease  is  much  more  exceptional  than  simple  hyperchlorhydria.  It 
appears  in  men  somewhat  oftener  than  in  women.  No  special  serological 
factors  can  be  named,  except  long-continued  mental  strain  and  excitement; 
often  no  cause  can  be  made  out. 

Symptoms. — The  symptoms,  as  in  hyperchlorhydria,  consist  of  cardialgia, 
sour  eructations,  heartburn,  and  not  infrequently  vomiting.  Pain  often  ap- 
pears when  no  food  has  been  taken.  When  vomiting  occurs  there  may  be 
little  or  no  food  in  the  vomitus,  but  merely  a  cloudy,  often  bile-stained  fluid, 
strongly  acid,  with  a  very  sharp  taste  and  so  irritating  that  it  causes  burning 
pain  in  the  pharynx.  The  appetite  is  generally  good,  and  the  patients  have 
usually  found  out  by  experience  that  if  they  drink  some  tea  so  as  to  dilute 
the  gastric  juice,  or  take  some  sort  of  food,  they  get  relief.  Often  there  is 
abnormal  thirst;  the  bowels  are  usually  constipated;  the  urine  faintly  acid 
and  turbid  with  deposits  of  phosphates;  the  pulse  is  often  slow;  in  many 
cases  there  is  a  distinct  general  neurasthenic  condition,  associated  with  the 
dyspepsia.  Here,  again,  the  only  method  of  arriving  at  a  certain  diagnosis 
is  by  examining  the  gastric  contents.  The  decisive  point  is  that  in  the  morn- 
ing before  breakfast  we  should  invariably  find  a  considerable  amount  of  fluid, 
containing  practically  no  portions  of  food,  but  a  large  percentage  of  hydro- 
chloric acid.  At  the  same  time  it  should  be  particularly  pointed  out  that  it 
is  not  abnormal,  now  and  then,  to  find  a  teaspoonful  or  two  of  fluid  in  the 
stomach,  containing  hydrochloric  acid,  while  fasting.  It  is  not  proper  to 
speak  of  the  case  as  one  of  hypersecretion  unless  we  can  obtain  from  the  fast- 


ANOMALIES   OF   THE   SECRETION   OF   GASTRIC  JUICE  561 

ing  stomach,  without  special  effort,  some  two  or  three  ounces  (50  to  100  c.c.) 
of  strongly  acid  fluid.  Along  with  the  hypersecretion  there  is  usually  hyper- 
chlorhydria,  so  that  we  find  a  high  acid  index  an  hour  after  the  test  hreakfast. 
If  we  give  a  test  meal,  and  examine  three  hours  later,  we  shall  find  that  the 
meat  has  vanished,  while  the  digestion  of  starches  has  been  decidedly  delayed 
by  the  hyperacidity.  Some  seven  hours  after  the  test  meal  the  stomach  is 
empty  of  food,  but  probably  contains  an  abundance  of  acid  secretion. 

If  we  inflate  the  stomach,  we  may  find  the  organ  dislocated  downward  (gas- 
troptosis).  This,  however,  is  merely  a  chance  complication.  There  is  never 
great  dilatation.  If  we  find  the  stomach  much  enlarged,  our  suspicions  are 
at  once  directed  to  pyloric  stenosis,  and  this  condition  is  usually  easily  diag- 
nosticated, one  important  indication  being  delay  in  the  emptying  of  the 
stomach.  Whenever  the  stomach  in  a  fasting  condition,  or  seven  or  eight 
hours  after  a  test  meal,  is  found  to  contain  not  only  an  abundance  of  hydro- 
chloric acid,  but  in  addition  considerable  amounts  of  partially  digested  food, 
the  condition  is  not  one  of  simple  hypersecretion,  but  of  hypersecretion  com- 
bined with  stenosis  of  the  pylorus  due  to  ulcer.  This  puts  an  entirely 
different  aspect  on  the  case.  The  assumption  that,  in  the  presence  of  hyper- 
secretion, a  marked  retardation  in  the  emptying  of  the  stomach  can  be  pro- 
duced by  a  purely  functional  cramp  of  the  pylorus,  I  consider  entirely 
unproved.  In  all  my  cases  of  hypersecretion  and  pronounced  disturbance 
of  the  motor  activity  of  the  stomach,  an  ulcer  was  eventually  demonstrated 
with  certainty,  even  if  in  the  beginning  it  seemed  reasonable  to  assume  the 
presence  of  a  purely  functional  hypersecretion. 

It  is  a  much  more  difficult  matter  to  distinguish  hypersecretion  from  a 
gastric  ulcer  without  stenosis.  Indeed,  sometimes  an  absolute  decision  is 
almost  impossible.  In  such  instances  we  may  be  enabled  to  form  an  opinion 
by  considering  the  general  course  of  the  disease,  the  associated  nervous  symp- 
toms, and  all  the  special  symptoms  (vide  supra). 

In  general,  the  course  of  acid  dyspepsia  with  hypersecretion  is  chronic, 
but  variable.  The  prognosis  is  not  unfavorable,  and  correct  management, 
based,  as  it  must  be,  upon  an  accurate  examination,  may  bring  about  very 
satisfactory  results. 

Treatment. — In  the  treatment  of  acid  dyspepsia,  including  hypersecretion 
as  well  as  simple  hyperchlorhydria,  we  meet  with  one  difficulty  in  the  fact 
that  we  can  seldom  absolutely  exclude  ulcer  of  the  stomach.  The  physician 
must,  therefore,  .determine  whether  he  shall  begin  with  a  course  of  treatment 
for  ulcer  or  not.  We  believe  that  in  all  cases  in  which  the  symptoms  have 
existed  for  a  considerable  time  and  are  severe,  and  in  which  there  has  been  no 
systematic  treatment  as  yet,  it  is  wise  to  treat  the  patient  as  if  there  were 
an  ulcer.  If  the  case  is  one  of  simple  acid  dyspepsia  this  can  do  no  harm, 
and  if  it  is  one  of  ulcer  it  is  the  only  method  that  can  do  good.  In  either 
case  the  quiet,  the  unirritating  diet,  and  the  administration  of  alkalies  are 
certainly  appropriate.  Moreover,  cases  are  not  infrequent  in  which  the  pa- 
tients are  anxious  and  hypochondriacal,  and  upon  them  a  methodically  con- 
ducted "  cure  "  for  ulcer  often  has  a  favorable  subjective  influence.  Still, 
this  just-mentioned  combination  of  acid  dyspepsia  with  decided  nervous  and 
hypochondriacal  disturbances  may,  on  the  other  hand,  render  the  effect  of 
a  strict  ulcer  treatment  quite  unfavorable.    This  applies  to  patients  who  have 


562  DISEASES  OF  THE   DIGESTIVE  ORGANS 

long  been  tortured  by  a  dread  of  gastric  ulcer,  have  consequently  gone  through 
the  appropriate  treatment  many  times  already,  and  have  grown  thin  and  feeble 
as  the  result  of  an  excessively  cautious  dietary.  For  such  unfortunates  there 
may  be  no  use  whatever  in  repeating  a  strict  course  of  treatment  suitable  to 
ulcer.  Such  a  procedure  confirms  the  patient  in  his  apprehensions,  and 
merely  makes  him  more  wretched. 

We  see,  then,  how  carefully  we  should  consider  the  individual  in  the 
treatment  of  acid  dyspepsia,  and,  above  all,  how  much  weight  we  should  as- 
sign to  the  general  condition  as  well  as  to  the  dyspeptic  symptoms.  It  is 
often  advisable  to  begin  with  a  course  of  treatment  for  ulcer  in  the  ordinary 
manner,  but  upon  the  prompt  cessation  of  symptoms  to  make  a  more  rapid 
transition  than  usual  to  nourishing  food  and  other  therapeutic  methods.  The 
more  convinced  the  physician  becomes  that  he  has  to  do  with  simple  "  nerv- 
ous "  hypersecretion  and  not  with  an  ulcer,  the  less  need  has  he  to  pursue 
a  strict  dietetic  treatment.  In  such  cases  it  is  best  to  prescribe  for  the  pa- 
tient a  diet  list,  containing  an  abundance  of  albuminoids,  including  meat, 
fish,  eggs,  and  milk ;  and  with  this,  rye  bread  and  butter,  and  easily  digested 
vegetables.  There  should  be  as  great  a  limitation  as  possible  of  alcoholic 
beverages,  spices,  strong  coffee,  and  sour  articles,  as  well  as  of  puddings  and 
starchy  vegetables.  Yet  in  such  cases,  also,  one  must  be  guided  by  the  indi- 
vidual experiences  of  the  patient  as  well  as  by  merely  theoretical  considerations. 
As  to  drugs,  of  course  alkalies  come  first.  We  should  be  guided  by  the  cir- 
cumstances of  the  particular  case  in  prescribing,  several  times  a  day,  particu- 
larly after  meals,  a  knife-point  full  of  bicarbonate  of  soda,  or  some  similar 
powder,  such  as  bicarbonate  of  soda  and  calcined  magnesia,  equal  parts;  or 
bicarbonate  of  soda,  30  parts;  subnitrate  of  bismuth,  5  parts;  and  similar 
drugs.  If  there  is  hypersecretion  we  like  to  give  the  patient  in  the  morning, 
before  breakfast,  a  half  liter  (pint)  of  warm  Carlsbad  water,  or  the  artificial 
Carlsbad  salt,  dissolved  in  water.  In  severe  cases  of  hypersecretion  regular 
washing  out  of  the  stomach  is  advantageous.  The  best  time  to  do  this  is  in 
the  early  morning.  We  may  employ  a  one-per-cent  solution  of  bicarbonate 
of  soda. 

Atropin  and  the  narcotics,  such  as  morphin  and  codein,  have  been  recom- 
mended for  the  purpose  of  diminishing  the  secretion  of  the  gastric  glands. 
We  have  used  both  belladonna  (for  example,  extr.  belladonnas,  gr.  v  [gm.  0.3]  ; 
aq.  amygd.  amar.,  1  ounce  [30.0  c.c]  ;  15  to  20  drops  t.i.d.  p.c.)  and  atropin 
with  success,  but  we  would  warn  the  physician  against  the  unnecessary  em- 
ployment of  narcotics. 

The  simultaneous  constitutional  treatment  is  very  important,  particularly 
in  all  cases  associated  with  neurasthenic  symptoms  {vide  infra,  the  chapter  on 
Nervous  Dyspepsia).  From  this  point  of  view  there  is  much  benefit  in  drink- 
ing the  waters  at  Carlsbad,  Tarasp,  and  similar  watering  places,  in  connection 
with  the  hope  of  constitutional  improvement  from  the  outdoor  life,  the  baths, 
cold  sponging  and  rubbing,  and  similar  agencies.  In  treatment  at  home  these 
last  factors  must  always  be  duly  considered. 

3.  Periodical  (Intermittent)  Hypersecretion  (Gastroxynsis). — In  the  con- 
dition here  to  be  described,  persons  who  at  other  times  feel  perfectly  well,  with- 
out any  digestive  disturbance,  are  rather  suddenly  attacked  by  violent  gastric 
pain,  sour  eructations,  and  vomiting.    The  intervals  between  attacks  may  be 


ABNORMALITIES  IN  SIZE  AND   POSITION  OF  STOMACH  563 

longer  or  shorter,  and  there  may  be  either  some  exciting  cause  or  do  apparent 
reason  for  the  disturbance.  The  vomitus  consists  of  large  amounte  of  watery 
fluid  containing  an  excess  of  hydrochloric  acid.  During  these  attacks  the  gen- 
eral condition  of  the  patient  is  wretched;  lie  looks  pale,  his  pul.-e  is  small  and 
frequent.  Often  there  is  extremely  violenl  headache  at  the  same  time.  An 
attack  of  this  sort  lasts  a  few  hours,  or  even  two  or  three  days.  Often  it  ends 
with  considerable  suddenness,  to  be  followed  by  a  period  of  good  health  which 
may  last  a  week  or  even  months,  or  longer. 

The  causes  of  this  strange  disease  are  entirely  unknown,  but  it  certainly 
seems  as  if  there  were  conditions  of  irritation,  originating  in  the  nervous  - 
tern.  It  seems  to  us  indubitable  that  there  is  a  close  relation  between  gas- 
troxynsis  and  migraine  (see  the  chapter  on  Migraine).  It  is  a  very  important 
fact  that  almost  precisely  the  same  group  of  symptoms  occurs  in  tabes  dorsalis 
(q.  v.),  under  the  name  of  gastric  crisis.  In  every  case,  therefore,  the  physician 
should  examine  the  tendon  reflexes  and  the  pupils.  In  pyloric  ulcer  with  ste- 
nosis attacks  may  also  occur  that  at  first  simulate  a  nervous  gastroxynsis.  I 
have  no  doubt  whatever  about  the  occurrence  of  a  purely  nervous  form  of  this 
malady,  although  in  its  well-marked  form  the  condition  is  quite  rare. 

If  possible  we  should  examine  the  gastric  secretion  in  the  time  between 
attacks,  as  well  as  during  the  attack.  It  appears  that  many  cases  of  periodical 
gastroxynsis  are  merely  acute  exacerbations  of  a  constant  hypersecretion.  In 
such  cases  there  are  likely  to  be  mild  dyspeptic  symptoms  in  the  intervals,  and 
a  careful  treatment  of  these  by  lavage,  alkalies,  and  Carlsbad  water  has  an 
excellent  effect  upon  the  paroxysms.  If  there  are  coincident  neurasthenic  symp- 
toms,  of  course  the  greatest  stress  must  be  laid  upon  constitutional  treatment. 
The  treatment  of  the  paroxysm  itself  is  seldom  very  successful.  The  best 
remedy  is  bromide  of  sodium  in  large  doses.  We  may  also  try  chloral,  chloro- 
form, belladonna,  codein,  antipyrin,  and  coryfin  (6  to  10  drops).  Externally, 
warm  compresses  or  hot  poultices  may  be  applied  over  the  stomach.  If  the 
pain  is  very  violent  a  subcutaneous  injection  of  morphin  may  be  almost  indis- 
pensable, although  we  should  avoid  it  if  possible. 


CHAPTEE   VIII 

ABNORMALITIES   IN   THE    SIZE   AND    POSITION   OF   THE    STOMACH— MOTOR 
DISTURBANCES    OF    THE    STOMACH 

1.     ABNORMALITIES  IN  THE  SIZE  OF  THE  STOMACH— ATONY 

OF   THE   STOMACH 

Like  any  other  organ,  the  stomach  may  present  considerable  differences  in 
its  size  without  being  pathological.  These  differences  partly  depend  upon  con- 
genital conditions,  and  partly  are  associated  with  the  mode  of  life.  It  has  long 
been  known  that  certain  classes  of  people  who  eat  very  bulky  articles  of  diet 
(e.  g.,  a  great  proportion  of  potatoes),  and  other  large  eaters,  including  many 
diabetics,  have  noticeably  large  stomachs ;  but  a  change  in  size  of  this  sort  can- 
not be  regarded  as  pathological,  provided  the  function  of  the  stomach  is  not 
impaired.     The  excessive  distention  of  the  organ,  or  the  excessive  demands 


564  DISEASES  OF  THE  DIGESTIVE  ORGANS 

upon  the  functional  activity  of  the  muscular  coat  of  the  stomach,  may  finally 
render  it  unequal  to  its  task.  Then  we  reach  a  pathological  disturbance,  a 
sort  of  overstrain  of  the  stomach,  a  muscular  insufficiency  analogous  to  the 
myopathic  diseases  of  the  heart,  which  have  been  so  much  studied.  Obviously 
one  important  factor  here  would  be  the  original  quality  of  the  muscular  fiber : 
if  the  muscles  of  the  stomach  are  weak  from  the  start,  they  will  become  in- 
sufficient all  the  sooner. 

We  must  state  that  in  our  experience  well-marked  cases  of  primary  idio- 
pathic dilatation  of  the  stomach,  as  an  expression  of  pure  muscular  insuffi- 
ciency, seem  to  be  far  from  frequent,  although  slight  degrees  of  muscular  weak- 
ness occur  quite  often. 

From  what  has  been  said,  it  is  evident  that  the  physician  should  lay  little 
stress  upon  the  mere  estimation  of  the  size  of  the  stomach.  And,  indeed,  its 
size  varies  greatly  according  to  the  amount  ingested.  We  can  form  an  opinion 
of  the  size  of  the  organ  by  percussion  of  the  empty  stomach,  or  by  percussing 
it  alternately  empty  and  filled  with  water  by  means  of  the  stomach  tube,  or, 
what  is  much  simpler  and  more  certain,  by  distending  it  with  air,  as  above  men- 
tioned (page  515).  In  general,  we  can  say  there  is  dilatation  of  the  stomach 
if  the  lower  border  of  the  fundus  extends  below  the  level  of  the  navel  while 
the  lesser  curvature  is  in  a  normal  position;  but,  as  we  have  said,  the  impor- 
tant question  is  not  the  size,  but  the  motor  ability  of  the  organ,  and  it  is  far 
more  important  to  determine  the  functional  activity  by  means  of  a  test  meal, 
in  the  manner  already  explained  (page  514),  than  to  find  out  the  mere  size 
of  the  stomach.  If  the  organ  empties  itself  in  a  normal  way,  any  dilatation 
that  there  may  be  has  no  significance.  If  there  is  some  tendency  to  stagnation 
of  the  gastric  contents  because  of  muscular  insufficiency,  we  may  have  mild  dys- 
peptic symptoms,  such  as  gastric  oppression,  eructations,  or  even  occasional 
vomiting. 

If,  however,  we  find  that  the  stomach  is  dilated  and  that  the  motor  ef- 
ficiency is  decidedly  impaired,  with  actual  stagnation  and  accumulation  of 
ingesta  in  the  stomach,  we  ourselves  think  it  is  always  justifiable  to  assume 
that  there  is  a  pyloric  stenosis.  In  such  case  the  disease  with  which  we  have 
to  deal  is  not  a  dilatation  of  the  stomach,  but  an  ulcer  or  cancer  of  the  pylorus, 
which  leads  to  stenosis  and  its  results,  as  we  have  already  described  at  length 
(pages  537  and  547).  It  has  often  been  maintained  that  in  cases  of  primary 
muscular  dilatation  there  may  occur  mechanical  kinks  in  the  pylorus  and 
sacculations  in  the  stomach,  so  as  to  cause  a  considerable  hindrance  to  the 
emptying  of  the  viscus.  This  may  be  possible,  but  we  have  never  seen  such 
a  case,  nor  read  a  conclusive  report  of  one. 

In  this  place  a  symptom  may  be  mentioned  which  is  often  regarded  as  a 
sign  of  dilatation.  We  refer  to  splashing  in  the  stomach  when  palpation  is 
practiced  by  a  sort  of  pushing  or  thrusting  motion.  Marked  splashing  is 
indeed  very  often  audible  in  cases  of  actual  dilatation  due  to  stenosis  of  the 
pylorus,  but  it  is  very  frequently  heard  in  persons  who  have  dyspepsia,  and 
even  in  persons  who  are  perfectly  well.  Children  sometimes  play  at  producing 
splashing  sounds  in  their  own  stomachs,  and  by  practice  acquire  great  tech- 
nical dexterity!  And  in  precisely  the  same  way  the  sound  is  produced  by 
nervous  and  hypochondriacal  patients,  to  whom  the  splashing  is  a  source  of 
anxiety.    Splashing  occurs  when  air  and  fluid  are  both  present  in  the  stomach, 


ABNORMALITIES  IN  SIZE  AND  POSITION  OF   STOMACH  565 

provided  the  abdominal  walls  as  well  as  the  gastric  walls  are  not  too  tense. 
Jn  this  sense  it  is,  therefore,  correct  to  associate  so-called  atony  of  the  stomach 
with  the  splashing,  because  it  may  often  be  due  to  a  certain  laxity  of  the 
muscular  coat  of  the  stomach,  but  we  should  never  lay  any  special  stress  upon 
the  sound,  unless  upon  examination  we  find  at  the  same  time  a  distinct  dis- 
turbance of  the  motor  efficiency  of  the  stomach. 

It  follows,  therefore,  that  mere  dilatation  of  the  stomach  is  not  an  inde- 
pendent disease.  In  practice  we  may  unhesitatingly  refer  every  case  of  well- 
marked  dilatation  with  decided  stagnation  of  the  gastric  contents  to  stenosis 
of  the  pylorus,  and  of  course  this  latter  is  to  be  regarded  as  the  true  disease. 
At  the  same  time,  however,  there  are  slight  degrees  of  gastric  dilatation,  or 
perhaps  a  better  expression  would  be  idiopathic  motor  insufficiency  of  the 
stomach  (muscular  atony  of  the  stomach),  which  occur  when  there  is  no  reason 
for  believing  that  there  is  any  anatomical  change  at  the  pylorus.  We  may 
assume  that  such  motor  insufficiency  exists  when  there  is  a  slight  but  distinct 
tendency  for  food  to  accumulate  in  the  stomach. 

In  treating  this  simple  muscular  atony,  we  should  first  regulate  the  diet. 
The  separate  meals  must  not  be  too  large,  but  they  should  be  nutritious,  and 
perhaps  even  somewhat  stimulating.  Eye  bread,  small  portions  of  vegetables, 
and  nourishing  meat  dishes  are  by  no  means  interdicted.  Large  amounts  of 
liquid  are  to  be  avoided,  as  they  needlessly  dilate  the  stomach.  In  simple 
atony,  lavage  is  seldom  necessary.  At  the  most,  we  might  at  the  beginning 
of  treatment  completely  empty  the  stomach  a  few  times.  Other  suitable 
measures  are  cold  sponging  and  rubbing  of  the  epigastrium,  the  application 
of  electricity  (particularly  the  galvanic  current)  to  the  stomach,  and  cautious 
massage  of  that  region.  Among  internal  remedies,  nux  vomica  deserves  to  be 
employed. 

Whether  there  is  such  a  thing  as  abnormal  smallness  of  the  stomach,  giving 
rise  to  symptoms,  is  not  yet  known.  Perhaps  there  may  be  such  a  condition  in 
cases  in  which  feeble  and  ill-nourished  individuals,  usually  of  the  female  sex, 
can  take  but  a  few  morsels  before  they  have  a  feeling  of  fullness  and  satiety, 
and  so  never  become  well  nourished  despite  every  effort.  We  may  find  the 
stomach  very  small  as  a  secondary  result  in  many  forms  of  inanition,  particu- 
larly in  association  with  stenosis  of  the  oesophagus  and  of  the  cardia. 

2.    ABNORMAL  POSITION  OF  THE  STOMACH— GASTROPTOSIS 

Kussmaul  was  the  first  to  call  attention  to  the  great  frequency  of  the  down- 
ward dislocation  of  the  stomach.  Glenard  has  written  much  about  it.  Either 
the  entire  organ  may  sink  down,  or,  what  is  more  common,  the  right  half  alone, 
so  that  the  organ  takes  a  vertical  position.  The  cause  of  this  anomaly  may  lie 
partly  in  congenital  conditions,  but  in  the  main  it  is  certainly  the  purely 
mechanical  result  of  the  pressure  of  clothing.  Gastroptosis  is  an  extremely 
common  phenomenon  in  grown-up  girls  and  women  who  wear  tightly  laced  cor- 
sets, and  fasten  the  bands  of  their  clothing  snugly  about  them.  It  also  occurs 
in  men,  but  far  less  often.  Usually,  with  the  gastroptosis  is  associated  a  change 
in  the  position  of  other  organs,  occurring  in  the  same  way.  In  particular,  the 
right  kidney  becomes  abnormally  movable,  and  consequently  readily  palpable 
(see  the  chapter  on  Movable  Kidney),  and  the  transverse  colon  sinks  down 
36 


566         .  DISEASES   OF  THE   DIGESTIVE   ORGANS 

either  in  its  right  half  or  in  its  middle  portion.  Glenard  has  termed  this 
condition  enteroptosis,  and  ascribed  to  it  an  important  role  in  the  aetiology  of 
nervous  dyspepsia  and  neurasthenia.  Well-marked  cases  of  enteroptosis  are 
most  frequent  in  women  who  have  lax  abdominal  walls  because  of  repeated 
confinements. 

The  experienced  eye  may  often  recognize,  or  at  least  surmise,  gastroptosis 
upon  external  inspection  of  the  abdomen.  One  is  struck  by  the  collapsed  ap- 
pearance of  the  epigastrium,  where  one  often  feels  marked  pulsation  of  the 
abdominal  aorta.  Below  the  navel,  on  the  other  hand,  is  seen  a  protuberance, 
the  shape  of  which  may  quite  distinctly  suggest  the  contours  of  the  stomach. 
At  this  spot,  below  the  navel,  distinct  splashing  may  not  infrequently  be  obtained 
by  proper  palpation.  An  absolute  diagnosis  of  gastroptosis,  however,  requires 
the  artificial  inflation  of  the  stomach  (vide  supra,  page  515)  or  an  X-ray  ex- 
amination of  the  stomach  filled  with  bismuth  paste.  Of  course,  the  most  impor- 
tant point  is  the  demonstration  of  a  downward  displacement  of  the  lesser 
curvature.  This  is  found  halfway  between  the  navel  and  the  epigastric  angle, 
or  often  even  at  the  level  of  the  navel.  The  downward  displacement  of  the 
greater  curvature  alone  does  not  establish  gastroptosis,  because  it  may  be  due 
to  dilatation  of  the  stomach. 

Inflation  of  the  stomach  is  such  a  simple  and  reliable  method  of  examina- 
tion that  there  scarcely  seems  any  real  necessity  for  other  methods.  For  this 
reason  Einhorn's  recommendation  of  electric  transillumination  of  the  stomach, 
by  means  of  an  incandescent  light  introduced  into  the  organ  ("  gastrodiapha- 
noscopy"),  is  scarcely  likely  to  become  generally  adopted  by  physicians.  It 
gives  some  indications  of  the  position  of  the  stomach,  but  the  conclusions 
drawn  from  its  use  are  by  no  means  infallible.  The  displacement  of  the  kidney, 
which  is  often  associated  with  gastroptosis,  can  be  easily  recognized  by  means  of 
palpation.  The  position  of  the  colon  (coloptosis)  can  be  demonstrated  by  dis- 
tending the  large  intestine  with  air  or  water. 

The  question  of  the  clinical  significance  of  gastroptosis  is  not  very  easy  to 
answer.  In  the  first  place,  it  should  be  remarked  that,  if  we  pay  attention  to 
the  subject,  we  shall  find  that  well-developed  gastroptosis  is  very  frequent  in 
persons  who  have  not  the  slightest  symptoms.  On  the  other  hand,  there  are 
many  patients,  especially  women,  who  complain  of  such  annoyances  as  pressure 
and  a  sense  of  fullness,  attacks  of  gastric  pain,  eructations,  and  occasional  vom- 
iting, and  who  are  found  to  have  a  distinct  gastroptosis.  In  such  a  case  we 
should  invariably  proceed  to  test  the  secretory  and  'motor  functions  of  the 
stomach.  Very  often  these  are  perfectly  normal,  and  such  a  condition  scarcely 
justifies  us  in  assuming  offhand  that  there  is  a  causative  relation  between  the 
gastroptosis  and  the  patient's  symptoms.  Gastroptosis  is  so  common  that  the 
relation  is  more  likely  one  of  simple  coincidence.  If  we  make  a  searching 
examination  into  the  patient's  condition  we  shall  usually  discover  that  the 
gastric  symptoms  are  associated  with  many  other  symptoms  of  a  neurasthenic 
kind,  and  hence  are  very  likely,  for  the  most  part,  of  purely  psychical  origin  (see 
the  following  chapter). 

Still,  it  cannot  be  absolutely  denied  that  certain  disagreeable  sensations  in 
the  abdomen  and  along  the  oesophagus  (perhaps  due  to  the  traction  exerted  on 
it)  may  be  directly  dependent  upon  gastroptosis.  Furthermore,  gastroptosis 
in  some  few  cases  seems  to  occasion  a  mechanical  hindrance  to  the  discharge 


NERVOUS   DYSPEPSIA  567 

of  the  stomach  contents,  especially  because  of  the  vertical  position  of  the  organ, 
so  that  we  have  a  sense  of  oppression  in  the  stomach,  eructations,  and  other 
symptoms;  but  this  motor  insufficiency  should  be  proved,  not  assumed.  As  a 
rule,  even  well-marked  gastroptosis  is  not  associated  with  any  disturbance  of 
the  motor  function  of  the  stomach.  There  is  more  likelihood  that  the  habitual 
constipation,  which  often  accompanies  the  dyspeptic  symptoms  of  gastroptosis, 
is  at  least  in  part  the  result  of  an  associated  coloptosis. 

Treatment. — For  the  treatment  of  the  dyspeptic  symptoms  which  may 
be  present  in  a  case  of  gastroptosis,  we  have  a  most  desirable  basis  in  the  gastrop- 
tosis itself,  although  the  author  at  least  is  convinced  that  its  main  efficacy  is 
subjective.  If  gastroptosis  has  been  made  out,  we  must  absolutely  forbid  the 
wearing  of  tightly  laced  corsets  or  too  snugly  fitting  gowns.  It  is  often  useful 
to  apply  a  wide  abdominal  band  with  leg  straps  above  the  symphysis.  This  in 
many  cases  fully  replaces  the  more  complicated  "  abdominal  corsets  "  and  sim- 
ilar apparatus.  With  regard  to  diet,  we  forbid  the  taking  of  large  amounts  of 
liquid,  and  prescribe  nourishing  food  that  is  not  bulky.  Particularly  when 
patients  are  emaciated  and  apprehensive,  we  often  do  the  greatest  good  by 
ordering  a  highly  nutritious  diet.  If  the  emaciation  is  marked,  and  there  is 
general  weakness,  a  complete  rest  cure  for  several  weeks  (lying  in  bed  or  on 
a  sofa  at  the  open  window  or  outdoors,  without  any  constricting  clothes), 
with  careful  forced  feeding  at  the  same  time,  is  often  attended  by  remarkably 
good  results.  The  region  of  the  stomach  should  be  rubbed  briskly  once  or 
twice  a  clay  with  cold  water  or  brandy.  The  employment  of  faradic  and  gal- 
vanic electricity  or  massage  is  particularly  indicated  when  constipation  is 
present.  "We  often  prescribe  small  doses  of  nux  vomica  internally  (e.  g.,  tr. 
nucis  vom.  and  aqua  amygdal.  amar.,  equal  parts.  Ten  drops  of  this  to  be 
given  thrice  daily). 

Of  course  we  must  pay  attention,  as  we  have  said,  to  the  general  neuras- 
thenic condition,  which  is  usually  also  present.  In  this  regard  great  importance 
attaches  to  a  suitable  mental  treatment,  in  order  to  free  the  patient  from  her 
exaggerated  anxiety  and  apprehension. 


CHAPTEE    IX 

NERVOUS    DYSPEPSIA 

{Gastric  Neurasthenia) 

We  have  repeatedly  indicated  in  the  preceding  chapter  that  many  disturb- 
ances of  the  gastric  functions  may  be  due  to  changes  in  the  innervation  of  the 
stomach,  or  to  actual  disease  of  its  nerves;  thus  some  have  been  inclined  to 
refer  the  disturbances  of  the  secretion  of  the  gastric  juice,  such  as  hyperacidity 
and  hypersecretion,  to  abnormal  conditions  of  the  secretory  nerves.  Many  cases 
of  "  cardialgia "  have  been  regarded  as  pure  "neuralgia"  of  the  sensory 
nerves  of  the  stomach ;  and  also  in  the  domain  of  the  muscular  activity  of  the 
stomach,  authors  have  distinguished  conditions  of  nervous  weakness  (nervous 
atony  of  the  stomach)   and  of  nervous  irritability  of  the  muscular  coat  (so- 


568  DISEASES  OF  THE  DIGESTIVE  ORGANS 

called  "  peristaltic  unrest "  of  the  stomach ;  constant  rumbling  in  the  stomach 
and  similar  symptoms).  There  is  no  doubt  that  in  cases  of  severe  organic  dis- 
ease of  the  nervous  system  there  may  be  well-marked  gastric  symptoms  as 
direct  consequences  of  nervous  irritation — for  example,  we  have  nervous  vomit- 
ing in  cerebral  tumor  and  meningitis,  and  gastric  crises  in  tabes.  It  is,  there- 
fore, not  impossible  that  there  may  also  be  primary  diseases  of  the  sensory, 
motor,  and  secretory  nerves  of  the  stomach  with  corresponding  symptoms,  but 
this  is  by  no  means  proved,  and  it  is  certain  that  such  actually  "  nervous  "  gas- 
tric diseases  are  very  rare,  if  they  occur  at  all.  At  present,  clinical  experience 
does  not  justify  us  in  putting  in  this  category,  with  any  degree  of  certainty, 
any  disorder  except  the  state  above  described  (page  562),  in  which  there  is 
periodical  vomiting  with  gastric  pain  and  hypersecretion. 

There  are  numerous  cases  which  are  at  present  habitually  termed  nervous 
dyspepsia,  but  in  our  opinion  the  overwhelming  majority  of  these  have  an  ori- 
gin different  from  the  one  implied.  Such  patients  assert  that  after  every  meal 
they  have  pressure  and  pain  in  the  stomach,  that  after  a  few  mouthfuls  the 
stomach  feels  full  and  distended,  and  consequently  they  often  have  palpitation 
and  a  troublesome  feeling  of  constraint  in  the  chest.  The  patients  frequently 
complain  of  eructations  also,  and  occasionally  of  vomiting.  These  symptoms 
are  all  such  as  occur  in  the  same  way  in  actual  diseases  of  the  stomach,  but  in 
these  patients  there  are  usually  certain  other  symptoms  present,  which  indicate 
the  nervous  character  of  the  disease.  In  the  first  place,  it  is  noticeable  that  the 
above  symptoms  display  striking  variations  in  their  severity.  The  same  patient 
who  to-day  complains  of  great  distress  in  his  stomach  after  a  few  spoonfuls  of 
soup,  at  another  time,  when  he  is  in  a  happy  and  lively  frame  of  mind,  will  eat  a 
large  dinner  without  being  reminded  that  he  has  a  stomach ;  but  as  soon  as  he 
gets  angry  or  irritated,  or,  in  brief,  in  a  "  sensitive  "  condition,  the  gastric  symp- 
toms appear  at  once  in  an  exaggerated  form.  On  all  such  occasions,  therefore, 
we  see  most  clearly  the  influence  of  the  imagination  and  of  general  psychical 
irritation  on  the  behavior  of  the  stomach.  Every  one  knows  that  a  violent  rage 
or  any  experience  arousing  anxiety  or  hope — any  excitement,  sad  or  joyful — may 
immediately  destroy  the  appetite ;  and  very  great  mental  disturbance  not  infre- 
quently also  causes  vomiting  or  similar  symptoms.  In  the  same  way  in  sensitive 
individuals  even  the  mildest  psychical  influences  produce  similar  results ;  but 
in  this  regard  there  is  nothing  which  has  so  unfavorable  an  influence  as  that 
state  of  psychical  disturbance  which  is  associated  with  great  concern  for  one's 
own  health — that  is,  a  condition  of  hypochondriacal  anxiety — anxiety  lest 
something  which  has  been  eaten  may  do  damage ;  constant  dread  that  a  grave 
disorder  of  the  stomach  may  be  developing.  These  mental  disturbances  are  es- 
pecially influential  in  maintaining  and  progressively  aggravating  the  abnor- 
mal condition.  This  is  the  explanation  of  that  peculiar  psychical  hyperesthesia 
which  feels  the  acutest  "  pain  "  in  the  stomach,  when  there  is  really  nothing 
but  a  perfectly  normal  general  sensation.  And  the  same  explanation  applies 
to  certain  muscular  contractions — half  unconscious,  half  voluntary — which 
occasion  eructations,  vomiting,  and  similar  phenomena.  The  patient  has  some 
symptoms  which  he  feels  subjectively,  and  some  which  seem  to  him  to  be  actually 
objective,  and  they  are  in  part  the  result  of  pure  imagination  (or  "  autosug- 
gestion ")  and  in  part  the  physiologically  necessary  consequence  of  the  great 
psychical  disturbance. 


NERVOUS   DYSPEPSIA  509 

What  we  wish  to  emphasize  is  our  conviction  thai  in  the  greal  majority  of 
cases  of  nervous  dyspepsia  wo  are  not  dealing  with  any  functional  disturbance 
of  the  gastric  nerves,  but  with  abnormal  " psychogenetic "  irritations  of  the 
central  nervous  system,  the  results  of  which  are  apparent  mainly  in  the  domain 
of  the  gastric  functions.  Nervous  dyspepsia  is  merely  one  example  of  that  great 
group  of  nervous  diseases  which  owe  their  origin  mainly  to  hypochondriacal 
disturbances  of  mind,  and  which  may  appear  in  the  most  diverse  organs.  It  is 
properly  nothing  hut  a  symptom  of  constitutional  "  nervousness  "  or  neurasthe- 
nia, and  is  therefore  termed  by  many  physicians,  with  absolute  correctness,  gas- 
tric neurasthenia.  By  careful  clinical  observation  it  is  easy  to  demonstrate  that 
almost  all  the  ordinary  gastric  symptoms  may,  under  favorable  circumstances, 
be  excited  by  purely  psychical  influences.  It  is  evident  that  anorexia  is  often 
the  result  of  simple  mental  disturbance,  especially  when  of  a  hypochondriacal 
character;  but  excessive  craving  for  food  (bulimia)  is  certainly  in  most  cases 
also  of  purely  psychical  origin,  arising  from  special  imperative  conceptions. 
There  is  no  doubt  that  the  most  varied  abnormal  sensations,  ranging  from  sim- 
ple oppression  to  a  most  acute  pain  in  the  stomach,  may  have  a  purely  subjective 
origin.  The  best  proof  of  this  lies  in  the  often  apparently  miraculous  effect  of 
remedies  which  have  a  purely  suggestive  and  psychical  influence  (simple  reas- 
surance of  the  patient,  hypnotism,  and  various  external  and  internal  remedies). 
It  is  very  important  to  know  that  in  many  cases  also  eructations  and  vomiting 
have  a  merely  psychical  and  central  origin.  They  are  due  to  the  influence  of 
certain  ideas  which  make  the  eructations  or  vomiting  appear  unavoidable,  and 
the  action  at  first  is  due  to  unconscious  volition,  and  finally  becomes  a  sort  of 
diseased  habit.  Many  nervous  and  hypochondriacal  patients  who  regard  them- 
selves as  dyspeptics  become  true  virtuosi  in  eructations  and  vomiting,  the  reflex 
process  becoming  easier  and  easier  because  of  repetition,  and  being  excited  by 
unconscious  volition.  General  psychical  disturbance  may  also  cause  eructations 
and  vomiting  by  direct  stimulation.  We  know  persons  who  are  attacked  with 
nausea  and  vomiting  upon  any  great  excitement.  Even  in  children  it  is  by  no 
means  rare  to  observe  persistent  vomiting  after  almost  every  meal,  and  that  this 
is  of  a  purely  "  nervous  "  character  appears  from  the  rapid  beneficial  effect  of 
exclusively  psychical  treatment — e.  g.,  if  the  child  is  strictly  forbidden  to  vomit. 
"We  often  see  just  the  same  condition  in  adolescent  girls,  frequently  associated 
with  other  hysterical  symptoms.  In  this  connection  it  should  be  briefly  men- 
tioned that  there  may  be  a  "  nervous  " — that  is,  hysterical — hematemesis.  ( For 
particulars  in  regard  to  this,  the  reader  is  referred  to  the  chapter  on  Hysteria ; 
and,  in  general,  the  chapters  on  Hysteria  and  Neurasthenia  should  be  referred 
to  as  supplementing  what  has  been  said  here.) 

Very  often  other  nervous  symptoms  are  observed  besides  those  referred  to 
the  stomach.  There  are  signs  of  excessive  mental  irritability,  symptoms  ref- 
erable to  the  head,  such  as  headache,  pressure  in  the  head,  vertigo ;  abnormal 
sensations  in  the  extremities,  of  pain,  coldness,  numbness,  and  the  like.  There 
are  almost  invariably,  also,  certain  attendant  intestinal  symptoms.  The  pa- 
tient complains  of  bloating  of  the  abdomen,  and  of  irregular  and  sluggish 
bowels. 

Nervous  dyspepsia  becomes  a  more  serious  matter  when  the  patient  is  pre- 
vented from  taking  sufficient  nourishment,  by  fear  of  committing  errors  in  diet, 
and  because  of  the  loss  of  appetite  which  his  mental  uneasiness  occasions. 


570  DISEASES   OF  THE  DIGESTIVE   ORGANS 

There  are  sometimes  complete  nervous  anorexia,  a  constant  dread  of  eating  or 
an  actual  aversion  toward  any  food,  and  a  considerable  or  excessive  emaciation, 
usually  associated  with  great  bodily  weakness.  Such  patients  finally  take  to 
their  beds  and  give  the  impression  of  severe  illness. 

Diagnosis. — In  many  cases  the  experienced  physician  can  make  an  ex- 
tremely probable  diagnosis  of  nervous  dyspepsia  merely  from  the  symptoms 
which  the  patient  enumerates.  The  true  condition  is  suggested  by  the  general 
nervousness,  by  the  prominence  of  anxiety  and  of  hypochondriacal  notions,  oc- 
casionally the  occurrence  of  marked  attacks  of  fear  with  strong  general  psychi- 
cal disturbances,  the  variability  of  the  symptoms  and  their  relation  to  states  of 
consciousness  (excitement,  on  the  one  hand,  distraction  and  diversion  on  the 
other),  and  the  other  attendant  symptoms  of  a  nervous  character,  such  as  head- 
ache, vertigo,  palpitation,  and  a  sense  of  oppression.  Still,  it  is  easy  to  be 
deceived,  because  the  symptoms  seem  to  be  so  objective  that  the  physician  feels 
constrained  to  believe  that  there  is  some  organic  disease  of  the  stomach,  although 
none  exists,  and  because,  on  the  other  hand,  an  actual  disease  of  the  stomach 
may  be  present  in  a  very  nervous  individual  and  fail  to  be  recognized,  being 
wholly  obscured  by  the  general  nervous  phenomena.  For  this  reason,  even  in 
cases  which  seem  to  be  the  most  simple,  we  would  do  well  to  make  a  careful 
objective  examination,  and  this  is,  of  course,  an  absolute  necessity  in  all  cases 
which  are  obstinate  and  severe. 

Often  the  objective  examination  shows  clearly  normal  conditions  in  every 
respect:  the  external  examination  is  normal,  and  the  position,  secretion,  and 
motility  of  the  stomach  are  normal.  In  such  a  case  the  diagnosis  is  established, 
and  the  mere  result  of  examination  will  often  have  a  most  beneficial  effect  upon 
the  patient.  For  this  reason  a  painstaking  examination  is  often  the  best  rem- 
edy for  many  patients  with  nervous  dyspepsia.  It  is  more  difficult  to  reach  a 
conclusion  when  certain  abnormalities  are  found,  although  there  are  no  signs 
of  indubitable  organic  disease — that  is,  there  is  no  tumor  nor  evidence  of  steno- 
sis of  the  pylorus  nor  genuine  hemorrhage — but  we  do  find,  for  example,  dis- 
tinct hyperacidity  or  hypersecretion;  less  often  achlorhydria ;  very  frequently 
gastroptosis ;  and  often,  it  is  said  (although,  according  to  the  author's  experi- 
ence, this  is  rare),  some  slight  disturbance  of  motility,  so-called  atony  of  the 
muscular  coat  of  the  stomach.  How  shall  such  cases  be  interpreted  ?  Shall  we 
alwaj^s  lay  stress  exclusively  upon  the  objective  anomalies  which  are  discovered, 
and  refer  to  them  every  one  of  the  many  symptoms  the  patient  enumerates  ?  In 
the  author's  opinion,  this  would  often  be  erroneous.  It  has  been  especially 
emphasized  in  the  preceding  chapters  that  the  conditions  mentioned  are  frequent 
and  are  apt  to  cause  no  symptoms  at  all,  so  that  if  we  find  associated  with  well- 
marked  nervous  dyspepsia  a  gastroptosis,  or  a  moderate  hypersecretion,  or 
achlorhydria,  in  many  cases  the  association  is  a  mere  chance  coincidence  with- 
out significance.  We  think  that  such  conditions  should  not  be  wholly  dis- 
regarded, but  yet  their  clinical  importance  should  not  be  overestimated; 
and  from  a  therapeutic  point  of  view,  also,  they  should  be  borne  in  mind, 
but  never  to  the  neglect  of  that  general  psychical  treatment  which  is  usually 
much  more  important.  Such  conditions  also  are  very  useful  as  a  handle 
for  mental  therapeutics  (as  we  have  already  pointed  out),  because  of 
the  favorable  effect  which  treatment  of  them  has  upon  the  mind  of  the 
patient. 


NERVOUS    DYSPEPSIA  571 

A  most  difficult  question  in  diagnosis,  in  our  opinion.  La  to  distinguish 
between  ulcer  and  nervous  dyspepsia  when  there  is  distinct  hypersecretion 
without  evident  signs  of  ulcer  (see  page  532).  In  such  a  case  all  the  separate 
symptoms  must  be  duly  considered,  and  yet  we  may  be  obliged  to  await  the 
further  development  of  the  disease  and  the  results  of  treatment  before  arriv- 
ing at  a  conclusion.  Patients  with  nervous  dyspepsia  are  apt  to  grow  worse 
and  worse  under  strict  treatment  for  ulcer,  while  an  opposite  mode  of  treat- 
ment (vide  infra)  often  has  the  most  brilliant  results. 

Prognosis. — The  prognosis  depends  mainly  on  the  strength  of  the  general 
neuropathic  tendency  in  the  case  and  on  the  surroundings  in  which  the  pa- 
tient lives.  If  the  patient  is  amenable  to  an  appropriate  suggestive  treatment, 
brilliant  therapeutic  results  can  be  readily  obtained  in  "  nervous  dyspepsia," 
especially  in  those  cases  in  which  the  patient  has  previously  become  extremely 
emaciated  through  a  too  rigid  diet,  and  subsequently  rapidly  gains  in  strength 
and  weight  on  a  correct  diet.  If,  however,  the  abnormal  concepts  and  the 
excited  general  psychical  condition  are  too  firmly  rooted  to  be  readily  disposed 
of,  only  slight  and  uncertain  results  are  obtained.  Likewise,  a  permanent 
improvement  can  rarely  be  expected  in  those  cases  in  which  the  injurious 
psychical  causes  or  other  aetiological  factors  continue,  while  the  removal 
of  these  causes  will,  on  the  contrary,  frequently  result  in  a  complete  cure 
even  of  apparently  very  grave  conditions.  A  liability  to  relapses  is,  of 
course,  almost  always  left  behind,  as  most  patients  are  constitutionally 
nervous. 

Treatment. — If  nervous  dyspepsia  has  once  been  diagnosticated,  the 
proper  aim  of  our  therapeutic  efforts  becomes  perfectly  definite.  We  must, 
in  the  first  place,  convince  the  patient  that  he  has  no  incurable  or  even  dan- 
gerous gastric  disease,  but  that,  on  the  contrary,  his  stomach  is  perfectly 
capable  of  performing  its  functions  in  a  normal  manner.  Nothing  could  be 
more  harmful  to  a  sufferer  from  nervous  dyspepsia  than  to  have  his  physician 
manifest  great  anxiety  about  treatment,  and  prescribe  a  very  strict  diet.  The 
patient  must  rather  be  gradually  led  to  use  an  abundance  of  nutritious  food. 
It  is  in  this  way  alone  that  he  regains  confidence  in  himself,  when  he  sees 
that  the  hearty  food  does  him  no  harm,  that  he  is  gaining  flesh,  and  that  the 
bowels  are  becoming  regular. 

Internal  remedies  are  best  omitted  altogether  if  the  patient  has  already 
taken  a  good  deal  of  medicine.  If  they  are  successful,  it  is  usually  because  of 
their  influence  on  the  mind.  If  we  must  prescribe  some  medicine,  the  bitter 
tonics  (the  preparations  of  quinin,  tincture  of  nux  vomica,  etc.)  are  most  suit- 
able. They  serve  particularly  to  stimulate  the  appetite.  If  painful  sensa- 
tions in  the  stomach  are  experienced  after  eating,  we  attempt  to  relieve  them 
with  warm  applications  or  a  Priessnitz  bandage,  twenty-per-cent  alcohol  ap- 
plications, by  administering  some  hydrochloric  acid,  pepsin,  etc.;  here,  as 
before  mentioned,  suggestive  influence  is  naturally  of  paramount  importance. 
In  this  respect,  the  galvanic  current  (large  anode  to  the  region  of  the  stomach, 
cathode  to  the  back)  is  often  particularly  efficacious.  The  treatment  of  con- 
tinuous ("habitual")  nervous  vomiting  is  very  important,  but  frequently 
difficult.  In  cases  of  this  sort  also  psychical  treatment  is  of  the  greatest  im- 
portance. Even  if  we  gravely  command  the  patient  not  to  yield  to  the  impulse 
to  vomit,  but  to  resist  it  as  much  as  possible,  such  an  injunction  will  often  do 


572  DISEASES  OF  THE   DIGESTIVE  ORGANS 

away  with  the  symptom,  and  it  is  not  rare  to  find  in  cases  of  nervous  vomiting 
that  it  will  cease  as  soon  as  nourishing  diet  is  allowed,  although  previously  it 
has  occurred  invariably  after  the  most  delicate  kinds  of  food.  It  is  often  very 
advantageous  in  nervous  vomiting  to  limit,  as  far  as  possible,  the  amount  of 
liquids,  such  as  soup  and  milk,  and  to  prescribe  a  dry  substantial  diet.  In 
many  cases  the  vomiting  will  then  cease  very  promptly. 

Obstinate  cases  of  nervous  vomiting,  it  is  true,  are  cured  with  difficulty 
at  home,  while  they  can  frequently  be  rapidly  relieved  by  the  psychical  influ- 
ence of  good  sanatorium  or  hospital  treatment.  If,  in  addition  to  the  purely 
nervous  symptoms,  certain  objective  symptoms  (anaemia,  gastroptosis,  habit- 
ual constipation,  etc. )  are  present,  these  will  also  have  to  be  considered  to  a 
certain  degree  (vide  supra). 

Those  methods  of  treatment  are  of  great  value  which  are  directed  to  the 
toning  up  of  the  body  in  general  and  the  nervous  system  in  particular.  The 
patient  may  go  into  the  country  or  to  the  mountains  or  the  seashore.  Method- 
ical treatment  with  cold  water  is  good. 

Frictions  of  the  abdomen  and  entire  body  with  cold  water  and  alcoholic 
solutions  are  almost  always  attended  by  good  results.  On  the  other  hand, 
those  health  resorts  which  often  do  good  in  the  case  of  organic  gastric  disease 
are  but  seldom  beneficial  in  nervous  dyspepsia.  Thus,  we  have  frequently 
seen  such  patients,  who  had  been  sent  by  their  physicians  to  Carlsbad,  return 
worse  rather  than  better.  We  have  repeatedly  found  electricity  valuable,  al- 
though we  surmise  that  its  subjective  effect  may  be  of  chief  importance.  Gal- 
vanism is  applied  along  the  spinal  column,  and  also  through  the  stomach 
horizontally,  one  large  electrode  being  placed  upon  the  epigastrium  and  the 
other  on  the  back.  It  is  well  to  reverse  the  current  frequently.  Faradization 
and  massage  of  the  abdominal  walls  are  indicated,  especially  when  there  is 
constipation. 

We  need  hardly  add  that  the  aetiological  factors  must  not  be  overlooked. 
The  patient  must  be  warned  against  mental  or  bodily  overexertion,  emotional 
excitement,  etc.  The  main  point  is  to  aim  at  a  methodical  moral  training  of 
the  patient.  He  should  learn  to  feel  and  to  behave  like  a  healthy  person.  He 
should  regain  his  self-control,  and  not  allow  himself  to  be  upset  by  every 
slight  psychical  shock,  whether  subjective  or  coming  from  without.  It  is  self- 
evident  that  this  goal  is  to  be  attained  not  by  baths  and  prescriptions,  but  by 
proper  moral  guidance.  The  best  proof  of  the  correctness  of  our  views,  with 
regard  to  the  true  nature  of  this  disease,  lies  in  the  therapeutic  successes  which 
can  be  obtained  in  this  manner  alone,  although  it  is  a  pity  that  they  are 
more  often  achieved  by  empirics  and  quacks  than  by  scientifically  educated 
physicians.  It  is  therefore  true  of  nervous  dyspepsia,  as  of  all  similar 
neurasthenic  conditions,  that  it  is  to  be  cured  not  by  physic  but  by  the 
physician. 


INTESTINAL   CATARRH  573 

SECTION   V 
Diseases  of  the  Intestines 

CHAPTER    I 

INTESTINAL    CATARRH 

(Catarrhal  Enteritis.     Enteritis  catarrhalis) 

iEtiology. — The  majority  of  cases  of  intestinal  catarrh,  like  gastric  catarrh, 
are  due  to  an  abnormal  irritation  of  the  mucous  membrane  of  the  intestine 
by  its  contents.  In  many  cases  the  irritants  are  of  a  mechanical  or  a  chemical 
nature,  and  depend  upon  the  quantity  and  quality  of  the  food  taken,  which 
explains  why  catarrh  of  the  stomach  and  catarrh  of  the  intestine  are  so  often 
combined  with  each  other.  Noxious  substances  are  often  introduced  into  the 
system  by  the  ingestion  of  spoiled  food,  such  as  spoiled  meat,  fish,  beer,  etc. 

To  the  intestinal  catarrhs  caused  by  improper  food  we  may  add  the  toxic 
catarrhs  which  are  produced  by  the  direct  ingestion  of  poisonous  substances 
into  the  digestive  tract,  or  by  the  imprudent  use  of  certain  drugs,  especially 
active  cathartics. 

A  great  many  cases  of  intestinal  catarrh  are  due  to  infectious  influences; 
these  include  most  of  the  apparently  spontaneous  catarrhs,  and  also  many, 
if  not  all,  of  the  catarrhs  attributed  to  taking  cold  or  getting  wet,  and,  finally, 
those  affections  which  often  develop  epidemically  or  endemically  in  hot 
weather,  and  which  we  term  summer  complaint,  cholera  morbus,  etc.  Cholera 
morbus  is  an  especially  severe  form,  and  it  will  be  described  more  fully  later 
on.  We  must  also  mention  here  that  intestinal  catarrh  is  often  one  symptom 
of  other  general  infectious  diseases,  such  as  typhoid,  dysentery,  septic  dis- 
eases, or  severe  malaria. 

In  a  final  class  of  cases  intestinal  catarrh  develops  from  disturbances  of 
the  circulation,  which  cause  a  passive  hyperemia  of  the  intestinal  mucous 
membrane.  Diseases  of  the  liver  and  portal  vein,  and  also  chronic  diseases 
of  the  heart,  kidneys,  and  lungs,  are  the  chief  affections  which  produce  a  stasis 
in  the  portal  system,  and  thus  an  intestinal  catarrh;  but  here  the  stasis  is 
probably,  in  most  cases,  only  a  predisposing  factor  in  the  development  of  the 
catarrh,  since  the  action  of  all  other  irritants  is  made  easier  by  the  disturb- 
ance of  the  circulation. 

The  frequency  of  intestinal  catarrh  in  both  sexes,  and  at  every  age,  is 
well  known.  Children,  above  all,  have  a  pronounced  tendency  to  diseases  of 
the  intestine,  so  that,  by  a  probable  estimate,  almost  one  third  of  the  illnesses 
of  children  are  to  be  referred  to  the  intestinal  canal.  We  will  give  a  special 
description  of  intestinal  catarrh  in  children  on  account  of  this  fact. 

Pathological  Anatomy. — The  pathological  changes  in  catarrhal  inflamma- 
tion of  the  intestines  are  essentially  the  same  as  are  met  with  in  the  inflam- 
mation of  any  other  mucous  membrane.  Redness  and  swelling  of  the  mucous 
coat,  increased  secretion  of  mucus,  and  in  severe  cases  purulent  products  on 
the  surface  of  the  membrane,  and  a  cellular  infiltration  of  the  tissue  itself, 


574  DISEASES  OF  THE  DIGESTIVE  ORGANS 

are  the  well-known  processes  characteristic  of  all  catarrhal  inflammations. 
The  solitary  and  agminated  follicles  often  swell  in  follicular  catarrh,  and 
they  may  finally  become  the  seat  of  superficial  follicular  ulcers.  We  often 
find,  especially  in  children,  superficial  erosions  on  the  rest  of  the  mucous 
membrane,  and  in  severe  cases  the  so-called  catarrhal  ulcers. 

If  the  catarrh  has  lasted  a  long  time,  we  sometimes  find  a  considerable 
thickening  of  the  nracous  membrane,  which  is  due  to  hyperplasia  of  the  con- 
nective tissue,  and  gives  an  uneven,  puffy  appearance  to  the  internal  surface 
of  the  intestine.  Circumscribed  hyperplasia  of  the  connective  tissue  may 
actually  lead  to  the  formation  of  polypi.  If  the  orifices  of  Lieberkuhn's  folli- 
cles are  stopped,  we  have  a  cystic  degeneration  of  the  follicles  from  the  re- 
tention of  the  intestinal  juice. 

We  very  often  find,  however,  a  considerable  atrophy  of  the  mucous  mem- 
brane, especially  in  the  chronic  intestinal  catarrh  of  children.  This  atrophy, 
which  has  been  carefully  investigated,  especially  by  Nothnagel,  affects  chiefly 
the  glandular  layer  of  the  mucous  coat.  In  place  of  the  glands,  which  in 
many  parts  may  wholly  disappear,  we  find  connective  tissue  more  or  less  rich 
in  cells.  The  atrophy  is  usually  most  pronounced  in  the  colon  and  the  lower 
part  of  the  ileum.     The  muscular  coat  may  also  take  part  in  the  atrophy. 

Certain  peculiarities  of  catarrh  affecting  single  portions  of  the  intestines 
will  be  mentioned  later  on. 

Symptomatology. — The  symptom  by  which  chiefly  we  determine  an  affec- 
tion of  the  intestinal  canal,  and  which  in  the  milder  cases  is  often  almost  the 
only  sign  of  an  intestinal  catarrh,  is  diarrhea — that  is,  abnormally  frequent 
stools  of  a  looser  consistence  than  usual;  yet,  strictly  speaking,  we  should  not 
attribute  every  diarrhea  to  a  catarrh  of  the  intestinal  mucous  membrane,  since 
a  large  number  of  influences  may  directly  produce  an  increased  peristalsis  and 
a  consequent  diarrhea.  Thus,  for  instance,  it  is  a  well-known  fact  that  sudden 
terror  or  great  anxiety  may  sometimes  cause  an  obstinate  diarrhea  in  a  very 
short  time.  In  nervous  and  neurasthenic  conditions,  we  sometimes  have  a 
chronic  diarrhea  which  can  be  due  only  to  abnormal  processes  of  innervation — 
"nervous  diarrhea."  The  diarrhea  which  may  arise  immediately  after  taking 
cold  is  also  merely  the  result  of  abnormally  great  peristaltic  movements  ex- 
cited in  a  reflex  manner.  Probably  a  number  of  chemical  and  infectious 
irritants  may  also  stimulate  the  movements  of  the  intestines,  and  thus  set  up 
a  diarrhea,  without  causing  at  the  same  time  a  catarrh  of  the  mucous  mem- 
brane. Practically,  however,  we  cannot  make  a  sharp  distinction  between 
diarrhea  and  intestinal  catarrh;  and,  in  most  of  the  diarrheas  which  have 
lasted  for  some  time,  we  are  certainly  right  in  supposing  that  there  are  actual 
anatomical  lesions  of  the  intestine  as  well  as  functional  disturbances. 

There  are  two  chief  factors  which  cause  diarrhea  in  intestinal  catarrh.  In 
the  first  place,  as  has  already  been  intimated,  the  same  injurious  substances 
which  cause  the  catarrh  also  excite  peristalsis.  The  many  products  of  the 
abnormal  processes  of  decomposition  in  the  intestine  also  exert  a  like  influ- 
ence. Besides  the  abnormal  irritants,  however,  we  ought  also  to  consider  an 
abnormally  great  irritability  of  the  diseased  intestinal  walls  in  catarrh.  Thus 
it  happens  that  the  fluid  contents  of  the  intestine  are  expelled  by  the  vigorous 
peristaltic  movements  (which  the  patient  himself  often  feels  as  a  "  rumbling 
in  the  abdomen")  before  the  normal  consolidation  of  the  feces  is  completed 


INTESTINAL   CATARRH  575 

by  the  absorption  of  water.  The  food,  under  normal  conditions,  passes 
through  the  small  intestine  in  two  or  three  hours,  and  thus  the  consolidation 
of  the  feces  takes  place,  as  is  well  known,  almost  exclusively  in  the  colon. 
We  see,  therefore,  why  the  diarrhea  owes  its  origin  chiefly  to  the  increased 
peristalsis  of  the  large  intestine,  although  in  many  cases  the  peristaltic  action 
of  the  small  intestine  is  also  increased.  Besides  increased  peristalsis,  an- 
other circumstance,  in  certain  cases,  contributes  to  the  diarrhea,  viz.,  the 
greater  fluidity  of  the  contents  of  the  intestine  due  to  the  increased  secretion 
of  mucus  and  the  exudation  caused  by  the  catarrhal  inflammation. 

In  some  intestinal  catarrhs,  especially  those  due  to  congestion,  the  dimin- 
ished absorption  of  water  from  the  intestines  in  consequence  of  the  circulatory 
disturbance  must  be  taken  into  account  as  a  possible  factor  in  addition  to 
the  increased  peristalsis. 

The  diarrheal  dejections  show  a  considerable  difference  in  regard  to  their 
minor  characteristics.  Their  number  varies  very  much.  There  are  sometimes 
two  or  three,  and  sometimes  ten  or  more,  evacuations  in  the  twenty-four  hours. 
The  consistence  of  the  stools  is  paplike,  or  almost  wholly  watery.  This  is  due 
to  the  abnormal  amount  of  water  in  them,  amounting  to  ninety  or  ninety-five 
per  cent,  while  the  amount  in  normal  stools  is  about  seventy-five  per  cent. 
The  color  of  the  thin  stools  in  intestinal  catarrh  is  usually  bright  yellow,  but 
they  are  sometimes  greenish  from  the  admixture  of  bile  pigment,  and  some- 
times slimy  (vide  infra). 

The  odor  of  the  dejections  is  frequently  extremely  foul;  in  other  cases 
(with  very  watery  movements)  it  is  comparatively  insignificant.  In  only 
a  part  of  the  cases  does  microscopic  examination  give  us  information  as  to 
the  extent  and  intensity  of  the  catarrh.  We  usually  find  the  remains  of  the 
food,  muscular  fibers,  starch  granules,  and  fat,  and  also  countless  bacteria,  and 
often  triple  phosphates,  occasional  blood  and  pus  corpuscles,  and  cylindrical 
epithelium.     Further  peculiarities  will  be  mentioned  below. 

Besides  the  diarrhea,  there  is  often,  but  by  no  means  always,  abdominal 
pain  in  intestinal  catarrh,  either  continuous  or  having  the  character  of  parox- 
ysmal, so-called  colicky  pains.  In  catarrh  of  the  rectum  there  is  that  constant 
painful  desire  to  go  to  stool  which  we  term  tenesmus. 

Physical  examination  of  the  abdomen  gives,  on  the  whole,  few  results. 
Sometimes  the  abdomen  is  flat,  and  sometimes  there  is  meteorism.  Marked 
peristaltic  action  of  the  intestines  often  causes  gurgling  and  rumbling  noises — 
borborygmi.  On  palpation,  the  abdomen  is  often  sensitive.  The  peculiar 
colicky  pains,  however,  are,  as  a  rule,  alleviated  by  external  pressure.  In  rare 
cases  we  may  detect  a  fluctuation  on  palpation  if  the  intestine  contains  much 
fluid.  The  results  of  percussion  depend  largely  upon  the  contents  of  the  intes- 
tines. There  is  dullness  on  percussion  if  the  intestines  are  full,  and  also  if 
they  are  contracted  and  devoid  of  air. 

In  many  cases  of  simple  diarrhea  the  general  health  is  practically  unaf- 
fected, but  in  other  cases  of  acute  intestinal  catarrh,  especially  in  the  severe 
infectious  forms,  the  disturbance  of  the  general  health  may  be  considerable. 
The  patient  feels  so  dull  and  weak  that  he  stays  in  bed.  We  often  see  a 
moderate  rise  of  temperature,  between  100°  and  102°  P.  (38°  to  39°  C). 
There  are  very  often  gastric  symptoms  also,  especially  loss  of  appetite,  coated 
tongue,  and   vomiting.     Other  organs  are  quite  rarely  affected,   except  in 


576  DISEASES  OF  THE  DIGESTIVE  ORGANS 

duodenal  catarrh,  when  the  liver  is  involved  (vide  infra).  In  acute  infec- 
tious intestinal  catarrhs  there  is  sometimes  an  eruption  of  herpes  on  the  lips. 
We  have  repeatedly  seen,  in  severe  cases  of  acute  enteritis,  marked  muscular 
and  articular  pains,  and  even  slight  but  manifest  swelling  of  the  joints. 
There  may  also  be  albuminuria,  casts,  and  even  the  signs  of  acute  nephritis, 
as  a  sequel  of  enteritis. 

Different  Forms  of  Intestinal  Catarrh. — Since  the  intestine  is  an  organ 
which  is  only  slightly  accessible  to  physical  examination  during  life,  and  since 
we  can  only  rarely  make  a  post-mortem  examination  in  the  mild  diseases  of 
the  intestine,  our  knowledge  as  to  the  different  forms  of  enteritis  is  defective 
in  many  respects.  In  practice  we  content  ourselves  in  most  cases  with  diag- 
nosticating an  intestinal  catarrh  simply  from  the  existence  of  diarrhea,  with- 
out laying  much  stress  upon  the  special  variety;  but  in  many  cases  some 
points  can  be  obtained  which  give  more  accurate  information  as  to  the  seat 
of  the  catarrh.  The  distinction  between  acute  and  chronic  intestinal  catarrh 
is  also  of  practical  significance. 

Duodenal  catarrh  can  be  diagnosticated  only  if  it  is  combined  with  jaun- 
dice. The  details  regarding  it  may  be  found  in  the  chapter  on  catarrhal 
jaundice. 

Isolated  catarrh  of  the  small  intestines,  of  the  jejunum  and  ileum,  is  prob- 
ably only  of  rare  occurrence,  except  when  the  upper  portions  of  the  colon  are 
involved.  We  can  very  rarely  diagnosticate  it  with  certainty,  but  there  are 
a  number  of  factors  which  permit  us  to  decide  that  the  small  intestine  is 
chiefly  affected,  or  at  least  that  it  is  involved  in  the  disease.  In  the  first 
place,  we  may  assume  an  affection  of  the  small  intestine,  for  obvious  reasons, 
in  all  those  cases  in  which  there  are  also  gastric  disturbances.  It  is  evident 
that,  in  the  frequent  combination  of  gastric  and  intestinal  catarrh,  the  por- 
tions of  the  intestine  nearest  the  stomach  will  be  chiefly  affected.  Physical 
examination  of  the  abdomen  also  gives  some  indications,  since  the  slight 
sensitiveness  and  swelling  of  the  abdomen,  as  well  as  the  visible  abnormal 
peristaltic  action,  affect  chiefly  the  middle  and  lower  portions  of  the  abdo- 
men in  catarrh  of  the  small  intestines,  while  the  analogous  symptoms  in 
catarrh  of  the  large  intestine  affect  the  lateral  and  upper  portions  of  the 
abdomen,  corresponding  to  the  anatomical  course  of  the  colon.  We  cannot 
make  a  sharp  distinction,  however,  in  this  respect.  The  results  which  auscul- 
tation and  percussion  over  the  abdomen  give  in  regard  to  the  point  of  origin 
of  the  gurgling  sounds  and  the  fullness  of  the  loops  of  intestine  are  very  rarely 
unequivocal. 

Careful  examination  of  the  stools  gives  us  more  information.  As  has  al- 
ready been  said,  we  need  not  have  diarrhea  in  a  catarrh  confined  to  the  small 
intestines,  since  diarrhea  is  due  only  to  the  increased  peristalsis  of  the  large 
intestine;  hence,  diarrhea  is  absent,  for  example,  in  most  cases  of  duodenal 
catarrh  (catarrhal  jaundice).  In  more  extensive  catarrh  of  the  small  intes- 
tines the  firm  stools  passed  may,  however,  be  regarded  as  pathological,  because, 
on  microscopic  examination,  they  appear  intimately  mixed  with  little  lumps 
of  hyaline  mucus  (Nothnagel).  As  a  rule,  of  course,  catarrh  of  the  small 
intestines  is  combined  with  a  catarrh  of  the  upper  portion  of  the  large  intes- 
tine. Then  we  have  a  diarrhea,  but  the  thin  stools  show  certain  peculiarities 
which  point  to  an  implication  of  the  small  intestines.     As  a  result  of  the 


INTESTINAL   CATARRH  577 

increased  peristalsis  of  the  small  intestines,  we  find  certain  constituents  in 
the  stools  which  are  normally  contained  in  the  small  intestines,  but  which 
under  normal  conditions  are  no  longer  to  be  met  with  in  the  feces  in  the  large 
intestine.  We  find  here,  in  the  first  place,  undigested  constituents  of  the  food 
(so-called  lientery),  large  masses  of  muscular  fiber,  or  even  fragments  of  meat 
which  may  be  recognized  by  the  naked  eye,  and  also  starch  and  fat.  Of  course 
the  opposite  hypothesis  does  not  hold  good,  that,  if  we  find  a  large  amount 
of  the  undigested  portions  of  the  food  in  the  stools,  it  must  necessarily  always 
point  to  a  catarrh  of  the  small  intestines,  since  the  digestion  may  be  impaired 
by  other  circumstances,  and  increased  peristalsis  of  the  intestines,  from  any 
cause,  must  result  in  the  same  symptoms. 

Eecently,  much  attention  has  been  devoted  to  the  careful  microscopical 
examination  of  the  stools  (A.  Schmidt,  Strassburger,  and  others).  If  the 
patient  receives  a  fixed  test  diet  of  meat,  fat,  and  carbohydrates  for  several 
days,  we  can,  by  a  microscopical  examination  of  the  feces,  determine  which 
class  of  food  stuffs  show  a  particularly  marked  disturbance  in  their  absorption. 
These  examinations,  which  are  interesting  but  difficult  of  interpretation,  have 
not  been  as  yet  extensively  employed  in  general  practice. 

If  the  stools  contain  bile  in  addition  to  some  portions  of  the  food,  it  is  to 
a  certain  degree  characteristic  of  catarrh  of  the  small  intestines.  Under 
normal  conditions  the  contents  of  the  small  intestines  alone  show  Gmelin's 
test  for  bile  pigment,  while  the  contents  of  the  large  intestine,  and  also  the 
normal  stools,  do  not.  In  intestinal  catarrh,  with  increased  peristalsis  of 
the  small  and  large  intestines,  there  is,  however,  often  quite  a  large  admix- 
ture of  still  undecomposed  bile  pigment.  The  green  stools  which  are  so  often 
seen  in  the  diarrhea  of  children,  and  more  rarely  in  that  of  adults,  are  also 
well  known.  Such  stools  usually  show  a  marked  color  reaction  with  nitric 
acid.  In  other  cases  we  find  only  certain  constituents  of  the  stools  stained 
with  bile — a  fact  to  which  Nothnagel  has  called  special  attention.  Yellow 
pigmented  bits  of  mucus,  and  cylindrical  epithelium  and  round  cells  stained 
with  bile,  are  especially  characteristic  of  the  diarrhea  of  catarrh  of  the  small 
intestines. 

Catarrh  of  the  large  intestine  is  probably  present  in  every  diarrhea,  as  has 
been  repeatedly  stated,  inasmuch  as  the  thin  stools  can  be  explained  only  by 
an  increased  peristalsis  of  the  large  intestine;  but  in  a  number  of  cases  we 
have  symptoms  which  point  especially  to  a  disease  of  the  large  intestine, 
particularly  of  its  lower  portion. 

Physical  examination  of  the  abdomen  shows  changes,  such  as  swelling, 
sensitiveness  to  pressure,  etc.,  chiefly  in  the  lateral  portions,  corresponding 
to  the  course  of  the  colon. 

A  marked  tenderness  to  pressure  in  the  region  of  the  sigmoid  flexure  is  of 
the  greatest  diagnostic  importance.  Undoubtedly,  severe  localized  inflamma- 
tion of  the  sigmoid  flexure  and  different  portions  of  the  colon  does  occur, 
although  the  pathology  of  this  affection,  which  is  known  as  acute  colitis  and 
sigmoiditis,  is  still  extremely  obscure.  Nevertheless,  the  diagnosis  can  occa- 
sionally be  made  with  reasonable  certainty,  by  careful  palpation  of  the  thick- 
ened and  tender  descending  colon,  in  connection  with  the  other  symptoms 
(mucus  in  the  stools,  fever,  etc.).  In  respect  to  setiology,  preceding  constipa- 
tion deserves  especial   consideration.     The  peritoneal  coat  of  the  colon   is 


578  DISEASES   OF   THE   DIGESTIVE   ORGANS 

occasionally  involved  in  the  inflammatory  process  (so-called  pericolitis).  Re- 
cently, such  cases  of  acute  febrile  pericolitis  have  been  repeatedly  observed. 
In  all  inflammatory  affections  of  the  large  intestine,  a  considerable  admixture 
of  macroscopically  recognizable  mucus  in  the  stools  is  of  diagnostic  im- 
portance. 

As  we  have  seen  above,  the  stools  in  catarrh  of  the  small  intestines  also 
contain  mucus,  but  it  is  intimately  mixed  with  the  other  constituents  of  the 
feces,  and  hence  it  can  usually  be  recognized  only  by  the  microscope.  In 
catarrh  of  the  large  intestine,  however,  the  mucus  rather  adheres  to  the  out- 
side of  the  other  constituents,  and  is  often  present  in  large  masses  visible  to 
the  naked  eye.  If  the  catarrh  affects  the  lower  part  of  the  large  intestine 
chiefly,  it  may  be  that  the  intestinal  contents  are  already  formed  into  firm 
lumps,  which  may  sometimes  be  wholly  or  partly  inclosed  in  a  layer  of  mucus. 
In  acute  catarrh  of  the  lowest  part  of  the  large  intestine  the  evacuations  are 
sometimes  composed  chiefly  of  pure  mucus,  with  a  greater  or  less  admixture 
of  pus,  as  is  seen  especially  in  the  "catarrhal  flux"  (see  the  chapter  on 
Dysentery).  The  more  the  rectum  is  involved  in  the  inflammation,  the  worse 
is  that  painful  feeling  of  tension  and  pressure  at  the  anus  during  and  after 
the  evacuation,  which  we  term  tenesmus. 

Isolated  inflammation  of  the  rectum  (proctitis)  is,  at  least  in  part,  di- 
rectly accessible  to  examination  by  the  finger  or  by  the  speculum.  Painful 
tenesmus  and  an  admixture  of  mucus,  and  especially  of  pus  in  the  stools,  are 
the  chief  symptoms  of  the  disease.  In  most  cases,  however,  we  have  to  do, 
not  with  a  primary  disease,  but  with  a  secondary  catarrh  of  the  rectal  mucous 
membrane,  as  a  result  of  different  morbid  conditions  in  the  vicinity  of  the 
rectum,  or  of  new  growths,  syphilitic  processes,  etc.,  in  the  rectum  itself. 
Periproctitis  (ischiorectal  abscess)  belongs  to  the  domain  of  surgery,  and 
cannot  be  described  here. 

Intestinal  catarrh  is  divided  into  an  acute  and  a  chronic  form. 

In  the  acute  intestinal  catarrhs,  excluding  the  toxic  inflammations,  we 
class  simple  diarrhea,  which  usually  passes  off  in  a  few  days,  and  the  severe 
enteritis,  which  is  probably  usually  infectious,  and  is  attended  by  a  marked 
disturbance  of  the  general  health,  by  fever,  and  sometimes  by  gastric  symp- 
toms also,  as  well  as  by  herpes,  by  occasional  slight  albuminuria,  by  articular 
pains,  etc.  It  lasts  from  three  to  ten  days.  Furthermore,  the  different  forms 
of  acute  catarrhal  colitis  described  above  belong  to  this  category. 

Cholera  morbus  (vide  infra)  is  to  be  regarded  as  a  special  form  of  acute 
infectious  inflammation  of  the  gastric  and  intestinal  mucous  membranes. 

Chronic  intestinal  catarrh  either  comes  from  an  acute  disease  of  the  in- 
testinal mucous  membrane  or  gradually  develops  independently.  In  adults 
it  is  by  no  means  a  very  common  disease,  at  least  as  regards  pronounced 
cases.  It  is  observed  with  comparatively  greatest  frequency  in  drinkers,  es- 
pecially in  habitually  excessive  beer  drinkers.  We  personally  know  patients 
of  this  sort  who  have  had  four  or  five  watery  stools  for  many  years.  More- 
over, chronic  intestinal  catarrhs  occur  occasionally  in  adults,  as  sequels  to 
severe  acute  intestinal  disease,  particularly  after  typhoid,  dysentery,  malaria, 
etc.  The  most  pronounced  symptom  of  the  disease  is  the  disturbance  of  the 
bowel  movements.  In  some  cases  there  is  continual  diarrhea ;  in  others,  diar- 
rhea alternates  with  obstinate  constipation.     With  a  careful  mode  of  living, 


INTESTINAL   CATARRH  579 

tlio  movements  arc  frequently  almost  normal,  bul   then  even  a  trivia]  error 

in  diet,  catching  cold,  or  psychical  excitement  (vide  supra,  inr.Mii-  diar- 
rhea) may  suffice  to  produce  a  diarrhea.  Jn  resped  to  the  character  of  the 
stools,  we  may  refer  to  what  has  been  said  above.  The  demonstration  of 
mucus  in  the  stools  is  always  the  most  important  sign.  The  test-irrigation 
of  the  intestines,  introduced  by  Boas,  furnishes  reliable  information  in  this 
respect.  After  previous  evacuation  of  the  bowels,  a  rectal  tube,  connected 
to  a  large  glass  funnel  by  means  of  rubber  tubing  (as  in  gastric  lavage,  vide 
supra,  page  509),  is  slowly  introduced  per  rectum  as  far  as  possible  into  tin- 
large  intestine,  small  quantities  of  lukewarm  water  being  meanwhile  allowed 
to  flow  in.  The  funnel  is  lowered  as  soon  as  a  desire  to  defecate  is  evinced. 
The  water  flows  back  into  the  funnel,  and  frequently  contains  a  distinct  ad- 
mixture of  mucus,  etc.,  which  permits  us  positively  to  conclude  that  a  catar- 
rhal affection  of  the  large  intestine  is  present.  The  subjective  symptoms  of 
chronic  intestinal  catarrh  consist  of  various  unpleasant  and  painful  sensa- 
tions (pressure,  borborygmi,  colics),  which  appear  particularly  after  errors 
in  diet,  and  may  become  extremely  disagreeable  to  the  patient.  In  some  cases 
the  general  nutrition  suffers  very  little,  while  in  others  gradually  marked 
emaciation  and  pronounced  ansemia  develop. 

Treatment. — Most  of  the  milder  cases  of  acute  intestinal  catarrh  need  only 
a  dietetic  treatment.  If  the  patient  avoids  all  injurious  substances  for  a  few 
days,  he  recovers  completely.  The  different  gruels,  such  as  barley  and  oat- 
meal gruel,  and  also  weak  broths,  milk,  and  thoroughly  toasted  bread,  or  the 
German  zwieback,  are  generally  regarded  as  the  most  suitable  food.  The 
coarser  vegetables  and  fruits,  fat  meat,  and  brown  bread,  are  to  be  avoided  as 
much  as  possible.  The  best  beverage  is  tea,  or  claret  diluted  with  water.  In 
other  respects  we  may  refer  to  the  dietetic  rules  laid  down  under  the  treat- 
ment of  chronic  gastric  catarrh. 

It  is  also  an  important  rule,  confirmed  by  much  experience,  to  keep  the 
abdomen  warm.  Children  should  always  stay  in  bed,  and  adults  should  do  so, 
at  least  in  all  severe  cases.  It  is  a  good  plan,  particularly  in  children,  to  pro- 
tect the  abdomen  from  cold  by  a  flannel  band. 

In  many  of  the  mild  cases  it  is  scarcely  necessary  to  use  internal  reme- 
dies. Gum  mixture  (P.  G.)  or  almond  mixture  is  a  good  prescription  if  there 
is  no  other  special  indication,  but  in  severe  cases  further  medication  may  be 
proper.  If  we  have  reason  to  suspect  some  irritating  ingesta  or  a  collection 
of  feces  as  a  cause  of  the  intestinal  catarrh,  a  cathartic  acts  favorably  at  the 
beginning  of  the  treatment  in  spite  of  the  existence  of  diarrhea.  Our  best 
cathartic  in  such  cases  is  castor  oil  or  calomel.  In  all  those  cases  in  which 
many  thin  dejections  point  to  a  greatly  increased  peristalsis  of  the  intestine, 
we  use  astringents,  especially  opium,  which  we  give  in  the  form  of  the  simple 
tincture  or  the  wine  in  doses  of  10  to  15  drops,  one  to  three  times  a  clay; 
or  as  a  powder,  0.5  to  1  gr.  (gm.  0.03  to  0.05)  of  opium  with  1  gr.  (gm.  0.05) 
of  sugar,  two  or  three  times  a  day.  It  is  also  well  to  combine  the  opium  with 
some  mucilaginous  vehicle,  as  2  parts  of  laudanum  to  150  of  gum  mixture  or 
decoction  of  salep  (P.  G.),  a  tablespoonful  every  two  or  three  hours.  Tannic 
acid  and  the  like  are  seldom  employed  in  acute  enteritis. 

If  there  is  severe  colic,  opium,  or,  under  some  circumstances,  an  injection 
of  morphin  is  the  best  remedy.     In  milder  cases  it  is  sufficient  to  apply 


580  DISEASES   OF  THE   DIGESTIVE   ORGANS 

warmth  to  the  abdomen  by  warm  poultices  or  hot  towels.  The  colic,  however, 
often  depends  upon  the  presence  of  old  fecal  masses  in  the  intestine,  when  it 
is  necessary  to  prescribe  a  cathartic,  such  as  castor  oil. 

If  there  is  painful  tenesmus,  it  is  usually  relieved  by  suppositories  of 
cacao  butter  containing  extract  of  opium. 

In  chronic  intestinal  catarrh  a  careful  regulation  of  the  diet  is  of  the 
greatest  importance.  To  be  avoided  are  fruits  and  sour  or  greasy  dishes,  in- 
digestible vegetables  and  puddings,  coarse  bread,  and,  above  all,  beer;  and  to 
be  recommended  are  tender  lean  meat  (sirloin),  sweetbread,  fish  that  are  not 
oily  (such  as  trout  and  pike),  potato  puree,  and  particularly  soft-boiled  rice 
and  sago.     In  regard  to  eggs  and  milk,  individual  experience  must  decide. 

As  beverages,  warm  or  cold  tea,  cocoa,  red  wine  and  water,  and  particularly 
huckleberry  wine,  which  we  have  used  a  great  deal  with  good  results,  are  to 
be  recommended.     Acorn  cocoa  is  also  frequently  of  value. 

Medicinal  treatment  is  directed  chiefly  against  the  chronic  diarrhea.  Next 
to  opium,  the  astringents  rank  first,  especially  tannin,  tannigen  (acetyltan- 
nin)  and  tannalbin  (tannin  albuminate).  The  two  last-named  remedies  have 
now  almost  entirely  replaced  tannin.  They  are  employed  in  doses  of  7  to  15 
gr.  (gm.  0.5  to  1)  several  times  daily,  either  alone  or  in  combination  with 
opium.  The  older  astringents,  such  as  radix  Colombo,  Lignum  campechi- 
anum,  catechu,  etc.,  are  now,  perhaps  undeservedly,  only  rarely  prescribed. 
Among  the  metallic  remedies,  acetate  of  lead  deserves  a  trial.  The  prepara- 
tions of  bismuth  are  frequently  of  decided  benefit — viz.,  bismuth  subnitrate, 
bismuth  salicylate,  and  betanaphthol  bismuth  (orphol)  ;  these  remedies  are 
also  frequently  combined  with  opium  (e.  g.,  bismuthi  salicyl.,  gr.  v  [gm.  0.3]  ; 
extr.  opii,  gr.  ^  [gm.  0.02]  ;  sacch.  albi,  gr.  v  [gm.  0.3],  three  powders  daily). 
In  some  cases  of  chronic  diarrhea  the  use  of  lime  is  recommended  (calcium 
phosphate  and  carbonate,  equal  parts,  a  teaspoonful  in  a  glass  of  plain  or 
carbonated  water  three  times  daily). 

In  case  the  offensive  odor  of  the  discharges  indicates  abnormal  decomposi- 
tion in  the  intestinal  canal,  we  employ  naphthalin  in  doses  of  1.5  to  5  gr. 
(gm.  0.1  to  0.3)  several  times  a  day.  We  often  have  to  try  various  remedies 
in  a  particular  case  before  we  find  one  that  is  efficient.  Great  care  should  be 
exercised  that  there  be  no  long  periods  of  constipation;  if  necessary,  we  may 
use  injections,  saline  laxatives,  or  castor  oil. 

In  all  cases  in  which  the  symptoms  point  to  a  serious  affection  of  the 
large  intestine,  local  medication  can  be  employed. 

We  irrigate  the  large  intestine  daily  with  weak  astringents,  and  sometimes 
with  disinfectants.  The  necessary  apparatus  is  very  simple.  It  consists  of 
a  large  glass  funnel,  to  which  a  rubber  tube,  about  half  a  meter  long  and  with 
a  proper  tip,  is  attached.  We  may  very  well  use,  for  an  end  piece  to  be  intro- 
duced into  the  rectum,  a  long,  soft,  elastic  oesophageal  tube,  which  can  easily 
be  pushed  quite  high  up.  The  fluids  used  for  irrigation  must  always  be 
warmed  to  about  85°  F.  (30°  C),  and  should  be  allowed  to  run  in  gradually 
and  slowly.  The  amount  of  fluid  used  for  one  irrigation  should  be  2  to  3 
pints  (1  to  1.5  liter),  or  sometimes  more.  The  patient  keeps  on  his  back 
during  the  irrigation.  The  knee-elbow  position,  which  is  much  more  uncom- 
fortable than  the  dorsal,  is  only  occasionally  necessary.  The  fluids  most  used 
are  a  one-  or  two-per-cent  solution  of  salicylic  acid,  solutions  of  salicylic  and 


INTESTINAL   CATARRH  581 

boric  acids  combined,  a  one-per-cent  tannin  solution,  or  a  solution  of  ace- 
tate of  lead  (1  to  1,000),  diluted  limewater,  etc.  Injections  of  bismuth 
(10  to  15  parts  in  1,000  of  water)  are  also  occasionally  employed  with  sue© 

Good  results  are  often  obtained  in  chronic  intestinal  catarrh  by  drinking 
the  waters  at  Carlsbad,  Tarasp,  Kissingen,  Marienbad,  or  Homburg,  particu- 
larly in  cases  with  occasional  constipation. 

It  is  of  great  practical  importance  to  distinguish  the  genuine  cases  of  chronic 
intestinal  catarrh  with  an  anatomical  basis,  from  the  common  nervous  disturb- 
ances of  the  digestive  tract.  Not  infrequently  the  most  diverse  symptoms  on 
the  part  of  the  intestine,  including  colic,  irregularity  of  the  bowels,  etc.,  appear 
as  part  of  a  general  neurasthenia  or  nervousness.  As  a  rule,  the  nervous  intes- 
tinal disturbances  come  on  in  attacks.  The  patients  are  very  well  at  times,  while 
at  other  times  without  any  sufficient  cause,  or  after  slight  colds,  errors  in  diet, 
and  even  psychical  excitement,  very  disagreeable  symptoms  occur,  such  as  pain- 
ful sensation  in  the  abdomen,  borborygmi,  colics,  sudden  diarrhea,  passage  of 
mucus,  etc.  Evidently  we  are  dealing  with  conditions  of  increased  intestinal 
irritability  which  manifest  themselves  in  some  cases  more  in  abnormal  peristal- 
sis, in  others  more  in  abnormal  secretion.  In  most  of  such  cases  there  is  little 
benefit  from  internal  remedies  and  strict  diet,  while  appropriate  general  treat- 
ment with  cold  water,  electricity,  gymnastics,  and  massage  is  often  attended  with 
the  best  results.  With  regard  to  this,  compare  also  the  chapters  on  Nervous 
Dyspepsia  and  on  Habitual  Constipation. 


APPENDIX 

Membranous  Enteritis  and  Mucous  Colic. — The  name  of  membranous  en- 
teritis or  mucous  colic  is  applied  to  a  condition  which  is  not  very  uncommon, 
and  is  therefore  of  practical  importance.  It  is  characterized  chiefly  by  the 
habitual  or  periodic  discharge  with  the  feces  of  a  great  abundance  of  mucus, 
in  the  form  of  membranes.  The  disease  is  observed  especially  in  women,  but, 
in  rare  cases,  also  in  men.  It  is  noticeable  that  the  patient  is  almost  always  a 
nervous,  hysterical,  or  hypochondriacal  individual. 

In  many  cases  a  discharge  of  the  membranes  takes  place  in  separate  attacks, 
which  occur  either  daily  or  at  longer  intervals,  and  are  associated  with  severe 
colic  ( "  mucous  colic  " ) .  The  membranes  are  gray  or  reddish  gray,  and  often 
cylindrical  or  rolled  up  in  a  ball.  They  consist  mainly  of  mucin — sometimes, 
it  is  said,  of  albuminoid  matters  also — and  examined  under  a  microscope  they 
are  usually  found  to  contain  an  unusual  amount  of  desquamated  cylindrical 
epithelium,  with  a  very  small  number  of  leucocytes,  and  perhaps  also  a  few 
crystals  of  triple  phosphate  and  cholesterin.  In  other  cases  there  are  scarcely 
any  attacks  of  colic,  but  merely  a  persistent  discharge  of  the  above-described 
membranes  and  bits  of  mucus.  The  true  discharges  of  the  bowels  are  almost 
always  very  sluggish  and  very  hard. 

There  is  still  much  uncertainty  as  to  the  true  nature  of  this  diseased  condi- 
tion. Whether  there  is  a  genuine  "  enteritis  "  is  doubtful,  at  least  with  regard 
to  many  cases.  The  noticeably  frequent  association  of  the  disease  with  hys- 
teria and  neurasthenia  seem  to  indicate  nervous  causes  for  the  exaggerated  pro- 
duction of  mucus.  The  formation  of  the  membranes  probably  takes  place 
37 


582  DISEASES  OF  THE  DIGESTIVE  ORGANS 

through  the  rolling  up  of  the  mucus  in  the  depths  of  the  longitudinal  folds  of 
the  colon  during  its  cramp-like  contractions. 

The  course  of  the  disease  is  usually  tedious,  hut  complete  recovery  may 
occur ;  there  is  no  danger.  The  nutrition  of  the  patient  may  remain  perfectly 
normal,  but  in  some  cases  it  is  greatly  impaired.  This  depends  chiefly  upon  the 
character  of  the  food  taken  and  the  other  nervous  symptoms  present. 

The  treatment  is  partly  local  and  partly,  or  rather  chiefly,  general,  for  the 
cure  of  the  associated  neurasthenia. 

For  local  treatment,  oil  injections  are  to  be  particularly  recommended 
(daily  injections  of  about  500  c.c.  warmed  olive  or  poppy  oil),  or  injections  of 
weak  solutions  of  bicarbonate  of  soda  or  greatly  diluted  limewater.  The  ex- 
isting constipation  should  also  be  treated  with  a  suitable,  not  too  careful,  diet, 
by  massage  and  only  in  cases  of  absolute  necessity  with  internal  cathartics.  For 
severe  colicky  pains  we  prescribe  hot  poultices  and  suppositories  of  opium  or 
extract  of  belladonna.  The  very  important  general  treatment  consists  princi- 
pally in  cold-water  cures  (half  baths,  rub  downs,  compresses),  fresh-air  treat- 
ment (seashore,  mountains),  electricity,  etc. 

Of  late,  severe  cases  of  membranous  colitis  have  been  repeatedly  treated, 
as  have  indeed  severe  inflammatory  affections  of  the  colon,  by  making  an  arti- 
ficial anus.  In  this  way  the  diseased  mucous  membrane  of  the  colon  is  pro- 
tected from  irritation,  and,  moreover,  drugs  can  be  applied  to  it  through  the 
artificial  opening.  The  author  has  been  able  to  convince  himself  of  the  efficacy 
of  this  treatment  in  some  very  obstinate  cases. 


CHAPTEE    II 

CHOLERA    MORBUS 

(Cholera  nostras.     Cholera  infantum) 

By  the  name  "  cholera  morbus  "  we  mean  an  acute  disease  of  the  stomach 
and  intestinal  canal  of  a  definite  form,  whose  symptoms  in  severe  cases  greatly 
resemble  those  of  genuine  Asiatic  cholera.  It  is  in  the  highest  degree  probable, 
from  the  whole  course  of  the  disease,  that  cholera  morbus  also  depends  upon  an 
acute  infection  of  the  body  by  a  specific  germ ;  but  this  germ  has  not  yet  been 
identified. 

Cholera  morbus  comes  on  usually  as  an  epidemic,  and  almost  exclusively  in 
the  hot  summer  months — June  to  August.  Hence  it  is  often  termed  summer 
cholera.  Children  in  the  first  two  years  of  life  are  chiefly  attacked,  especially 
those  who  are  artificially  fed  or  who  have  recently  been  weaned.  The  disease 
also  attacks  older  children  and  adults,  but  much  more  rarely. 

The  symptoms  of  cholera  morbus  are  those  of  a  severe  acute  gastroenteritis. 
The  disease  begins  suddenly,  or  after  some  slight  warning,  with  violent  vomit- 
ing and  severe  diarrhea.  In  some  cases  one  of  these  symptoms  predominates, 
and  in  others  the  other.  The  vomitus  consists  partly  of  the  food  taken,  and 
partly  of  a  slimy,  watery  substance.  The  stools  at  first  retain  their  fecal  char- 
acter, but  they  soon  become  more  colorless  and  more  watery,  so  that  they 
sometimes  approach  the  well-known  rice-water  appearance  of  the  stools  in  gen- 


CHOLERA   MORBUS  583 

nine  cholera.    Abdominal  pain  is  usually  absent,  but  a  feeling  of  pressure  and 

constraint  in  the  epigastrium  is  often  present.  The  diminished  secretion  of 
urine  and  the  frequent  muscular  pains  cause  the  whole  type  of  the  disease  to 
resemble  genuine  cholera  still  more  closely.  There  is  sometimes  a  cutaneous 
eruption  resembling  roseola. 

The  severe  constitutional  disturbance  is  especially  characteristic.  The 
patient  becomes  extremely  dull  and  has  a  wasted  look,  the  voice  is  weak  and 
hoarse,  an  unquenchable  thirst  sets  in,  the  pulse  is  very  small,  the  skin  of  the 
face  and  the  extremities  is  cool  and  livid;  in  short,  we  have  the  pronounced 
picture  of  a  general  collapse.  The  body  heat  also  falls,  although  at  the  first 
stage  of  the  disease  there  is  often  a  rise  of  temperature. 

[The  temperature  is  always  high,  even  during  the  stage  of  collapse,  when 
the  skin  and  extremities  are  cool  to  the  touch ;  if  the  thermometer  is  introduced 
into  the  rectum — generally  the  best  place,  by  the  way,  to  take  the  temperature 
in  young  children — it  will  rise  to  101°  to  102°  F.,  and  is  more  apt  to  reach 
104°  to  107°  F.  This  shows  that  inflammation  plays  a  large  part  in  the  pathol- 
ogy of  the  disease.] 

The  picture  of  a  severe  general  disease  is  especially  prominent  in  cholera 
infantum.  In  severe  cases  of  this  form  of  the  disease  the  general  restlessness, 
which  at  first  exists,  rapidly  passes  into  somnolence.  The  child  lies  with  sunken, 
half-closed  eyes,  the  conjunctivae  are  slightly  injected,  the  corneas  are  cloudy, 
the  face  is  pale  and  cyanotic,  the  fontanelles  are  depressed,  the  skin  is  cool,  and 
the  pulse  is  small  and  frequent  and  it  can  scarcely  be  counted.  Amidst  these 
symptoms,  death  comes  on  in  coma  or  with  slight  convulsions.  There  can 
scarcely  remain  room  for  doubt  that  these  severe  cases  of  gastro-enteritis  are  of 
infectious  origin,  and  that  the  constitutional  symptoms  are  the  result  of  toxic 
matters  generated  in  the  intestine  under  the  influence  of  the  microorganisms. 
Another  peculiar  symptom  which  occurs  in  severe  cholera  infantum  is  the  so- 
called  sclerema  adiposum.  While  the  temperature  keeps  sinking  the  extremities 
become  peculiarly  stiff  and  rigid,  and  the  skin  grows  pale  and  firm.  This 
phenomenon  is  caused  by  the  fat  in  the  fat  cells  of  the  subcutaneous  connective 
tissue  stiffening  as  a  result  of  the  low  [superficial]  temperature. 

The  mortality  of  children  with  cholera  infantum  is  very  marked,  especially 
in  large  cities,  and  among  the  poorer  classes  of  society.  Severe  cases  usually 
end  fatally  in  a  few  days,  but,  on  the  other  hand,  many  cases  recover,  either 
because  the  course  of  the  disease  from  the  first  is  not  so  severe,  or  because  cases 
ajoparently  hopeless  take  a  favorable  turn.  In  adults  it  is  extremely  rare  to 
see  cholera  morbus  terminate  unfavorably.  Patients  also  recover  quite  rapidly 
from  apparently  severe  conditions,  although  the  stomach  and  intestines  often 
remain  rather  sensitive  for  a  long  time. 

The  anatomical  appearances  in  children  who  die  of  cholera  infantum  usu- 
ally contrast,  from  their  insignificance,  with  the  severe  symptoms  observed 
during  life.  The  catarrhal  affection  of  the  gastric  and  intestinal  mucous  mem- 
branes is  not  at  all  prominent  in  the  cadaver,  and  the  solitary  follicles  and 
Peyer's  patches  show  only  a  slight  swelling.  A  careful  microscopic  examina- 
tion of  the  intestinal  mucous  membrane  shows,  however,  quite  severe  inflam- 
mation. The  other  lesions  which  are  most  frequently  seen  are  lobular  atelec- 
tases in  the  lungs,  venous  hyperaamia  and  oedema  of  the  pia  mater,  and  slight 
lesions  of  the  kidneys. 


584  DISEASES   OF   THE   DIGESTIVE   ORGANS 

The  diagnosis  of  cholera  morbus  presents  no  difficulty  if  the  characteristic 
symptoms  of  the  disease  are  present.  The  distinction  between  it  and  genuine 
Asiatic  cholera  used  to  be  occasionally  quite  difficult,  and  it  was  rendered  pos- 
sible only  by  considering  the  getiological  factors,  and  the  evident  connection 
between  the  individual  case  and  other  cases  of  undoubted  cholera.  By  Koch's 
discovery  of'  the  comma  bacillus  in  Asiatic  cholera  the  distinction  between  the 
two  diseases  has  now  become  absolutely  certain.  In  all  suspicious  cases,  there- 
fore, we  must  examine  the  dejections  for  comma  bacilli,  and  upon  the  result  of 
this  examination  depends  the  determination  of  the  proper  means  of  prophy-- 
laxis. 

The  treatment  of  cholera  morbus  in  adults  must  be  first  to  take  special  care 
to  limit  the  diet.  The  food  should  be  only  gruels,  or  at  most  broth  and  milk. 
It  is  a  good  plan  to  give  the  milk  iced,  and  in  small  amounts.  The  distressing 
thirst  is  best  relieved  by  cracked  ice  or  cold  tea.  Wine  (iced  champagne)  is  to 
be  given  if  the  general  weakness  becomes  marked. 

Among  drugs,  opium  is  the  most  effective  remedy,  and,  whether  in  powder, 
as  the  extract,  or  in  liquid  form,  as  laudanum,  it  is  the  first  thing  to  use  to 
relieve  the  diarrhea  and  vomiting.  All  other  remedies,  such  as  nitrate  of  silver, 
are  quite  subordinate  to  opium.  We  may  combine  small  doses  of  calomel  with 
the  opium.  If  there  is  a  severe  collapse  which  threatens  life,  it  is  advisable  to 
make  a  subcutaneous  injection  of  water  containing  0.6  per  cent  of  salt. 

In  the  case  of  children,  it  is  best  to  discontinue  milk  entirely  for  several 
days,  or,  at  the  most,  to  give  ice-cold  milk  by  the  teaspoonful.  A  supply  of 
fluids  is  alone  essential,  either  in  the  shape  of  boiled  water  or  weak  tea  (chamo- 
mile tea).  Mucilaginous  drinks  (thin  gruels)  and  albumin  water  must  also 
be  used  only  with  care. 

We  should  rather  hesitate  in  prescribing  opiates,  although  here  small  doses 
of  opium,  1  or  2  drops  of  laudanum  according  to  the  age  of  the  child,  may  often 
be  indispensable.  In  fresh  cases  calomel  has  obtained  a  great  reputation,  a 
sixth  of  a  grain  (gm.  0.01)  two  or  three  times  a  day.  If  nothing  will  stay  on 
the  stomach,  we  may  try  a  subcutaneous  injection  of  0.6  per  cent  saline  solu- 
tion. If  there  are  symptoms  of  severe  collapse,  we  should  immediately  employ 
hot  baths  at  100°  F.  (30°  E.),  with  the  addition  of  10  to  15  ounces  of  mustard 
(gm.  300  to  500)  and  hot  packs,  as  well  as  such  stimulants  as  camphor  or  alco- 
hol subcutaneously.  To  guard  against  desiccation  of  the  sclera  and  cornea, 
the  eyes  should  be  covered  with  compresses  moistened  with  solutions  of  acetate 
of  lead,  corrosive  sublimate,  etc. 


CHAPTEK    III 

INTESTINAL    CATARRH    OF    CHILDREN 

(Pedalrophy.     Acute  and  Chronic  Intestinal  Disturbances  of  Children) 

The  great  frequency  and  the  practical  importance  of  the  "  dyspeptic  con- 
ditions "  in  children  in  the  first  years  of  life,  which  conditions  are  associated 
with  severe  disturbances  of  nutrition,  justify  a  short  description  of  them,  but 
we  must  refer  to  the  special  manuals  on  children's  diseases  for  a  detailed 
account. 


INTESTINAL   CATARRH   OF   CHILDREN  585 

TEtiology  and  Pathological  Anatomy. — Thai  diseases  of  the  digee 
organs  play  so  large  a  part  in  children's  troubles  is  owing,  on  the  one  hand,  to 
the  great  sensitiveness  which  the  infantile  organism,  and  particularly  its  digest- 
ive apparatus,  shows  to  the  irritants  which  are  broughl  in  contact  with  them, 
and,  on  the  other,  to  the  too  common  mistakes  which  the  child's  parents  and 
nurses  show  in  its  feeding.  Of  course  it  is  not  always  ignorance  and  neglect, 
but  often,  unfortunately,  poverty  and  want  which  cause  children  to  suffer,  and 
explain  the  terrible  mortality  in  the  first  years  of  life. 

The  simple  fact  that  by  far  the  larger  number  of  children  who  suffer  from 
dyspeptic  and  atrophic  conditions  are  fed  artificially,  lead-  us  to  the  belief  that 
the  cause  of  most  intestinal  diseases  of  children  is  to  be  sought  U>v  in  a  defective 
and  insufficient  dietary. 

It  has  been  determined  statistically  that  the  mortality  of  bottle-fed  in- 
fants is  approximately  twenty  times  greater  than  that  of  breast-fed.  For  a 
time  there  was  a  tendency  to  ascribe  the  detrimental  influence  of  artificial 
feeding  principally  to  impurity  of  the  milk,  i.  e.,  to  infectious  causes.  Fliigge, 
Czerny,  and  others  have,  however,  shown  that  the  use  of  sterilized  food  has 
no  marked  influence  on  infant  mortality.  Though  the  deleterious  action  of 
bacteria  (vide  infra)  can  by  no  means  be  entirely  disregarded,  the  chemical 
and  biological  differences  between  mother's  milk  and  all  artificial  foods,  and, 
above  all,  the  quantitative  differences  in  the  composition  of  the  different  arti- 
ficial foods,  furnish  in  themselves  a  number  of  causes  for  disease.  These 
noxious  causes  and  their  sequelae  have  been  studied  in  detail  for  the  different 
classes  of  artificial  foods  (Czerny).  The  harmful  action  of  cow's  milk  is  due, 
perhaps,  partly  to  the  chemical  peculiarities  of  its  proteids  (vide  infra), 
partly  to  its  distinctive  enzymes,  and  partly  to  an  admixture  of  noxious  sub- 
stances derived  from  the  fodder  eaten  by  the  cows,  etc.  In  the  first  place, 
the  "  overfeeding "  of  infants  with  proteids,  and,  above  all,  the  continuous 
overabundant  supply  of  fats,  play  a  very  important  role  in  the  "  milk-diet 
disorders."  Another  class  of  nutritive  disorders  is  to  be  ascribed  to  the  very 
common  use  of  gruels  (Melilsuppen)  and  similar  preparations  as  food  for 
infants  (so-called  farinaceous-diet  disorders).  Here  both  the  continued  lack 
of  fats  and  also  an  insufficient  supply  of  proteids  and  salts  play  a  role.  To 
what  extent  the  too  early  administration  of  eggs  and  meat  can  produce 
proteid-diet  disorders,  due  to  the  specific  action  of  "  hetero-albumins,"  has 
not  yet  been  determined  with  certainty.  The  assumption  of  some  pediatrists, 
that  the  proteid  of  cow's  milk — i.  e.,  casein— is  particularly  indigestible  and 
harmful,  has  not  been  conclusively  proved.  In  isolated  cases,  again,  nutritive 
disorders  due  to  gelatin  have  occurred  from  the  continued  administration  of 
strongly  gelatinous  broths  prepared  from  calves'  bones. 

Besides  incorrect  feeding,  in  regard  simply  to  quality  or  quantity,  in- 
fectious influences,  as  already  stated,  also  play  a  great  part.  Pathogenic  bac- 
teria are  occasionally  introduced  as  such  into  the  stomach  and  intestines  with 
the  food.  Or,  we  are  dealing  with  bacteria  normally  present  in  the  digestive 
tract  which,  however,  under  peculiar  conditions  have  increased  in  numbers 
and  possibly  also  in  virulence.  In  spite  of  many  investigations,  it  has  not 
been  conclusively  determined  which  particular  group  of  bacteria  is  to  be  con- 
sidered the  principal  cause  of  the  dyspeptic  conditions  in  children.  In  many 
cases  virulent  types  of  the  bacillus  coli  appear  to  play  the  chief  role;  in  other 


586  DISEASES  OF  THE  DIGESTIVE  ORGANS 

cases,  streptococci,  diplococci,  etc.  The  infectious  nature  of  the  disease  has 
a  relation  to  the  fact  that  dyspeptic  conditions  are  much  more  frequent  during 
the  summer  than  the  winter  months.  It  should  be  remarked,  however,  that 
the  deleterious  action  of  the  bacteria  must  be  frequently  regarded,  not  as  a 
true  infection,  but  rather  as  an  intoxication,  since  the  food  becomes  decom- 
posed by  bacteria  either  before  being  administered  or  afterwards  in  the  di- 
gestive tract.  In  this  way  a  number  of  toxic  substances  are  produced  ("ali- 
mentary toxicosis,"  according  to  Czerny  and  Keller).  It  is  mainly  the  acids 
produced  by  decomposition  of  the  milk  sugar  and  the  fats  (lactic  acid,  fatty 
acids,  etc. ) ,  but  occasionally  also  the  fermentation  products  of  the  farinaceous 
carbohydrates,  which  cause  diarrhea,  increased  production  of  mucus  in  the 
intestines  and  general  toxic  disorders.  Some  of  the  clinical  pictures  have  a 
strong  resemblance  to  acid  intoxications  (acidosis,  as  in  diabetic  coma).  Par- 
ticular attention  should  also  be  paid  to  the  loss  of  water  from  which  the  body 
suffers. 

Symptomatology. — With  this  conception  of  the  symptomatology  of  the 
disease  as  the  expression  of  a  bacterial  intoxication,  the  strikingly  insignificant 
anatomical  changes  found  at  the  autopsies  of  children  who  have  died  of  "  in- 
testinal catarrh "  entirely  coincide.  What  were  formerly  considered  to  be 
signs  of  organic  intestinal  disease  have  been  shown  in  many  instances  to  be 
merely  post-mortem  changes.  Nevertheless,  the  swelling  of  the  follicles  (fol- 
licular catarrh)  is  occasionally  striking.  Follicular  ulcers  also  occur.  In 
other  cases  an  atrophy  of  the  mucous  membrane  is  the  main  change.  Chronic 
thickening  and  redundancy  of  the  mucous  membrane  are  of  rarer  occurrence. 
In  most  of  the  severe  cases  the  large  intestine,  and  also  the  lower  portion  of 
the  ileum,  are  the  chief  seat  of  the  changes.  We  often  find  a  swelling  of  the 
mesenteric  lymph-glands,  and  also  a  fatty  liver.  In  the  lungs  extensive 
atelectases  or  nodules  of  catarrhal  pneumonia  often  develop  as  a  result  of  the 
imperfect  respiration.  Other  not  infrequent  complications  resulting  from 
the  general  infection  or  intoxication  are  otitis,  nephritis,  cystitis,  etc.  The 
symptoms  of  the  dyspeptic  disturbances  are,  in  the  first  place,  those  due  to 
the  intestinal  trouble,  and,  secondly,  the  quite  rapid  disturbance  of  the  child's 
general  nutrition. 

The  condition  of  the  stools  is  the  most  important  intestinal  symptom.  The 
normal  dejection  in  children  until  they  are  weaned  is  of  the  color  of  the  yolk 
of  an  egg,  of  a  rather  pasty  consistence,  and  of  a  faintly  sour  smell.  In  most 
intestinal  disturbances  the  stools  are  more  frequent,  six  or  seven,  and  even 
more,  a  day.  The  stools  are  not  of  an  even  consistence,  but  contain  flocculent 
and  lumpy  masses,  which  look  as  if  they  had  been  chopped  up.  Or,  they  are 
thinner,  more  watery,  contain  large  flakes  and  lumps  (undigested  bits  of 
casein  and  other  remains  of  the  food),  as  well  as  a  marked  admixture  of  mucus, 
either  as  "  sago  grains  "  or  larger  glassy  masses.  The  odor  of  the  stools  be- 
comes fetid,  the  reaction  is  frequently  alkaline,  the  color  throughout  or  in 
part  is  frequently  distinctly  green.  This  green  discoloration  probably  de- 
pends principally  on  a  decomposition  of  the  bile  pigments.  Whether  bacteria 
also  play  any  role  in  this  process  is  still  doubtful.  Sometimes  the  stools  do 
not  acquire  the  green  color  until  after  they  have  been  passed.  With  the 
microscope  we  find  in  severe  cases,  besides  particles  of  food,  leucocytes  and 
epithelial  cells,  threads  and  clumps  of  mucus,  and  innumerable  bacteria  of 


INTESTINAL  CATARRH   OF   CHILDREN  587 

all  shapes.  There  are  also  crystals  of  triple  phosphates,  when  the  stools  have 
an  alkaline  reaction,  and  needle-shaped  crystals  of  the  fatty  acids,  as  well  as 
plates  of  cholesterin,  when  the  discharges  are  acid.  Small  quantities  of  blood 
are  also  occasionally  found  in  the  stools,  which  naturally  always  points  to 
more  marked  anatomical  changes  in  the  intestinal  wall.  Certain  forms  of 
enteritis  are  characterized  by  exceedingly  imperfect  absorption  of  fats.  The 
stools  are  then  light  yellow  or  greenish  yellow,  and  of  a  thin  consistence; 
they  smell  strongly  of  fatty  acids,  and  contain  a  very  plentiful  amount  of 
undigested  fats   (so-called  "fatty  diarrhea"). 

There  is  no  definite  distinction  in  regard  to  the  dejections  in  catarrh  of  the 
large  and  of  the  small  intestines.  On  the  whole,  the  rule  holds  that,  in  catarrh 
of  the  small  intestines  chiefly,  the  stools  are  larger,  they  are  passed  with  more 
wind  or  gas,  and  show  a  more  uniform  consistence;  while  in  catarrh  of  the 
large  intestine  they  are  smaller  but  more  frequent,  ten  or  twenty  a  day,  are 
passed  noiselessly,  are  associated  with  tenesmus,  and  show  a  different  consist- 
ence in  their  various  parts,  partly  normal,  partly  thin,  partly  slimy,  etc.  Ex- 
amination of  the  abdomen  reveals,  as  a  rule,  in  catarrh  of  the  small  intestine 
that  the  abdomen  is  much  swollen,  while  in  catarrh  of  the  large  intestine  it 
is  often  deeply  sunken.  The  tissues  about  the  anus  are  often  red  and  sore 
and  the  mucous  membrane  prolapsed. 

The  liver  is  often  enlarged  and  distinctly  palpahle,  and  sometimes  the 
spleen  also.  The  swollen  mesenteric  glands  can  be  felt  in  isolated  cases.  We 
often  find  disturbances  in  the  stomach,  vomiting,  eructations,  etc.,  as  well  as 
trouble  in  the  intestines.  There  may  be  thrush  in  the  mouth,  or  the  develop- 
ment of  aphthous  ulcers.  Among  other  complications,  we  see  diseases  of  the 
respiratory  tract,  including  bronchitis,  atelectasis,  and  catarrhal  pneumonia; 
also  albuminuria,  eczema,  furunculosis,  otitis,  nervous  disturbances,  etc.  Ea- 
chitic  and  tuberculous  changes  in  the  lungs,  intestines,  and  lymph-glands  may 
be  combined  with  the  intestinal  catarrh. 

In  almost  all  long-continued  cases,  however,  the  general  disturbance  of 
nutrition,  the  atrophy  ("pedatrophy,"  "athrepsia")  of  the  child,  takes  the 
foreground  in  the  picture  of  the  disease.  Accurate  observation  of  the  body 
weight  through  weekly  or  biweekly  weighings  is  imperative  in  order  to  judge 
the  course  of  the  disease.  In  severe  cases  of  chronic  enteritis,  or  those  that 
have  been  treated  improperly,  the  atrophy  finally -attains  its  maximum  inten- 
sity. The  muscles  become  shriveled  and  flabby,  and  the  whole  body  finally 
becomes  so  much  emaciated  that  the  pale,  dry  skin  hangs  in  broad  folds  and 
wrinkles  about  the  bones,  whose  prominences  are  everywhere  visible.  The  face 
is  sharp,  and  has  an  aged  expression  ("Voltaire-face")  from  the  many  little 
folds  of  the  skin.  The  eyes  are  dull,  lusterless,  and  wide  open;  the  voice  is 
merely  a  low,  hoarse  whimper.  The  abdomen  is  deeply  sunken,  or  in  some 
cases  it  is  swollen  by  meteorism,  in  peculiar  contrast  to  the  emaciation  else- 
where, and  its  surface  is  traversed  by  bluish  veins. 

Treatment. — If  we  would  give  a  full  account  of  the  treatment  of  the 
atrophic  conditions  in  children  due  to  digestive  disturbances,  we  must  include 
in  our  consideration  the  entire  hygiene  and  care  of  children  in  health  and  dis- 
ease, for  all  children's  physicians  are  united  in  the  opinion  that,  as  the  cause 
of  most  intestinal  diseases  in  children  is  to  be  found  in  improper  feeding,  so 
recovery  from  existing  digestive  disturbances  can  take  place  primarily  only 


588  DISEASES   OF  THE   DIGESTIVE   ORGANS 

by  a  corresponding  proper  and  judicious  feeding.  In  what  follows  we  can 
refer  only  to  the  most  important  principles  and  general  points  which  are  here 
to  be  considered. 

The  only  proper  and  natural  food  for  a  child  in  its  first  year  is  breast  milk. 
All  dyspeptic  conditions  are  much  rarer  in  children  who  are  nursed  than  in 
bottle-fed  children,  and,  when  they  do  occur  in  children  at  the  breast,  they 
often  are  only  of  brief  duration.  They  are  then  to  be  referred  usually  to 
certain  disturbances  in  the  mother,  such  as  disease,  improper  food,  or  severe 
mental  excitement.  The  return  of  menstruation  or  a  new  pregnancy  has  some- 
times an  unfavorable  influence  on  the  character  of  the  milk.  It  is  very  im- 
portant to  see  that  the  breast  is  given  at  regular  intervals  to  the  infant.  Gen- 
erally the  feedings  should  be  given  every  three  hours  during  the  day,  so  that 
the  number  of  feedings  in  twenty-four  hours  approximate  six  or  seven.  The 
duration  of  each  nursing  is  approximately  ten  minutes,  and  should  not  exceed 
twenty.  Under  normal  conditions  the  increase  in  weight  for  the  first  quarter 
of  the  first  year  is  about  6  to  7  ounces  (gm.  180  to  200)  weekly,  for  the 
second  quarter  about  4  ounces  (gm.  120),  and  for  the  third  3.5  ounces  (gm. 
100).  By  weighing  the  infant  before  and  after  nursing  we  can  find  out 
whether  the  child  receives  a  sufficient  quantity  of  food.  The  quantity  of  milk 
taken  at  each  feeding  should  be  approximately  2  or  3  ounces  (gm.  50  to  80) 
during  the  first  quarter  of  the  year,  3  to  4  ounces  (gm.  80  to  120)  during  the 
second,  still  more  later  on.  If  the  secretion  of  milk  in  the  nursing  woman 
diminishes,  or  is  insufficient  from  the  outset,  we  can  give  diluted  cow's  milk 
(vide  infra)  in  addition  to  the  breast  milk.  Weaning  of  breast-fed  children 
occurs  gradually  during  the  seventh  to  the  ninth  month.  Cow's  milk,  weak 
broths,  soft-boiled  eggs,  etc.,  are  given  in  the  transition  to  ordinary  food. 

In  selecting  a  wet  nurse  the  general  nutrition  and  health  (tuberculosis, 
syphilis),  as  well  as  the  character  of  the  breasts  and  nipples,  must  be  con- 
sidered. If  possible,  the  child  of  the  nurse  should  also  be  examined ;  its  age  at 
the  time  of  taking  the  nurse  should  be  between  one  and  three  months.  The 
food  of  the  mother  or  wet  nurse  must  be  abundant,  excluding,  however,  all 
indigestible,  strongly  spiced  and  acicl  foods.  Attention  should  be  paid  to  a 
sufficient  but  not  overabundant  supply  of  fluids  (milk,  cocoa,  beer,  as  much 
as  a  quart  daily).  It  is  of  the  greatest  importance  to  get  a  wet  nurse  in 
those  cases  where  the  child  does  not  thrive  on  artificial  food  and  continually 
has  dyspeptic  troubles.  Feeding  by  the  milk  of  a  wet  nurse  is  then  the  only 
remedy  which,  at  least  in  many  cases,  by  saving  the  child's  life,  repays  the 
many  annoyances  and  quite  large  expense  which  a  wet  nurse  causes.  Com- 
plete, and  sometimes  even  quite  rapid,  recovery  may  often  be  obtained  through 
a  wet  nurse,  even  in  cases  of  severe  chronic  intestinal  catarrh,  when  atrophy 
and  weakness  are  already  very  far  advanced. 

If  the  mother  is  unable  to  nurse  the  child,  and  it  is  impractical  to  get  a 
wet  nurse,  the  question  of  artificial  feeding  of  the  infant  must  be  considered. 
The  best  substitute  for  mother's  milk  is  cow's  milk.  It  should  be  obtained 
from  healthy  cows,  which  have  been  fed  on  hay  (dry  fodder)  and  not  on 
fresh  grass,  distiller's  mash,  etc.  General  cleanliness  is  of  the  greatest  im- 
portance in  the  process  of  collecting  the  milk.  The  milk  must  reach  the  con- 
sumer in  the  shortest  possible  time,  and  then  be  boiled  immediately  for 
purposes  of  sterilization.     Soxhlet's  sterilizer  is  well  suited  to  this  purpose, 


INTESTINAL  CATARRH    OF   CHILDREN  589 

and  is  consequently  much  used.  As  cow's  milk  contains  a  considerably 
greater  percentage  of  proteids  and,  on  the  other  hand,  a  smaller  percent 

of  fats  and  sugar  than  mother's  milk,  it  is  never  given  pure  to  children,  hut 
in  diluted  form,  and,  if  necessary,  even  with  certain  additions.  As  a  general 
rule,  one  part  of  the  milk  must  he  diluted,  according  to  its  quality,  with  two 
or  three  parts  of  boiled  water  in  the  first  months,  in  children  from  four  to 
six  months  old  with  equal  parts  of  water,  and  in  older  children  with  about 
half  as  much  water.  At  the  age  of  about  nine  to  twelve  months,  the  child 
may  have  undiluted  milk.  In  general  we  give  the  milk  warmed  to  about 
95°  F.  (35°  C),  but  children  with  gastro-intestinal  catarrh  often  bear  cold 
milk,  given  in  small  amounts,  better  than  warm.  Since  the  percentage  of 
fats  and  milk  sugar  becomes  decidedly  too  low  by  dilution,  many  attempts 
have  been  made  to  obviate  this  difficulty  by  special  additions  and  methods  of 
preparation.  The  addition  of  milk  sugar  is  the  most  common.  Heubner 
recommends  a  mixture  of  equal  parts  of  cow's  milk  and  a  six-per-cent  solu- 
tion of  milk  sugar,  whereas  Soxhlet  attempts  also  to  replace  the  fat  deficit 
with  sugar,  and  consequently  uses  a  still  greater  addition  of  milk  sugar. 
Other  pediatrists  (Biedert,  etc.)  add  fat  in  the  shape  of  cream  to  cow's  milk. 
By  centrifuging  milk  diluted  to  half  strength  and  adding  milk  sugar,  the 
attempt  has  also  been  made  to  prepare  a  milk  richer  in  fats  and  more  closely 
resembling  mother's  milk  (Gartner's  fat  milk,  etc.) .  Finally,  preserved  cream 
and  vegetable  fats  (Lahmann's  "vegetable  milk")  have  been  recommended  as 
additions.  In  raising  children  on  cow's  milk,  also,  a  regular  division  of  the 
feedings  is  absolutely  necessary.  The  interval  between  the  feedings  must  be 
a  three-hour  one  in  the  day  and  at  night  from  six  to  eight  hours.  The 
quantity  of  milk  taken  at  each  feeding  is  slightly  larger  in  bottle-fed  than 
in  breast-fed  infants. 

If  pure  cow's  milk  cannot  be  obtained  or  is  not  well  borne,  the  artificial 
foods  (consisting  generally  of  milk  and  dextrinized  flour),  which  are  prepared 
in  great  number  by  the  modern  industrial  chemical  firms,  must  then  be 
considered.  In  spite  of  the  fact  that  all  artificial  foods  have  their  great 
drawbacks,  and  should  therefore  be  regarded  solely  as  emergency  foods,  their 
use,  under  certain  conditions,  cannot  be  entirely  obviated  in  practice.  It 
cannot  be  denied  that  in  certain  cases  good  results  are  obtained  with  arti- 
ficial foods.  Among  the  "  infant  flours  "  which  have  been  used  with  especial 
frequency,  we  may  mention  the  preparations  of  Nestle,  Kufeke,  Lofflund, 
Theinhardt,  Mellin,  etc. 

As  soon  as  disturbances  in  the  functions  of  the  stomach  and  intestines, 
as  well  as  interference  with  the  regular  increase  in  weight  and  impairment 
of  the  general  condition  of  the  child  occur,  the  treatment,  in  the  first  place, 
must  always  be  a  dietetic  one.  The  physician  should  always  first  ascertain 
if  the  feeding  of  the  child  has  been  conducted  in  a  correct  and  careful  man- 
ner, and  whether  the  simple  observance  of  the  previously  expressed  principles 
will  not  in  themselves  suffice  to  correct  the  disturbance.  Where  we  are  deal- 
ing with  artificially  fed  children,  we  must  first  see  whether  the  percentage 
composition  of  the  food  is  not  sufficient  in  itself  to  explain  the  disturbance, 
and,  if  so,  make  our  changes  accordingly.  The  "  milk-diet  disorders  " — char- 
acterized by  an  insufficient  increase  in  weight  of  the  child  despite  a  plentiful 
intake  of  milk,  by  a  bad  general  condition,  marked  anaemia,  a  distended 


590  DISEASES  OF  THE   DIGESTIVE   ORGANS 

abdomen,  and  gray,  dry,  foul-smelling  stools — require  a  diminution  in  the 
daily  quantity  of  milk,  and  the  addition  of  mucilaginous  and  farinaceous 
decoctions  (oatmeal,  rice  gruel,  etc.).  The  "malt  soups"  can  also  be  em- 
ployed here  with  benefit.  With  nutritional  disturbances  due  to  farinaceous 
foods,  the  children  appear  at  first  to  be  well  nourished.  Later,  a  marked 
atrophy  also  develops,  the  children  are  very  readily  susceptible  to  secondary 
infections,  occasionally  they  show  a  marked  hypertonicity  of  the  muscles.  A 
discontinuance  of  the  carbohydrates  and  a  change  to  milk  diet  (preferably 
mother's  milk,  of  course)  can  alone  help  here. 

If  severe  acute  digestive  disturbances  (vomiting,  diarrhea)  occur,  it  is 
best  entirely  to  discontinue  the  milk  and  every  other  food  for  twenty-four 
hours.  We  give  only  some  weak  tea  (chamomile  tea)  or  albumen  water  (the 
albumen  of  one  egg  is  beaten  to  a  froth,  mixed  with  one  third  of  a  quart  of 
boiled  water,  strained,  and  sweetened  with  a  little  sugar).  Even  after  an 
improvement  in  the  symptoms  has  set  in,  the  milk  should  be  given  diluted, 
and  every  four  to  five  hours.  If  there  is  diarrhea,  the  dilution  of  milk  with 
gruels  is  to  be  recommended  (barley  gruel,  prepared  by  boiling  a  tablespoonful 
of  barley  with  half  to  one  quart  of  water  for  one  hour,  and  then  straining, 
oatmeal  gruel,  rice  gruel,  or  decoction  of  salep,  etc.).  With  older  children, 
decoctions  of  acorn  coffee  may  also  be  tried.  In  severe  cases  of  acute  gastro- 
enteritis with  marked  retching  (especially  where  there  is  a  suspicion  of  a 
toxic  origin),  gastric  lavage  has  recently  been  repeatedly  used  with  very  good 
results  even  in  young  children.  A  Nelaton's  catheter  and  plain  water  or  a 
weak  solution  (0.01  to  0.2  per  cent)  of  hydrochloric  acid  are  used.  Medica- 
tion is  entirely  unnecessary  in  many  cases  of  acute  dyspepsia  or  acute  enter- 
itis. However,  if  the  symptoms  do  not  diminish  after  the  requisite  changes 
in  diet,  we  must  attempt  to  aid  the  treatment  by  internal  medication.  Calo- 
mel has  won  a  specially  wide  reputation.  It  is  given  in  doses  of  TV  to  £  of 
a  grain  (gm.  0.005  to  0.01)  in  powder.  If  the  diarrhea  lasts  a  long  time, 
we  may  very  well  use  opiates,  although  with  great  caution.  The  combination 
of  calomel  and  opium  often  does  good  service. 

^  Calomel  gr.    i    (gm.  0.01); 

Extracti  opii gr.    3V  (   "     0.002) ; 

Pulv.  acacise  gr.  ss.   (  "     0.03) . 

M.  et  ft.  pulv. 

Sig. :  One  such  powder,  three  or  four  times  a  day. 

With  little  children  we  may  put  2  to  4  drops  of  laudanum  in  3  ounces 
(gm.  100)  of  liquid,  such  as  gum  mixture,  salep  decoction,  muriatic-acid 
mixture,  etc.,  and  give  a  dessertspoonful  of  this  every  two  or  three  hours. 
The  tannic-acid  preparations,  tannigen  and  tannalbin  (gr.  jss.  to  v  [gm.  0.1 
to  0.3]  per  dose,  several  times  a  day),  are  also  much  used  in  infantile  diar- 
rheas, likewise  bismuth  subnitrate  and  bismuth  salicylate  (gr.  ss.  to  jss. 
[gm.  0.03  to  0.1]  per  dose).  For  colicky  pains  we  prescribe  warm  fermenta- 
tions to  the  abdomen,  embrocations  of  chloroform  oil  (massage),  injections 
of  chamomile  tea,  etc. 

Many  attempts  have  been  made  to  check  the  abnormal  processes  of  de- 
composition in  the  intestine  by  prescribing  remedies  which  possess  antiseptic 


TYPHLITIS   AND   PERITYPHLITIS  591 

and  antizymotic  properties.  Creosote  lias  been  warmly  recommended  by  many 
4  to  (i  drops  in  2  ounces  (gm.  .r)0)  of  water  with  half  an  ounce  (gin.  15)  of 
sirup,  a  teaspooni'ul  every  two  hours.  Other  drugs  used  for  the  same  purpose 
are  naphthalin,  one-half-  to  one-per-eent  solution  of  dilute  muriatic  acid  in 
water,  and  one-per-cent  solution  of  chloral  in  water.  The  results,  however, 
are  doubtful.  In  chronic  dyspeptic  conditions  of  longer  duration  and  in 
chronic  intestinal  catarrhs,  as  a  matter  of  course,  all  the  above-mentioned 
general  dietetic  regulations  also  must  first  of  all  he  tried  in  the  most  careful 
and  patient  manner.  The  medicinal  treatment,  unfortunately,  is  mainly  one 
of  experimentation.  The  drugs  used  most  frequently  have  already  been  men- 
tioned— viz.,  tannigen,  tannalbin,  bismuth  subnitrate,  etc.  It  is  to  be  noted 
that  occasionally  alkalies  (particularly  small  doses  of  Carlsbad  Miihlbrunnen) 
produce  surprisingly  good  results  even  in  young  children.  On  the  other 
hand,  we  have  little  confidence  in  efforts  to  arrest  abnormal  intestinal  decom- 
position by  the  use  of  antiseptics.  Nevertheless,  we  may  occasionally  try 
creosote  as  well  as  naphthalin  and  chloral  hydrate  (one  part  in  one  hundred), 
etc.  When  the  stools  are  of  a  greenish  color,  lactic  acid  (a  teaspoonful  of  a 
two-per-cent  solution  one  quarter  hour  after  each  feeding)  is  said  to  act 
well. 

If  a  large  amount  of  mucus  in  the  stools  points  to  a  catarrh  of  the  large 
intestine,  we  may  sometimes  employ  irrigation  of  the  colon  with  excellent 
results.  We  inject  the  fluid,  one-per-cent  solution  of  tannin  or  alum,  or  solu- 
tion of  acetate  of  lead  (1  to  3  to  1,000),  once  or  twice  a  day.  The  amount 
of  fluid  to  be  introduced  at  once,  by  a  Hegar's  funnel,  with  a  gum-elastic 
catheter,  may  reach  one  or  two  pints  (half  a  liter  to  a  liter). 

With  persisting  gastric  symptoms,  repeated  gastric  lavage  (vide  supra)  may 
be  employed.  The  various  symptomatic  details  (treatment  of  constipation, 
possible  collapse,  complications,  etc.)  need  not  be  more  fully  considered  in 
this  place. 


CHAPTEE    IV 

TYPHLITIS    AND    PERITYPHLITIS 

(Inflammation  of  the  Appendix.     Appendicitis) 

etiology  and  Pathological  Anatomy. — Inflammation  of  the  caecum  and  its 
vicinity  has  a  special  place  among  the  diseases  of  single  portions  of  the 
intestines.  The  reason  why  circumscribed  inflammation  so  often  develops 
here  is  to  be  found  in  the  peculiar  anatomical  arrangement  of  the  caecum  and 
its  appendix,  the  vermiform  process.  It  is  evident  that  the  conformation  of 
the  parts  makes  it  particularly  easy  for  inflammatory  germs  to  settle  in  this 
narrow  canal. 

Formerly  it  was  believed  that  the  inflammation  might  often  be  limited 
to  the  caecum  itself.  It  was  asserted  that  impacted  fecal  matter  occasioned 
mechanical  irritation  of  the  intestinal  wall,  and  thus  facilitated  the  attack 
of  chemical  and  infectious  agents.  In  this  way  arose  the  doctrine  of  "  typh- 
litis stercoralis,"  but  such  simple  typhlitis  has  been  demonstrated  post- 
mortem only  in  isolated  cases,  and  although  it  cannot  be  absolutely  denied, 


592  DISEASES   OF  THE   DIGESTIVE  ORGANS 

therefore,  that  under  certain  circumstances  there  may  occur  a  genuine  typh- 
litis, as  a  result  of  the  accumulation  of  feces,  yet  its  frequency  has  certainly 
been  formerly  much  overestimated  (Sahli).  It  is  years  since  the  author  has 
made  a  diagnosis  of  "  typhlitis  stercoralis." 

By  far  the  greatest  number  of  cases  of  acute  inflammation  in  the  ileo- 
caecal  region  are  perityphlitis;  that  is,  inflammation  of  the  peritoneum  and" 
the  connective  tissue  surrounding  the  caecum.  From  the  point  of  view  of 
pathological  anatomy,  we  might  term  the  inflammation  of  the  retrocecal  tis- 
sue paratyphlitis,  inasmuch  as  it  is  extraperitoneal,  in  distinction  from  the 
true  intraperitoneal  perityphlitis;  but  clinically  we  cannot  maintain  this 
distinction,  or,  at  most,  imperfectly.  The  starting  point  for  perityphlitis  is 
the  vermiform  appendix.  To  this  there  are  rare  exceptions  in  which  the 
inflammation  arises  from  perforation  of  the  caecum  itself.  The  appendix, 
although  of  so  little  physiological  importance  and  a  merely  rudimentary  por- 
tion of  the  intestine,  plays  an  important  part  in  pathology. 

The  appendix  has  not  been  improperly  compared  with  the  crypts  of  the 
tonsil,  in  which  likewise  inflammatory  agents  readily  find  a  nidus.  The 
analogy  is  all  the  more  appropriate,  since  the  mucous  membrane  of  the  appen- 
dix is  also  particularly  rich  in  lymphoid  tissue  (lymph  follicles).  The  length 
of  the  appendix,  its  mode  of  insertion  into  the  caecum,  and  its  position,  are 
subject  to  many  variations,  which  may  also  in  part  affect  its  susceptibility 
to  disease.  The  appendicular  artery,  a  branch  of  the  caecal  artery,  has  no 
anastomosis  with  any  other  artery,  is  a  so-called  terminal  artery,  which  is 
also  a  material  fact  in  the  causation  of  inflammation. 

According  to  Sonnenburg  and  others,  we  distinguish  a  simple  appendicitis 
and  a  gangrenous  or  perforative  appendicitis.  In  simple  appendicitis  the  in- 
flammation is  confined  to  the  appendix  itself.  The  mucous  membrane  is 
swollen  and  is  beset  with  hemorrhages,  the  follicles  are  enlarged  ("  appendi- 
citis granulosa"),  the  entire  wall  is  infiltrated  and  rigid,  and  the  serous 
coat  is  also  generally  markedly  injected.  In  perforative  appendicitis  there  is 
acute  necrosis  or  gangrene  of  more  or  less  extent,  commonly  at  the  tip  of 
the  appendix.  In  this  way  the  inflammatory  process  extends  to  the  surround- 
ing tissues,  and  a  perityphlitis  develops  from  the  appendicitis.  The  primary 
causes  of  the  acute  inflammation  are  still  but  little  known  to  us.  Occasion- 
ally there  appears  to  be  a  special  infectious  factor.  Thus,  for  example,  ap- 
pendicitis may  apparently  occur  as  a  sequel  to  a  preceding  sore  throat.  At 
times  a  certain  epidemic  spread  of  the  disease  can  also  not  be  denied.  In 
some  cases  slight  traumata  appear  to  be  the  exciting  cause  of  the  acute  in- 
flammation. Very  frequently  the  acute  attacks  are  merely  exacerbations  of 
a  chronic  inflammatory  process,  just  as  acute  cholecystitis  and  biliary  colic 
almost  always  originate  on  the  basis  of  a  chronic  gallstone  affection.  This 
comparison  is  all  the  more  apt,  since  the  formation  of  concretions  appears 
to  play  a  role  also  in  disease  of  the  appendix.  Even  though  present  opinion 
is  inclined  not  to  ascribe  as  great  significance  to  "  fecal  calculi "  as  was  for- 
merly done,  it  would,  nevertheless,  in  our  opinion,  be  incorrect  to  entirely 
deny  their  importance.  Small  fecal  masses  from  the  caecum  often  enter  the 
vermiform  appendix,  and,  under  some  circumstances,  they  may  remain  there, 
more  especially,  perhaps,  when  the  fold  of  mucous  membrane  (Gerlach's 
valve)  at  the  orifice  of  the  appendix  prevents  the  return  of  the  fecal  masses 


TYPHLITIS   AND   PERITYPHLITIS  593 

into  the  caecum.  The  fluid  in  them  is  absorbed,  they  are  very  often  Lncrusted 
with  lime  salts,  and  thus  so-called  "fecal  calculi  "  are  formed. 

Foreign  bodies,  such  as  small  fruit  pits  or  seeds,  etc.,  cuter  the  vermi- 
form appendix  and  perhaps  give  rise  occasionally  to  the  formation  of  a  fecal 
calculus;  but  one  must  be  cautious  in  assuming  that  any  small,  hard  mass  is  a 
foreign  body,  for  these  calculi  often  have  such  a  rounded  shape  that  they 
were  formerly  considered,  very  erroneously,  to  be  retained  cherry  stones,  etc. 

In  many  cases  fecal  calculi  may  remain  in  the  vermiform  appendix  for 
a  long  time  without  producing  any  injurious  results,  but,  as  a  rule,  they  cause  a 
mechanical  irritation  of  the  mucous  membrane  which  leads  to  inflammation, 
and  often,  in  some  circumscribed  spots,  to  a  pressure  necrosis,  and  later  to 
ulceration  of  the  vermiform  appendix. 

If  the  ulcer  of  the  mucous  membrane  cicatrizes,  stricture  formation,  and 
occasionally  hydrops  (with  suppurative  inflammation,  empyema),  of  the  ap- 
pendix occurs.  As  a  rule,  however,  the  inflammation  extends  to  the  adjacent 
tissues  of  the  appendix.  This  extension  of  the  inflammation  is  due  in  part 
to  a  migration  of  the  bacteria  and  their  toxins  through  the  walls,  or,  more 
commonly  (and  this  is  the  more  important  fact),  to  a  perforation  of  the 
appendix.  The  mechanical  pressure  necrosis  (anasmic  decubitus  and  ulcer) 
is  followed  immediately  by  the  entrance  of  the  bacteria  of  inflammation  and 
an  extension  of  the  inflammatory  necrosis  and  inflammation.  The  patho- 
genic bacteria  are  not  always  the  same.  Virulent  strains  of  the  B.  coli  prob- 
ably play  the  principal  role,  but  occasionally  pneumococci  and  other  pyogenic 
organisms  are  found  in  perityphlitic  abscesses. 

All  these  processes  may  be  very  acute,  or  they  may  also  take  a  fairly 
chronic  course.  Under  certain  conditions,  the  chronic  process  may  light  up 
into  an  acute  exacerbation;  this  may  frequently  be  repeated  in  the  course  of 
time.  According  to  the  acuteness  and  virulence  of  the  process,  we  may  merely 
find  adhesions  and  agglutinations  in  the  vicinity  of  the  inflammatory  focus, 
circumscribed  serofibrinous  exudates,  a  circumscribed  abscess,  or,  in  the  most 
severe  cases,  a  general  diffuse  peritonitis.  In  by  far  the  greater  number  of 
cases  agglutination  and  adhesions  in  the  neighborhood  of  the  appendix  occur 
in  time,  so  that  the  inflammation  remains  circumscribed.  We  designate  this 
as  a  perityphlitis.  In  some  of  the  milder  cases  there  is  only  an  infiltration 
of  the  tissues  with  pus  cells,  an  inflammatory  serous  imbibition,  perhaps  also 
with  a  circumscribed  fibrinous  exudate.  In  the  interior  of  the  inflammatory 
tumor,  which  consists  essentially  of  the  thickened  intestinal  walls  and  the 
coils  of  intestine  glued  together,  and  perhaps  sometimes  also  of  impacted 
fecal  matter,  there  is  indeed  often  an  actual  abscess,  small  and  localized,  and 
lying  usually  in  the  immediate  neighborhood  of  the  appendix. 

In  all  of  the  severer  cases,  however,  large  abscesses  are  formed.  The 
various  other  possible  pathological  changes  in  perityphlitis  will  be  best  con- 
sidered in  connection  with  the  clinical  symptoms. 

Perityphlitis  is  chiefly  a  disease  of  early  life.  Many  cases  occur  in  child- 
hood (between  five  and  twelve  years),  and  again,  more  particularly  between 
the  ages  of  eighteen  and  thirty.  Later  on  the  disease  becomes  rarer.  In  our 
experience,  the  disease  is  also  decidedly  more  common  in  the  male  than  in 
the  female  sex.  There  appears  to  be  a  certain  hereditary  tendency  to  the 
disease  in  some  families. 


594  DISEASES  OF  THE   DIGESTIVE  ORGANS 

Symptoms  and  Clinical  Course. — The  symptoms  of  perityphlitis  have  usu- 
ally a  rather  acute  development.  The  patient  has  felt  perfectly  well,  and, 
as  a  rule,  has  not  even  suffered  from  constipation,  when  he  has  a  rather  sud- 
den pain  in  the  ileocsecal  region.  There  may  be  no  reason  for  this,  or 
there  may  be  some  such  cause  as  stooping,  lifting,  or  a  long  walk;  in  rarer 
cases,  also  trauma.  Not  infrequently  there  is  slight  vomiting,  and  the  pa- 
tient feels  languid  and  feverish.  The  bowels  may  be  constipated,  but  some- 
times they  continue  regular.  Many  patients  are  obliged  to  go  to  bed  at  once, 
but  others  keep  about  for  some  days  till  they  are  forced  to  give  up  because  of 
the  aggravation  of  their  symptoms,  particularly  the  pain.  It  is  a  point 
of  some  practical  importance  that  the  pain  is  by  no  means  invariably  referred 
to  the  region  of  the  csecum  at  first,  particularly  as  the  position  of  the  appen- 
dix is  very  variable.  Not  infrequently  the  pain  is  localized  more  in  the 
middle  of  the  abdomen  or  toward  the  left,  or  upward.  It  is  not  until  subse- 
quent days  of  the  attack  that  the  pain  gradually  settles  in  the  true  ileocsecal 
region. 

The  pains  often  radiate  to  the  back,  the  region  of  the  bladder,  or  the 
thighs.  With  severe  pains  respiration  becomes  superficial  and  costal  in  type, 
since  deep  diaphragmatic  respiration  increases  the  pains. 

Upon  objective  examination  we  usually  find  distinct  local  changes  in  the 
ileocecal  region,  even  in  the  first  days  of  the  disease.  Our  manipulations 
should  be  extremely  cautious.  It  may  be  possible  by  careful  inspection  alone 
to  recognize  a  limited  swelling.  On  palpation  we  are  at  once  struck  by  the 
increased  muscular  rigidity  of  the  abdomen  on  the  affected  side  (also  recog- 
nizable by  a  diminution  of  the  abdominal  reflex).  In  that  case  it  is  very 
important  to  determine  whether  tenderness  is  present.  This  may  be  very 
considerable  or  comparatively  slight.  The  typical  painful  spot  (McBurney's 
point)  is  said  to  be  1.5  to  2.5  inches  (4  to  6  cm.)  inward  from  the  anterior 
superior  spinous  process,  on  the  line  joining  this  process  with  the  navel. 
This  localization  does  not  possess  great  importance,  because  the  painful  spot 
varies  in  different  cases.  Sometimes  the  greatest  pain  is  felt  posteriorly  more 
in  the  lumbar  region,  suggesting  a  retrocecal  paratyphlitic  abscess  (vide 
supra).  Lastly,  there  is  decisive  importance  in  the  discovery  of  abnormal 
resistance,  or  of  a  more  or  less  sharply  denned  tumor  due  to  the  inflammatory 
exudation  (vide  supra).  This  tumor  can  usually  be  made  out.  For  this 
purpose  we  recommend  particularly  the  employment  of  the  palm  of  the  hand 
in  gentle  pushing  movements,  beginning  on  the  left  side  and  gradually  pro- 
ceeding toward  the  ileocsecal  region.  This  is  the  best  way  of  determining  the 
size  of  the  inflammatory  mass.  In  milder  cases  it  is  also  permissible  to  make 
deeper  palpation,  if  we  are  cautious.  The  examination  per  anum  is  very 
important,  especially  in  all  suspicious  cases  in  which  the  results  of  ab- 
dominal palpation  are  uncertain.  We  have  repeatedly  seen  a  number  of  cases 
in  which  no  exudation  could  be  demonstrated  by  external  palpation,  while 
a  large  inflammatory  tumor  could  be  distinctly  felt  through  the  rectum. 
The  results  of  palpation  are  confirmed  by  percussion,  which  gives  either  a 
muffled  tympanitic  resonance  or  marked  dullness  over  the  seat  of  the  dis- 
ease. In  general,  however,  the  results  of  percussion  should  not  be  inter- 
preted too  strictly,  for  they  are  ambiguous,  because  of  the  variations  in  the. 
degree  of  intestinal  distention. 


TYPHLITIS   AND   PERITYPHLITIS  595 

In  addition  to  the  local  symptoms  just  described,  careful  attention  should 
be  paid  to  the  general  symptoms.  Of  great  importance  are  the  aspect  and 
general  condition  of  the  patient.  If  the  patient  lias  no  suggestion  of  the 
"abdominal  f  acies  "  (vide  infra,  chapter  on  Peritonitis),  it  is  very  probable 
that  the  inflammation  remains  circumscribed.  It  is  also  important  to  study 
the  chart  of  the  temperature  and  pulse. 

Some  cases  begin  with  a  sudden  fairly  high  elevation  of  temperature  (up 
to  104°  F.  [40°  C.]),  ushered  in  by  a  chill;  or  the  onset  of  the  lever  is  slower, 
but  the  temperature  remains  moderately  elevated  (about  101°  to  103°  F. 
[38.5°  to  39.5°  C.])  for  the  next  four  or  five  days,  and  then  subsides  on  the 
following  days  if  the  patient  remains  quiet.  Defervescence  occurs  more  or 
less  rapidly  by  lysis,  but  frequently  also  in  an  almost  critical  manner.  Not 
infrequently,  after  the  first  three  or  four  days  of  the  disease,  a  remarkable  re- 
mission in  all  the  symptoms  occurs,  and  in  the  more  favorable  cases  con- 
valescence may  then  ensue.  Very  often,  however,  there  is  a  recrudescence 
of  the  fever,  and  then  great  caution  is  urgently  demanded.  Por  renewed 
elevation  of  temperature  after  the  fourth  or  fifth  day  of  the  disease  always 
indicates  an  aggravation  of  the  local  process,  particularly  the  onset  of  marked 
suppuration.  The  pulse  ought  to  be  watched  as  carefully  as  the  temperature. 
The  pulse  rate  is  approximately  from  80  to  100  at  the  onset.  A  lowered 
pulse  rate  is  generally  a  favorable,  and  an  increased  an  unfavorable,  sign. 
A  rapid,  soft  at  times,  slightly  irregular  pulse  frequently  indicates  a  begin- 
ning septic  infection.  Severe  cases  of  septic  peritonitis  sometimes  run  their 
course  with  scarcely  any  temperature,  but  with  a  small,  rapid  pulse.  [In  such 
cases,  the  rectal  temperature  is  often  much  higher  than  the  oral.] 

The  bowels  are  almost  always  constipated  from  the  start.  Vomiting  occurs 
frequently  at  the  onset,  but  is  absent  entirely  or  nearly  so  in  the  lighter  cases 
during  the  further  course  of  the  disease.  Frequent  eructations  and  a  return 
of  vomiting  later  on  in  the  attack  are  unfavorable  symptoms,  since  they  gen- 
erally indicate  a  marked  involvement  of  the  peritoneum. 

In  many  cases  there  is  temporary  difficulty  in  micturition,  so  that  a  catheter 
must  be  employed.  Frequency  of  urination  occurs  in  those  cases  in  which 
the  abscess  points  toward  the  bladder.  There  is  usually  a  distinct  increase 
in  the  amount  of  indican  in  the  urine. 

A  question  of  the  greatest  clinical  importance  is  whether  the  perityphlitis 
will  lead  to  the  formation  of  a  large  abscess  or  not.  We  have  already  said 
that  in  a  pathological  sense  almost  all  cases  of  perityphlitis  are  suppurative, 
but  the  formation  of  a  large  collection  of  pus  is  of  practical  importance. 

The  temperature  conditions  are  most  significant  in  determining  the  ques- 
tion of  abscess  formation.  If  the  fever  lasts  more  than  a  week  or  a  week  and 
a  half,  suppuration  is  highly  probable.  If  there  is  a  temperature  of  104°  to 
105°  F.  (40°  to  40.5°  C.)  we  may  suspect  suppuration,  even  at  an  early  period, 
particularly  if  the  rate  of  the  pulse  corresponds  to  the  height  of  the  fever. 
Eigors  are  not  frequent  at  all,  but,  if  they  do  occur,  they  indicate  abscess 
formation.  The  local  signs,  on  the  other  hand,  are  not  very  valuable  in  the 
diagnosis  of  an  abscess.  Early  in  the  attack  it  is  scarcely  ever  possible  to 
detect  fluctuation,  for  the  abscess  is  deeply  situated  and  surrounded  by  in- 
filtrated tissue. 

A  definite  conclusion  can  be  reached  in  many  cases  by  exploratory  puncture, 


596  DISEASES  OF  THE  DIGESTIVE  ORGANS 

but  the  latter  is  generally  only  rarely  nsed.  On  the  other  hand,  it  is  very 
important  to  determine  the  number  of  leucocytes  in  the  blood  (Curschmann). 
With  increasing  leucocytosis  (16,000  to  20,000  leucocytes  or  more  to  the 
cubic  centimeter)  suppuration  is  most  probable.  However,  this  sign  can,  of 
course,  only  be  utilized  in  conjunction  with  all  the  other  symptoms. 

The  further  course  of  perityphlitis  is  favorable  in  the  overwhelming  ma- 
jority of  cases.  After  a  few  days,  or  a  week  or  so,  if  the  treatment  is  appro- 
priate, the  symptoms  abate.  The  fever  disappears,  as  already  mentioned, 
either  gradually  or,  not  infrequently,  quite  rapidly,  almost  like  a  crisis.  The 
inflammatory  tumor  shrinks,  the  pain  abates,  the  bowels  become  regular,  and 
the  patient  gradually  regains  complete  health.  On  the  other  hand,  often 
there  are  manifold  variations  in  the  disease,  by  which  its  duration  may  be 
prolonged  to  two  and  three  weeks  and  over.  But,  even  then,  complete  restitu- 
tion occurs  frequently  enough  without  further  intervention. 

With  regard  to  the  pathological  changes  in  all  these  cases  that  recover,  of 
course  we  have  no  accurate  knowledge.  Sometimes  it  is  probable  that  there 
never  is  a  well-marked  abscess  formation,  but  only  an  inflammatory  infiltra- 
tion of  the  tissue,  which  subsides  again.  It  is  probable  that,  in  many  cases, 
there  is  a  small  abscess  which  discharges  spontaneously  into  the  intestine, 
usually  into  the  caecum,  but  exceptionally  into  other  portions  of  the  intestine. 
One  thing  which  seems  to  us  to  suggest  such  a  spontaneous  discharge  of  an 
abscess  is  the  not  infrequent  occurrence  of  a  crisis,  with  rapid  fall  of  tem- 
perature and  simultaneous  cessation  of  all  the  other  symptoms.  Still,  we 
scarcely  ever  detect  pus  in  the  stools,  for  the  pus  corpuscles  are  changed  dur- 
ing their  passage  from  the  colon  to  the  rectum.  Perhaps  in  some  cases  small 
localized  abscesses  are  also  reabsorbed. 

On  the  other  hand,  an  unfavorable  termination  is  certainly  not  infrequent, 
and  this  fact  explains  the  widely  spread  popular  opinion  that  appendicitis 
is  a  dangerous  and  treacherous  disease.  The  most  dangerous  cases  are  those 
in  which  a  diffuse  septic  peritonitis  develops  at  the  onset  in  consequence  of 
an  extensive  gangrenous  perforation  of  the  appendix  before  any  adhesions 
have  formed.  These  are  the  cases  which  impress  one  as  being  very  serious 
from  the  start,  and  which  end  fatally  in  a  few  days.  The  primary  focus  of 
the  peritonitis  may  readily  be  entirely  overlooked.  Occasionally  the  disease 
may  commence  as  an  apparently  harmless  simple  appendicitis,  and  on  the 
second  or  third  day  the  mild  clinical  picture  may  suddenly  change  to  the 
grave  one  of  general  peritonitis  with  an  almost  always  rapidly  fatal  termina- 
tion. In  a  third  class  of  cases,  the  disease  is  at  first  of  moderate  severity, 
but  after  a  few  days  shows  a  marked  improvement,  so  that  one  is  led  to  ex- 
pect a  spontaneous  recovery.  Then,  suddenly,  a  turn  for  the  worse  ensues, 
either  rapidly  or  more  slowly  (renewed  elevation  of  temperature,  vomiting, 
peritoneal  irritation,  etc.),  and,  unless  there  is  prompt  surgical  intervention, 
the  danger  of  generalized  peritonitis  from  a  rupture  of  the  abscess  into  the 
peritoneal  cavity  is  very  great.  In  other  cases,  nowadays  very  rare,  the 
abscess  is  left  to  itself  and  burrows  a  way  for  itself.  Either  it  finally  breaks 
through  the  abdominal  wall,  or  it  may  extend  downward  into  the  iliac  fossa 
or  the  groin  [or  upward  toward  the  liver],  or  perforate  into  the  rectum, 
bladder,  or  other  parts.  It  has  also  happened  that  the  suppuration  has  in- 
volved the  ileocecal  vein,  with  consequent  pylephlebitis  and  the  formation  of 


TYPHLITIS   AND   PERITYPHLITIS  597 

abscesses  in  the  liver.  In  most  of  these  chronic  cases  the  symptoms  are  those 
of  a  tedious  septicopyaemia  such  as  is  nowadays,  thanks  to  the  progress  of 
surgery,  very  rarely  seen.  As  the  inflammation  originate-  from  perforation 
of  the  intestine,  the  pus  is  apt  to  be  extremely  offensive  whenever  there  is  any 
extensive  abscess  formation. 

Finally,  we  must  add  that,  in  isolated  cases  of  acute  appendicitis,  symp- 
toms of  intestinal  obstruction  (vide  infra)  may  develop,  such  as  tympanitic 
frequent  eructations,  or  even  fecal  vomiting.  Complications  in  other  organs 
are  exceptional. 

Diagnosis. — In  general,  there  is  no  difficulty  in  the  diagnosis  of  perityph- 
litis. Nevertheless,  the  differential  diagnosis  between  appendicitis  and  an 
acute  gallstone  or  renal  colic  will  occasionally  have  to  be  considered.  In 
women  the  differential  diagnosis  between  appendicitis  and  acute  inflamma- 
tions in  the  neighborhood  of  the  uterus  (parametritis,  etc.)  is  not  always 
simple.  Finally,  we  ourselves  for  several  days  had  regarded  an  attack  of 
appendicitis  without  marked  local  symptoms  in  a  child  as  a  case  of  typhoid, 
until  the  diagnosis  became  clear  from  the  local  conditions. 

The  principal  difficulties  in  the  diagnosis  consist  in  estimating  the  par- 
ticular anatomical  conditions,  the  formation  of  an  abscess,  its  position,  etc. 
A  thorough  examination  in  every  way  (per  anum  also)  is  indispensable.  In 
so  far  as  this  relates  to  the  extremely  important  question  of  surgical  inter- 
ference, we  shall  revert  to  the  matter  when  considering  treatment.  In  those 
rare  cases  of  perityphlitis  which  have  a  chronic  course,  the  disease  may  be 
confounded  with  new  growths,  particularly  carcinoma  originating  in  the  csecum 
or  the  appendix.  Mistakes  in  diagnosis  have  also  been  occasioned  by  tumors 
of  the  right  kidney  and  the  right  ovary,  and  by  psoas  abscess  due  to  Pott's 
disease. 

Tuberculosis,  and  in  rare  cases,  actinomycosis,  may  also  produce  clinical 
pictures  similar  to  those  of  appendicitis.  In  this  connection  it  may  be  men- 
tioned that  in  rare  cases  the  lumen  of  the  appendix  may  become  occluded, 
giving  rise  to  so-called  dropsy  of  the  vermiform  appendix.  This  may  occasion 
a  tumor  which  can  be  felt  in  the  ileocecal  region. 

Prognosis. — In  every  case  of  perityphlitis  the  prognosis  should  be  guarded, 
since  the  course  of  the  disease  cannot  be  foreseen.  Nevertheless,  in  by  far  the 
greater  number  of  cases,  the  termination  of  the  acute  perityphlitic  attack  is 
a  favorable  one,  and  the  lighter  cases,  with  circumscribed  inflammation,  are 
the  rule.  If  we  take  all  the  cases  of  acute  inflammation  of  the  ileocsecal  region, 
we  shall  find  that  some  eighty  or  ninety  per  cent  get  well  without  operation,  but 
still,  it  should  be  emphatically  stated  that  perityphlitis  is  a  dangerous  disease, 
and  every  year  it  brings  no  small  number  of  individuals,  both  children  and 
adults,  to  sudden  death.  The  main  danger  lies  in  the  rapid  onset  of  general 
peritonitis.  Even  after  the  patient  has  survived  the  attack  of  acute  perityph- 
litis he  may  be  troubled  in  various  ways.  For  instance,  the  resultant  adhesions 
and  other  chronic  inflammatory  changes  may  impede  the  action  of  the  bowels 
for  a  long  while,  may  cause  localized  pains,  etc.  In  such  cases  one  must  always 
be  prepared  for  a  renewed  onset  of  severe,  acute  symptoms,  which  may  occur 
quite  suddenly.  Chronic  appendicitis  is  like  a  quiescent-  volcano,  from  which, 
at  any  time  with  no  assignable  or  some  comparatively  insignificant  cause,  such 
as  constipation,  slight  trauma,  or  perhaps  a  second  infection,  a  fresh  outbreak 


598  DISEASES   OF   THE   DIGESTIVE   ORGANS 

may  be  expected.  Sometimes,  as  has  already  been  mentioned,  these  chronic 
changes  make  themselves  felt  through  constant  mild  subjective  symptoms  in  the 
ileocecal  region.  In  other  cases,  the  subjective  symptoms  cease  entirely,  and, 
notwithstanding,  after  a  shorter  or  longer  interval,  there  is  another  acute  at- 
tack. In  this  way  some  people  suffer  four  or  five  times,  and  even  oftener,  from 
acute  perityphlitis. 

Treatment. — As  soon  as  the  diagnosis  of  appendicitis  or  perityphlitis  has 
been  made  or  is  even  considered,  the  main  indications  are  immediate  complete 
rest  in  bed  and  the  strictest  diet  (a  little  cold  milk  or  soup,  interdiction  of  all 
solid  food).  A  not  too  heavy  ice  bag  is  placed  over  the  ileocsecal  region.  If 
this  is  not  well  borne,  a  Priessnitz  or  a  twenty-per-cent  alcohol  compress  is 
prescribed.  As  a  rule,  a  laxative  is  not  necessary.  Eecently,  however,  there 
is  an  increasing  tendency  again  to  permit  the  careful  use  of  castor  oil  (for- 
merly so  much  in  vogue),  when  constipation  is  present  at  the  onset,  provided 
there  are  no  symptoms  of  peritoneal  irritation.  At  present,  opium  is  prescribed 
in  most  cases  from  the  onset.  If  there  are  marked  pains  in  the  ileocsecal  region, 
the  action  of  the  opium  (tr.  opii  simplex,  5  to  10  drops,  and  more  according 
to  the  age  of  the  patient)  is  generally  very  favorable.  A  countercurrent  against 
prescribing  opium  has  arisen  only  from  the  fact  that  opium  relieves  the  pain, 
and  in  this  way  conceals  the  danger  of  the  onset  of  peritonitis,  so  that  the  proper 
moment  for  surgical  intervention  can  easily  be  overlooked.  In  our  opinion,  this 
is  not  a  sufficient  reason  to  exclude  opium  entirely  in  the  treatment  of  peri- 
typhlitis. But,  on  the  other  hand,  opium  should  not  be  needlessly  administered 
(i.  e.,  without  marked  pains)  in  too  large  doses. 

With  these  remedies — viz.,  rest,  diet,  ice,  and  opium — everything  has  been 
done  to  favor  spontaneous  cure  in  favorable  cases.  As  has  been  already  said, 
many  cases  recover  under  this  treatment.  There  is  no  necessity  at  first  to  be 
anxious  about  opening  the  bowels.  Usually  there  is  no  harm  if  the  patient 
goes  without  a  movement  for  five  to  eight  days,  providing  that  his  condition  is 
satisfactory  as  regards  his  general  health,  pulse,  and  temperature.  It  is  indeed 
not  unusual  to  have  a  natural  operation  of  the  bowels  while  rather  large  doses 
of  opium  are  being  administered,  but  if  the  abdomen  becomes  more  and  more 
distended  and  there  is  rather  long-continued  constipation,  we  need  not  hesi- 
tate to  make  a  cautious  use  of  glycerin  suppositories  or  injections.  For  injec- 
tion we  usually  choose  oil  or  soapsuds,  and  let  it  run  through  an  ordinary  foun- 
tain syringe  into  the  colon,  while  the  patient  is  lying  on  his  back.  If  necessary, 
the  injections  must  be  repeated,  and  of  the  beneficial  effects  of  these  oil  or  soap 
injections  we  have  often  been  convinced. 

We  have  already  insisted  that  every  patient  with  perityphlitis  should  be 
most  carefully  watched,  however  favorable  the  course  of  the  disease  seems  to 
be.  The  physician  must  ask  himself  every  minute  whether  further  symptomatic 
treatment  is  permissible,  or  whether  it  may  not  be  necessary  to  have  the  abscess 
opened  by  surgical  interference. 

Since  the  course  of  the  disease  cannot  be  told  beforehand,  and  since  the' 
dangers  of  the  operation  are  naturally  smaller  in  proportion  to  the  promptness 
of  its  performance,  many  eminent  surgeons  are  of  the  opinion  that  in  every  case 
of  perityphlitis  the  corpus  delicti  (the  inflamed  appendix)  should  be  removed 
if  possible  on  the  first  day,  or,  at  the  latest,  on  the  second  day  of  the  disease, 
before  it  can  do  any  further  damage.    The  results  of  these  early  operations  are- 


TYPHLITIS   AND   PERITYPHLITIS  599 

very  good  (casualties,  it  is  true,  do  occur  in  isolated  cases).  Most  of  the  cases 
would  certainly  also  have  recovered  without  operation.  But  in  -ohm-  cases  the 
termination  would  have  been  unfavorable  without  operation,  and  most  of  those 
operated  early  are  now  safe  from  later  recurrences,  which  is  a  great  advantage. 
Nevertheless,  the  obligatory  early  operation  will  always  remain  more  a  theoret- 
ical demand  than  a  procedure  which  can  be  practically  executed.  At  any  rate, 
numerous  cases  seek  medical  aid  only  on  the  third  day  or  even  later,  and  then 
the  question  whether  we  should  operate  at  all  and  when,  is  frequently  difficult 
to  decide.  The  general  answer  to  this  question  can  only  be  that  immediate 
operation  is  always  indicated  as  soon  as  the  presence  of  a  perityphlitic  abscess 
has  been  assumed,  the  absorption  or  spontaneous  rupture  of  which  into  the 
intestines  should  not  be  waited  for,  because  of  the  possibility  of  a  rupture  into 
the  free  peritoneal  cavity  with  subsequent  diffuse  suppurative  peritonitis,  or 
of  a  general  septic  intoxication,  or  a  protracted  chronic  suppuration.  When 
this  danger  point  is  reached  is  often  impossible  to  say  with  certainty;  never- 
theless, there  are  a  large  number  of  important  indications.  In  general,  we  rely 
personally  on  the  following  rules :  If  the  temperature  last  longer  than  five  or 
six  days  without  remission,  or,  particularly,  if  after  a  febrile  attack  during  the 
first  few  days,  a  renewed  elevation  of  temperature  occur,  then  there  is  strong 
suspicion  of  an  abscess  formation.  If  the  pulse  rate  (despite  the  low  temper- 
ature!) rises,  and  it  increases  to  100  to  120  while  the  tension  decreases,  this 
also  is  no  favorable  sign.  Continued  eructations  and  recurrent  vomiting  are 
likewise  unfavorable.  Accurate  observation  of  the  local  condition  (tumor, 
increasing  tenderness)  is  very  important,  but  attention  to  the  general  condi- 
tion (pallor  and  bad  look,  dry  tongue,  beginning  facies  abdominal  is)  is  of 
equal  importance.  Finally,  the  leucocytosis  should  be  considered  (vide  supra). 
An  uninterrupted  increase  of  the  leucocytes  to  18,000  to  20,000  to  the  cubic 
millimeter  and  over,  always  increases  the  suspicion  of  an  existing  suppura- 
tion. On  the  other  hand,  a  low  leucocyte  count  should  not  keep  us  from  oper- 
ating, if  the  condition  is  otherwise  unfavorable. 

It  is  impossible  to  give  more  detailed  rules,  of  general  application,  with 
regard  to  the  question  of  operating.  The  individual  circumstances  of  each  par- 
ticular case  and  the  personal  experience  of  the  physician  must  always  be  con- 
trolling factors.  No  physician  can  avoid  unfortunate  occurrences  in  perityph- 
litis, and  the  most  experienced  practitioner  will  never  escape  a  certain  feeling 
of  uneasiness  in  any  case  of  the  disease. 

In  general,  during  the  first  few  days  of  the  disease  (excepting  cases  of  pos- 
sible early  operation),  if  the  general  condition  of  the  patient  is  good,  ex- 
pectant treatment  is  certainly  to  be  recommended ;  and  even  in  the  ranks  of  the 
surgeons  the  eagerness  for  operation  has  grown  less  in  this  disease,  just  as  it  has 
in  many  others.  On  the  other  hand,  operation  must  not  be  delayed  in  those 
cases  in  which  severe  local  symptoms  or  general  septic  intoxication  occurs 
within  the  first  few  days ;  and  in  every  case,  as  Sahli  so  aptly  puts  it,  expectant 
treatment  should  always  be  an  "  armed  truce."  For  this  principle  is  certainly 
true :  better  to  operate  too  early  than  too  late. 

If  the  attack  has  passed,  the  question  of  an  interval  operation  ("a  froid") 
arises.  Since  in  many  cases  adhesions  of  the  appendix  persist,  or  a  fecal  con- 
cretion, or  even  a  small  inspissated  pus  focus,  remain  in  the  appendix,  a  constant 
danger  of  recurrence  (vide  supra)  is  thereby  occasioned.    This  danger  is  obvi- 


600  DISEASES  OF  THE   DIGESTIVE   ORGANS 

atecl  once  and  for  all  by  the  removal  of  the  appendix.  The  operation  is  to  be 
particularly  recommended,  if  several,  even  light,  attacks  of  appendicitis  or 
perityphlitis  have  occurred,  or  if  any  remaining  slight  discomforts  (pains,  ten- 
derness on  pressure,  palpable  appendix,  irregular  bowels,  etc.)  indicate  per- 
sisting morbid  changes  in  the  appendix.  There  can  hardly  be  any  doubt  that 
many  accidents  can  be  avoided  by  an  interval  operation  in  which,  as  a  rule, 
there  is  almost  no  danger. 

Moreover,  for  the  after-treatment  of  perityphlitis,  mild  Carlsbad  cures, 
mud  packs,  careful  massage,  etc.,  are  still  occasionally  employed. 


CHAPTER    V 
PERFORATING   ULCER    OF    THE    DUODENUM 

There  is  a  form  of  ulcer  of  the  duodenum,  especially  of  its  upper,  horizon- 
tal portion,  which  is  precisely  analogous  to  the  round  gastric  ulcer  in  regard  to 
aetiology,  pathological  anatomy,  and,  very  largely,  symptomatology.  The  ulcer 
is  probably  also  due  in  most  cases  to  the  action  of  the  acid  gastric  juice  on  the 
duodenal  mucous  membrane  under  conditions  which  have  been  detailed  more 
fully  in  the  aetiology  of  gastric  ulcer.  We  must  mention  here  the  noteworthy 
fact  that,  after  extensive  burns  of  the  external  skin,  ulceration  of  the  duodenum, 
rarely  of  the  stomach  also,  has  been  repeatedly  observed.  This  is  probably  due 
to  the  thrombosis  of  a  duodenal  vessel,  occasioned  by  the  setting  free  of  fibrin 
ferment. 

Ulcer  of  the  duodenum  is  much  rarer  than  the  round  gastric  ulcer,  and,  in 
distinction  from  the  latter,  it  has  been  found  decidedly  of tener  in  men  than  in 
women. 

Many  cases  of  ulcer  of  the  duodenum  run  their  course  entirely  without  symp- 
toms, or  they  cause  no  symptoms  until  sudden  hemorrhage  appears  (from 
erosion  of  the  pancreatico-duodenalis,  gastroduodenalis,  etc.)  with  hemateme- 
sis  and  bloody  stools  (quite  often  bloody  stools  alone  without  hematemesis), 
or  until  there  are  suddenly  signs  of  peritonitis  from  perforation.  In  many  cases 
a  type  of  disease  exists  for  a  long  time  whose  symptoms,  as  we  have  said,  are  so 
like  the  clinical  symptoms  of  gastric  ulcer  that  we  can  only  rarely  distinguish 
the  two  forms  with  certainty  during  life.  We  notice  continuous  or  neuralgic 
pain,  which,  in  ulcer  of  the  duodenum,  has  its  chief  seat  in  the  right  hypochon- 
drium.  Severe  gastric  symptoms,  especially  vomiting,  are  not  as  common  as  in 
gastric  ulcer.  Occult  hemorrhages,  demonstrated  by  the  different  chemical 
blood  tests  of  the  stools,  may  materially  support  the  suspicion  of  an  ulcer. 
Finally,  it  is  to  be  noted  that  recently  a  slight  glycosura  has  repeatedly  been 
observed  in  duodenal  ulcer  (in  contradistinction  to  ulcer  of  the  stomach) .  The 
general  health  and  general  nutrition  may  remain  quite  undisturbed  for  a  long 
time. 

Ulcer  of  the  duodenum  ends  by  cicatrization  and  recovery,  or  by  cicatriza- 
tion and  the  formation  of  stenosis,  and  obstructed  evacuation,  with  secondary 
dilatation  of  the  upper  portion  of  the  duodenum  and  of  the  stomach.  In  regard 
to  the  different  adhesions  and  the  perforations  of  the  ulcer  into  neighboring 
organs,  we  may  refer  to  what  has  been  said  of  gastric  ulcer. 


TUBERCULOSIS   OF   THE   INTESTINES  601 

The  treatment  must  be  governed  by  the  same  principles  which  were  laid 
down  in  the  treatment  of  gastric  ulcer,  especially  as  the  diagnosis  is  usually 
doubtful. 


CHAPTER    VI 
TUBERCULOSIS    OF    THE    INTESTINES 

Tuberculosis  of  the  intestines  is  in  most  cases  a  secondary  disease,  and  is 
one  symptom  of  a  more  extensive  general  tuberculosis.  It  develops  most  fre- 
quently in  the  course  of  chronic  pulmonary  tuberculosis,  and  depends  here,  as 
we  have  seen  (compare  page  307),  probably  upon  an  infection  of  the  intestines 
from  the  tuberculous  sputum  that  has  been  swallowed. 

Intestinal  tuberculosis,  however,  may  also  be  a  primary  disease,  and  the 
source  of  further  extension  of  tuberculosis  over  the  body.  "  Tuberculosis  of  the 
abdominal  organs/'  which  usually  starts  from  the  intestines,  has  a  clinical  sig- 
nificance, especially  in  children.  It  is  not  improbable  that  in  such  cases  the 
first  infection  of  the  intestine  comes  from  without,  and  that  the  tuberculous 
poison  is  taken  into  the  body  with  the  food.  Here  we  must  suspect  especially 
the  milk  from  cows  with  pearly  distemper — that  is,  with  tuberculous  disease. 

The  anatomical  changes  in  intestinal  tuberculosis  are  precisely  analogous  to 
the  tuberculous  changes  in  other  mucous  membranes.  The  tubercular  new 
growth  has  its  origin  usually  in  the  lymph  apparatus  of  the  intestine,  in  the 
solitary  follicles,  and  in  Peyer's  patches.  The  first  miliary  tubercles  form 
beneath  the  epithelium,  and  soon  fuse  with  one  another  into  a  diffuse  infiltra- 
tion. In  its  further  course  the  infiltration  on  one  side  extends  deeper  into  the 
surrounding  tissue,  so  that  it  attacks  the  submucous  and  muscular  coats  and 
even  extends  to  the  serous  coat,  and  on  the  other  side,  by  the  destruction  of 
the  new  growth  which  begins  at  the  surface  and  constantly  spreads,  tubercular 
ulcers  are  formed.  We  can  often  make  out  with  the  naked  eye  single  miliary 
tubercles  or  groups  of  them  at  the  base  or  in  the  infiltrated  edges  of  the  ulcer. 
This  is  especially  plain  in  deep-seated  ulcers  on  the  corresponding  portion  of 
the  serous  coat.  The  form  of  the  large  tubercular  ulcers  is  often  irregular.  In 
many  cases  the  long  diameter  of  the  ulcer  is  parallel  to  the  circumference  of  the 
intestine,  so  that  the  girdle-like  ulcers,  which  are  especially  characteristic  of 
tuberculosis,  are  formed. 

Tubercular  ulcers  are  situated  both  in  the  large  and  in  the  small  intestines. 
They  are  usually  most  marked  in  the  vicinity  of  the  ileocecal  valve.  Isolated 
tubercular  lesions,  which  may  impress  one  absolutely  like  an  ileocecal  tumor, 
are  not  infrequent  in  this  locality.  The  thickened,  matted  coils  of  intestine, 
in  conjunction  with  the  swollen  lymphatic  glands  and  other  tissues,  occasion- 
ally form  large  irregular  tumors,  which  may  give  rise  to  confusion  with  chronic 
perityphlitis. 

Tubercular  ulcers  in  the  stomach  are  extremely  rare.  Besides  the  intestinal 
tuberculosis  there  is  very  often  tuberculosis  of  the  mesenteric  lymph-glands, 
and  also  frequently  tuberculosis  of  the  peritoneum. 

The  symptoms  of  intestinal  tuberculosis  are  usually  quite  subordinate  to  the 
symptoms  caused  by  other  coexisting  tuberculous  affections.     There  may  often 


602  DISEASES  OF  THE   DIGESTIVE  ORGANS 

be  quite  extensive  tubercular  ulcers  without  any  marked  symptoms,  but,  as  a 
rule,  the  onset  of  diarrhea  turns  the  attention  to  the  intestinal  complication 
(see  the  chapter  on  Pulmonary  Tuberculosis). 

Marked  admixture  of  blood  with  the  stools  occurs  only  rarely  in  tubercular 
ulcers  of  the  intestine.  In  tuberculosis  of  the  large  intestine,  blood  and  pus 
are  occasionally  found  in  small  amounts  in  the  stools. 

Tubercle  bacilli  have  been  repeatedly  demonstrated  in  the  fecal  discharges, 
but  it  is  not  very  easy  to  find  them,  and,  moreover,  their  diagnostic  significance 
is  impaired  by  the  fact  that  they  may  be  referable  to  sputum  which  has  been 
swallowed. 

Pains  are  often  entirely  absent.  In  other  cases  there  is  considerable  abdom- 
inal pain  as  well  as  much  tenderness  on  pressure.  Marked  tenderness  on  pres- 
sure indicates  an  involvement  of  the  peritoneum.  Not  infrequently,  a  persistent 
moderate  meteorism  is  present.  To  a  certain  extent,  circumscribed  ileocecal 
tuberculosis  furnishes  a  very  characteristic  clinical  picture.  It  generally  pro- 
duces the  symptoms  of  a  chronic  intestinal  obstruction  (colic,  constipation,  vis- 
ible intestinal  peristalsis),  and  is  generally  associated  with  a  distinct  circum- 
scribed tumor  in  the  ileocecal  region.  The  course  is  generally  very  protracted, 
lasting  possibly  for  years.    Secondary  suppuration  is  not  infrequent. 

Primary  tuberculosis  of  the  abdominal  organs  sometimes  presents  quite  a 
characteristic  type  of  disease,  especially  in  children.  This  was  termed  by  the 
older  physicians  tabes  mesent erica.  The  chief  feature  of  this  type  of  disease 
consists  in  a  progressive  general  emaciation  and  anaemia,  which  are  usually 
associated  with  a  persistent  hectic  fever,  which  obstinately  resists  all  the  rem- 
edies employed.  The  abdomen  is  usually  swollen  by  meteorism,  but  it  is  some- 
times flat  and  sunken.  In  some  cases  we  can  feel  the  swollen  mesenteric 
lymph-glands  through  the  abdominal  wall  during  life.  The  involvement  of 
the  mesenteric  lymph-glands  obstructs  the  lymph-channels  which  serve  for  the 
absorption  of  fat,  a  circumstance  which  contributes  to  the  excessive  emaciation 
frequently  seen.  The  liver  may  be  enlarged  and  its  lower  border  can  often  be 
felt.  The  bowels  are  irregular,  and  there  is  usually  a  moderate  diarrhea,  per- 
sisting in  spite  of  all  remedies.  The  invariably  fatal  termination  is  due  to  an 
increase  of  the  general  marasmus,  or  to  a  final  acute  tuberculous  affection,  such 
as  miliary  tuberculosis  or  tuberculous  meningitis.  The  autopsy  shows  tubercu- 
losis of  the  intestines,  peritoneum,  lymph-glands,  liver,  etc.,  to  a  greater  or  less 
extent.  The  lungs  may  be  quite  free  from  tuberculosis.  We  will  return  to  this 
affection  in  the  description  of  tuberculosis  of  the  peritoneum. 

The  treatment  of  intestinal  tuberculosis  can,  as  a  rule,  be  only  symptomatic. 
Besides  the  general  dietetic  treatment  which,  in  addition  to  sparing  the  intes- 
tines, seeks  to  keep  up  the  patient's  strength  as  far  as  possible,  medical  interfer- 
ence is  demanded  by  the  abdominal  pain  and  diarrhea.  The  chief  remedy  is 
opium,  either  alone  or  combined  very  frequently  with  tannin,  tannigen,  tan- 
nalbin,  acetate  of  lead,  subnitrate  of  bismuth,  bismutose,  coto  bark  (gr.  vijss. 
[gm.  0.5] ),  etc.  Sometimes  a  decoction  of  logwood  is  beneficial.  Talc  also  has 
lately  been  recommended;  about  6  or  7  ounces  (gm.  200)  are  given  daily,  sus- 
pended in  milk.  We  have  seen  some  good  results  from  it.  The  most  serviceable 
local  applications  are  poultices  and  alcoholic  and  Priessnitz  compresses.  In 
ileocecal  tuberculosis  (vide  supra),  surgical  intervention  (extirpation,  entero- 
anastomosis,  etc.)  has  frequently  given  good  results. 


SYPHILIS   OF   THE   RECTUM  603 

In  other  respects  the  treatment  coincides  with  the  general  treatment  of 
tuberculosis  (vide  supra). 


CHAPTER    VII 
SYPHILIS    OF    THE    RECTUM 

In  not  very  rare  cases  we  see  in  the  rectum,  especially  in  its  lower  portions, 
extensive  syphilitic  ulcerations,  which  produce  a  severe  and  practically  impor- 
tant type  of  disease.  The  more  intimate  relation  between  syphilis  of  the  rec- 
tum and  the  general  syphilitic  process  is  not  perfectly  clear.  According  to 
quite  a  widespread  opinion,  the  infection  of  the  rectum  comes  from  the  secretion 
trickling  down  from  the  ulcers  of  the  genitals.  The  facts  seem  to  support  this 
view,  since  syphilis  of  the  rectum  is  seen  much  more  frequently  in  women  than 
in  men.  Some  authors  have  even  asserted  that  all  the  so-called  "  syphilitic  " 
ulcers  in  the  rectum  have  no  connection  at  all  with  genuine  syphilis,  but  are 
chancroids.  It  is,  in  fact,  striking,  even  if  it  by  no  means  proves  such  a  hypoth- 
esis, that,  at  the  autopsy  of  persons  who  have  died  of  "  syphilis  of  the  rectum," 
we  rarely  find  definite  syphilitic  changes  in  other  internal  organs — a  fact  which 
we  also  can  confirm. 

The  most  characteristic  mark  of  syphilitic  ulcers  in  the  rectum  is  their 
tendency  to  form  cicatrices  and  stenoses.  This  result  of  the  ulcer  is  also  impor- 
tant in  its  clinical  relations,  since  the  chief  symptoms  of  the  disease  usually 
begin  with  the  development  of  the  stenosis.  The  seat  of  the  stenosis  is  usually 
so  low  down  that  we  can  conveniently  reach  it  with  the  finger,  on  a  digital  ex- 
amination of  the  rectum  during  the  patient's  life.  The  rectum  narrows  like  a 
funnel  upward,  and  we  can  feel  the  quite  sharp  edge  of  the  ring-like  cicatrix 
with  the  point  of  the  finger.  This  funnel-shaped  stenosis  of  the  rectum  is  so 
characteristic  of  syphilis  of  that  organ  that,  in  almost  all  cases,  we  can  make 
the  diagnosis  with  perfect  certainty  from  this  alone. 

The  rectum  and  the  descending  colon  are  usually  dilated  above  the  stenosis, 
and  here  extensive,  irregular  ulcerations,  with  undermined  edges,  are  usually 
found  in  the  mucous  membrane.  These  are  partly  of  a  specific  nature,  and 
partly  diphtheritic  ulcers  caused  by  the  pressure  of  the  accumulated  fecal 
masses. 

The  symptoms  of  syphilis  of  the  rectum  usually  develop  quite  gradually.  At 
first  the  bowels  are  irregular,  and  there  are  disturbances  of  defecation  which 
stubbornly  resist  the  ordinary  remedies  employed.  There  are  sometimes,  in  the 
first  stage  of  the  disease,  frequent  and  severe  hemorrhages  with  the  dejections, 
as  we  have  seen,  and  for  a  long  time  these  may  falsely  be  considered  to  be 
"  bleeding  from  hemorrhoids."  The  symptoms  become  more  marked  as  cica- 
trization of  the  ulcer  increases  and  as  stenosis  of  the  rectum  develops.  There 
is  usually  a  decided  catarrh  of  the  rectum,  so  that  the  thin  stools  contain  a  large 
admixture  of  mucus  and  pus.  The  patient's  condition  is  extremely  distressing, 
from  the  pains  with  the  frequent  but  always  scanty  dejections,  and  from  the 
severe  tenesmus.  Nodular  thickenings  and  prolapse  of  the  mucous  membrane, 
and  sometimes  true  hemorrhoids,  form  about  the  anus.  The  patient's  strength 
constantly  diminishes  from  the  pain  and  the  continual  diarrhea.    He  finally 


604  DISEASES   OF  THE   DIGESTIVE   ORGANS 

becomes  emaciated,  looks  very  pale  and  wretched,  and  has  fever  toward  night. 
Death  ensues  from  increasing  general  weakness,  or  rarely  from  a  terminal  peri- 
tonitis due  to  perforation,  after  the  whole  disease  has  lasted  one  and  a  half  to 
two  and  a  half  years. 

This  unfavorable  termination  unfortunately  seems  to  be  the  rule  in  all  the 
cases  described ;  hence  the  prognosis  is  to  be  regarded  as  very  serious  in  all  cases 
of  syphilis  of  the  rectum.  Improvement  worthy  of  mention,  or  even  perhaps 
recovery,  is  possible  only  when  the  disease  is  recognized  at  the  outset  and  prop- 
erly treated. 

At  the  outset  of  the  disease  the  treatment,  of  course,  must  consist  chiefly  of 
an  energetic  general  attack  upon  the  syphilis  by  mercurial  inunctions  and  iodid 
of  potassium;  but,  when  once  the  characteristic  funnel-shaped  stenosis  of  the 
rectum  has  formed,  we  cannot  expect  much  from  antisyphilitic  medication,  since 
this  cannot  exert  any  influence  on  the  cicatrices  and  their  results.  Improve- 
ment is  now  to  be  obtained  only  by  mechanical  dilatation  of  the  stenosis  by 
bougies,  or,  if  this  is  not  enough,  by  a  surgical  operation. 

Treatment  with  bougies,  in  order  to  produce  results,  must  be  carried  out 
very  carefully  for  a  long  time.  The  operative  treatment  consists  in  incision 
and  dilatation  of  the  stenosis,  or  in  a  complete  resection  of  the  diseased  rectum ; 
in  certain  cases,  also,  in  the  formation  of  an  artificial  anus.  When  only  symp- 
tomatic treatment  is  possible,  it  consists  of  local  irrigations,  similar  to  those 
employed  in  catarrhal  colitis,  and  in  the  careful  administration  of  mild  laxa- 
tives (rhubarb,  compound  licorice  powder,  castor  oil,  etc.). 


CHAPTEE    VIII 
CANCER    OF    THE    INTESTINES 

The  development  of  cancer  is  far  more  rare  in  the  intestine  than  in  the 
stomach.  Nevertheless,  cancer  of  the  intestines  is  a  disease  of  great  practical 
importance,  since  a  cure  is  possible  only  in  case  of  a  correct  early  diagnosis. 
The  rectum  is  the  most  frequently  affected  of  all  portions  of  the  intestines. 
Next  in  frequency  is  carcinoma  of  the  colon,  particularly  the  csecum,  the  sig- 
moid flexure,  and  the  hepatic  and  splenic  flexures.  Carcinoma  is  very  much 
less  common  in  the  small  intestine,  though  it  occurs  in  all  parts  of  it.  In 
the  duodenum  it  particularly  affects  the  neighborhood  of  the  common  duct. 

Most  cancers  of  the  intestine  appear  in  the  form  of  ringlike  swellings  that 
take  in  the  whole  circumference  of  the  intestine.  More  rarely  we  find  a  more 
diffuse  papillary  proliferation,  extending  over  a  larger  surface  of  the  intestine. 
There  is  often  quite  an  extensive  destruction  of  the  new  growth  on  the  surface 
of  the  cancer,  from  which  deep  ulcerations  arise.  Often  metastases  are  found 
in  the  lymph-glands,  liver,  and  other  organs.  Above  a  cancerous  obstruction 
the  intestine  is  usually  dilated,  with  thickening  of  its  muscular  coat,  and  in- 
flammation or  ulceration  of  its  mucous  membrane  due  to  the  impacted  fecal 
matter.  In  its  histological  structure,  cancer  of  the  intestine  is  to  be  regarded 
as  invariably  a  cylindrical-celled  carcinoma,  which  sometimes  shows  a  plainly 
glandular  structure — adeno-carcinoma — and  sometimes  that  of  the  other  forms 
of  cancer — scirrhous,  medullary,  or  colloid. 


CANCER   OF   THE   INTESTINES 

Cancer  of  the  intestines,  like  all  cancers,  occurs  chiefly,  if  not  invariably,  in 
advanced  life. 

Symptomatology. — The  clinical  symptoms  of  cancer  of  the  intestines  are 
only  in  a  part  of  the  cases  so  pronounced  that  we  can  make  a  positive  diagno-i- 
of  the  disease.     The  symptoms  vary  with  the  location  of  the  growth. 

Cancer  of  the  rectum  begins  usually  with  distress  at  stool  (tenesmus)  and 
pain  in  the  rectum,  which  at  first  comes  only  with  defecation,  but  later  becomes 
almost  continuous.  The  disturbances  of  defecation  consist  at  first  apparently 
only  in  simple  constipation.  Often  there  is  frequent  desire  to  defecate,  the 
movements  consisting  always  of  small  tapelike  or  nodular  masses,  which  are 
evacuated  with  great  difficulty.  Gradually  a  painful  tenesmus  sets  in.  The  pain 
often  shoots  into  the  neighboring  parts — the  sacrum,  the  thighs,  the  genitals, 
etc.  The  local  symptoms  gradually  increase,  the  stools  often  contain  some 
mucus  and  blood,  and  diarrhea  alternates  with  obstinate  constipation.  The 
patient  also  becomes  emaciated,  and  constantly  grows  weaker  and  more  mis- 
erable. Finally,  we  often  find  a  complete  paralysis  of  the  sphincter  ani,  so  that 
a  mucous,  bloody  fluid  constantly  oozes  from  the  half-open  anus.  An  absolute 
diagnosis  can  usually  be  made  with  ease  by  digital  examination  of  the  rectum. 
This  examination  should  never  be  omitted  in  any  suspicious  case,  or  otherwise 
it  is  only  too  easy  to  make  a  mistake.  Many  a  fatal  case  might  perhaps  have 
been  saved  by  a  timely  diagnosis.  External  piles  are  common  in  cancer  of  the 
rectum,  and  their  presence  should  by  no  means  prevent  the  physician  from  an 
internal  examination.  If  there  is  cancer  of  the  rectum,  the  finger  upon  being 
introduced  detects  an  irregular,  firm  growth,  and  we  can  usually  make  out 
with  approximate  accuracy  its  extent  and  mobility  and  its  invasion  of  neigh- 
boring organs,  such  as  the  vagina  and  bladder.  We  differentiate  cancers  of 
the  rectum  into  those  situated  far  up  (generally  markedly  exuberant),  and 
those  located  low  down  (generally  annular).  Examination  with  the  rectal 
speculum  sometimes  makes  the  diagnosis  more  accurate,  but  is  usually  unneces- 
sary. In  some  cases  the  destruction  of  the  new  growth  may  cause  perforation 
into  the  adjoining  organs  mentioned,  and  we  can  easily  understand  the  results 
of  this,  such  as  cystitis,  purulent  discharges  from  the  vagina,  etc.  We  may 
also  have  peritonitis  from  perforation.  Secondary  cancer  appears  with  especial 
frequency  in  the  liver,  also  in  the  peritoneum  and  elsewhere. 

Carcinoma  of  the  colon  causes,  as  a  rule,  only  very  indefinite  symptoms, 
which  for  a  long  time  are  hard  to  interpret.  These  symptoms  consist  chiefly 
of  distress  at  stool,  obstinate  constipation,  dull  pains  in  the  abdomen,  and  the- 
signs  of  slowly  increasing  general  weakness  and  emaciation.  With  the  growth 
of  the  neoplasm  there  are  usually  attacks  of  colic,  with  the  gradual  or  perhaps 
rapid  development  of  all  the  symptoms  of  obstruction  of  the  bowels  (vide  infra, 
Chapter  XI).  The  pains  are  rarely  sharply  localized;  but  sometimes,  how- 
ever, the  principal  location  of  the  pain,  and  particularly  the  localized  tender- 
ness, point  approximately  to  the  seat  of  the  neoplasm.  Not  infrequently  the 
pain  is  principally  referred  to  the  umbilical  region.  Vomiting  occurs  fairly 
often  in  cancer  of  the  colon.  At  first  the  vomitus  consists  of  stomach  con- 
tents, mucus,  bile,  later  (with  increasing  intestinal  obstruction)  it  may  as- 
sume a  fecal  character. 

In  many  cases  the  shape  of  the  feces  is  peculiar.  They  are  ribbon-shaped, 
or  consist  of  queer  flattened  nodules  which  have  a  certain  resemblance  to  sheep's 


606  DISEASES   OF  THE   DIGESTIVE   ORGANS 

dung  (scybala) .  Not  infrequently  we  find  in  the  dejections  an  admixture  of 
mucus,  pus,  and,  what  is  still  more  important,  blood;  if  blood  is  persistently 
present  in  the  movements  (to  be  determined  by  the  guaiac-turpentine  test, 
vide  supra),  or  if  there  are  bloody  or  mucopurulent  masses  in  the  discharges, 
cancer  is  suggested.  Exceptionally  there  may  be  found  in  the  stools  small  de- 
tached portions  of  the  new  growth.  Not  very  rarely  in  cancer  of  the  intestines 
the  local  symptoms  for  a  long  time  remain  in  the  background ;  only  an  increas- 
ing general  weakness,  or  a  striking  anaemia,  arouse  suspicion  of  a  more  serious 
affection,  the  true  nature  of  which  remains  unrecognized  for  a  long  time,  since 
the  most  careful  examination  of  the  abdomen  frequently  at  first  yields  no  re- 
sult. However,  on  careful  palpation  it  is  sometimes  possible  to  feel  the  new 
growth  through  the  abdominal  walls  as  a  distinct  tumor.  One  characteristic 
of  the  tumor  occasioned  by  intestinal  carcinoma  is  that  it  may  be  very  mov- 
able, and  change  its  position  because  of  its  own  weight  or  of  the  collections  of 
fecal  matter.  As  a  rule,  the  growth  does  not  move  with  respiration,  except 
possibly  in  carcinoma  of  the  transverse  colon.  Most  cancers  of  the  colon  are 
more  distinctly  felt  with  an  empty  gut  than  with  a  full  one.  Insufflation  of 
air  through  the  rectum  may  facilitate  the  exact  localization  of  the  seat  of  the 
neoplasm  in  isolated  cases.  In  doubtful  cases  an  examination  under  narcosis  is 
indicated. 

It  is  easy  to  confound  colon  carcinoma  with  carcinoma  of  the  stomach,  the 
mesentery,  the  mesenteric  lymph-glands,  kidney,  etc.  It  is  very  important  to 
know  that  in  case  of  intestinal  carcinoma  the  tumor  which  is  felt  may  be  not 
the  new  growth  at  all,  but  the  hardened  fecal  masses  collected  above  it.  Such 
fecal  accumulations  may  cause  all  sorts  of  errors  as  to  the  situation  and  dimen- 
sions of  the  new  growth.  In  such  cases  a  correct  conclusion  may  not  be  ob- 
tained until  after  continued  observation  and  the  use  of  laxatives  and  enemata. 
It  is  also  true  that  ordinary  fecal  masses  may  be  mistaken  for  cancer  of  the 
intestine  when  there  is  no  intestinal  disease  of  any  sort.  If  the  neoplasm  in- 
creases in  extent,  the  symptoms  of  intestinal  stenosis  become  gradually  more 
and  more  prominent  (colic,  vomiting,  visible  rigidity,  distention,  and  peri- 
stalsis of  the  intestinal  coils  situated  above  the  obstruction).  The  symptoms 
of  stenosis  may  be  relieved  from  time  to  time,  owing  to  ulceration  of  the 
cancer.  In  exceptional  cases  there  may  be  perforation  of  cancer  of  the  colon 
into  the  stomach,  with  the  formation  of  a  gastrocolic  fistula;  of  perforation  of 
cancer  of  the  sigmoid  flexure  into  the  bladder  or  into  the  peritoneum,  with  a 
secondary  peritonitis,  which  may  be  localized  or  diffuse.  Carcinoma  of  the 
caecum  is  often  indistinguishable  for  a  long  while  from  tumors  due  to  chronic 
typhlitis  or  perityphlitis.  Cancers  of  the  appendix  may  also  be  confused  with 
a  circumscribed  chronic  tuberculosis  of  the  ileocecal  region.  Cancer  is  sug- 
gested, above  allj  by  the  age  of  the  patient,  the  progressive  aggravation  of  the 
illness,  and  sometimes  also  by  swelling  of  the  inguinal  lymph-glands.  In  the 
surgical  wards  in  Leipsic  we  observed  a  case  of  cancer  originating  in  the  ver- 
miform appendix,  which  penetrated  through  the  skin. 

Cancer  of  the  small  intestine  is  very  rare.  It  is  distinguished  by  the  very 
great  mobility  of  the  tumor,  if  one  is  found.  The  symptoms  are  those  of  grad- 
ually increasing  stenosis  (vide  infra).  Cancer  of  the  duodenum  is  similar  in 
many  respects  to  cancer  of  the  stomach,  particularly  of  the  pylorus.  It  leads 
to  stenosis  of  the  duodenum,  and  consequently  to  dilatation  of  that  portion  of 


HEMORRHOIDS  GOT 

the  duodenum  which  is  above  tiie  new  growth,  and  of  the  stomach,  and  so  occa- 
sions the  well-known  symptoms  of  gastrectasia.  Cancer  which  is  seated  in  the 
neighborhood  of  the  common  duct  usually  causes  excessive  and  persistent 
jaundice. 

Prognosis. — The  course  of  all  cases  of  intestinal  cancer,  provided  operative 
removal  of  the  tumor  is  impossible,  is  absolutely  unfavorable.  The  disease  may 
last  for  a  considerable  time,  about  two  or  three  years.  On  the  other  hand,  the 
duration  of  the  special  symptoms  may  be  comparatively  brief — that  is,  a  few 
months  or  weeks;  undoubtedly  because  the  condition  existed  long  before  it 
caused  symptoms.  Most  of  the  cases  run  their  course  under  the  clinical  pic- 
ture of  a  more  or  less  slowly  developing  intestinal  stenosis,  which  may  lead  to 
almost  complete  obstruction.  The  final  fatal  result  in  intestinal  carcinoma 
takes  the  form  either  of  increasing  general  weakness  or  of  perforation  with 
fatal  suppurative  peritonitis.  Death  may  also  be  occasioned  by  extensive  and 
foul  suppuration  in  the  surrounding  connective  tissue,  or  by  phlebitis  and 
pyaemia. 

Treatment. — The  only  possibility  of  successful  treatment  in  intestinal  car- 
cinoma is  by  surgical  methods.  The  results  of  operation  are  very  favorable 
in  cases  of  cancer  of  the  rectum  if  the  disease  is  not  situated  too  high,  and  has 
not  extended  too  far.  Cancer  of  the  other  parts  of  the  intestine  has  a  less 
promising  outlook.  Still,  a  large  series  of  permanent  cures  have  already  been 
obtained  by  resection  of  intestinal  cancers.  In  isolated  cases,  with  stenotic 
symptoms,  good  palliative  results  have  also  been  obtained  by  means  of  the 
so-called  entero-anastomosis.  If  surgical  interference  is  impracticable,  treat- 
ment must  be  merely  symptomatic  (suitable  diet,  mild  laxatives,  narcotics,  hot 
compresses,  etc.),  with  a  view  to  alleviating  suffering. 

We  will  append  a  few  remarks  about  sarcoma  of  the  intestine.  This  is  a 
very  rare  disease,  which  originates  from  the  submucous  layer,  or  else,  in  the 
form  of  lympho-sarcoma,  from  the  lymph-follicles  of  the  intestine,  particu- 
larly of  the  small  intestine.  Both  varieties  exhibit  a  tendency  to  extend 
cylindrically  over  considerable  areas  along  an  intestinal  coil.  They  usually 
do  not  lead  to  stenosis,  and  they  may  even  cause  dilatation  of  the  affected 
portion  of  the  intestine.  The  tumors  which  are  formed  may  attain  to  very 
considerable  size.  The  most  prominent  symptoms  are  general  weakness  and 
anaemia,  associated  with  slight  fever.  These  constitutional  symptoms  are 
more  prominent  than  the  local  ones.  The  course  is  usually  rapid,  and  ends, 
after  six  to  twelve  months,  in  death. 


CHAPTER    IX 

HEMORRHOIDS 

By  the  name  "  hemorrhoids  "  we  mean  diffuse  or  varicose  dilatations  of 
the  hemorrhoidal  veins,  especially  of  the  venous  plexuses  at  the  lower  end  of 
the  rectum.  Hemorrhoids  are  single  large  varices,  which  usually  rise  from 
the  submucous  layer,  and  push  the  mucous  membrane  out  before  them.  If 
they  are  situated  outside  of  the  sphincter  ani  we  speak  of  external  hemor- 


608  DISEASES   OF  THE   DIGESTIVE   ORGANS 

rhoids,  in  distinction  from  internal  hemorrhoids,  which  lie  above  the  sphincter. 
The  size  of  the  nodules  varies  with  the  fullness  of  the  dilated  veins;  hut 
hemorrhoids,  as  a  rule,  do  not  consist  exclusively  of  dilated  vessels,  for  we 
often  find,  at  the  same  time,  considerable  thickening  of  the  surrounding  con- 
nective tissue,  so  that  the  whole  mucous  membrane  has  a  swollen  appearance, 
with  a  polypoid  proliferation  in  parts.  The  hemorrhoids  usually  present  them- 
selves as  bluish  tumors,  from  the  size  of  a  pea  to  that  of  a  walnut,  which  sur- 
round the  anus  like  a  garland.  Most  of  them  have  a  broad  base,  while  others 
are  apparently  pedunculated. 

The  chief  cause  of  hemorrhoids  is  frequently  repeated  stasis  in  the  veins 
affected.  The  position  of  the  hemorrhoidal  veins  is  such  that  their  contents 
are  constantly  pressing  downward  by  the  action  of  gravity,  and  the  develop- 
ment of  varices  is  further  promoted  by  their  complete  lack  of  valves.  Special 
local  conditions  often  contribute  also  to  render  the  escape  of  blood  difficult; 
thus  hemorrhoids  are  particularly  frequent  during  pregnancy,  also  in  persons 
with  habitual  constipation,  and  consequently  in  individuals  who  follow 
sedentary  pursuits.  Local  disease  of  the  mucous  membrane  of  the  rectum 
(catarrh,  neoplasms,  etc.)  also  gives  rise  in  some  cases  to  the  formation  of 
hemorrhoids.  Hemorrhoids  are  sometimes  found  as  a  result  of  portal  con- 
gestion (in  hepatic  cirrhosis  and  similar  conditions),  and  finally  in  general 
circulatory  disturbances  due  either  to  pulmonary  or  cardiac  disease;  but  these 
cases  are  not  so  frequent  as  was  formerly  supposed.  Quite  often,  however,  we 
can  discover  no  sufficient  cause  for  the  development  of  the  disease,  and  we 
are  then  forced  to  the  hypothesis  of  a  local  disease  of  the  affected  venous 
plexus,  which  is  probably  often  connected  with  an  individual,  and  apparently 
sometimes  hereditary,  predisposition.  We  most  frequently  see  hemorrhoids 
in  men  in  middle  life. 

Hemorrhoids  sometimes  cause  only  slight  symptoms,  or  none  at  all,  but 
in  other  cases  they  are  a  tedious,  burdensome,  and  even  distressing  evil.  The 
chief  symptom  is  pain,  which  is  felt  as  a  constant  burning  at  the  anus,  but 
which  increases  to  great  severity  at  each  dejection.  There  is  much  pain  when 
the  hemorrhoids  and  the  surrounding  tissue  gradually  get  into  an  inflamed 
condition.  In  the  skin  about  the  anus,  erythema,  excoriations,  and  some- 
times small  but  very  painful  fissures  are  formed.  The  mucous  membrane  at 
the  lower  end  of  the  rectum  is  often  found  in  a  catarrhal  state,  which  gives 
rise  to  the  presence  of  pus  and  mucus  in  the  dejections — "  mucous  hemor- 
rhoids." The  worst  symptoms  are  caused  when  by  pressing  and  straining  at 
stool  an  internal  pile  is  forced  outward  and  contricted  by  the  sphincter.  If 
the  constriction  is  not  speedily  relieved  the  extruded  varix  becomes  much 
swollen  and  inflamed.  This  change  is  favored  by  a  cramp-like  contraction  of 
the  sphincter.  Under  such  circumstances  there  may  result  a  purulent  phlebitis 
associated  with  very  great  pain,  high  fever,  and  severe  constitutional  disturb- 
ance. Sometimes  we  find  a  thrombus,  thrombophlebitis,  or  suppurative  peri- 
proctitis, even  if  there  is  no  previous  constriction. 

Hemorrhoidal  bleeding  is  a  frequent  and  familiar  symptom.  It  arises 
from  small  fissures  of  the  dilated  and  thinned  venous  walls,  and  is  frequently 
produced  by  defecation.  Sometimes  it  occurs  at  apparently  regular  intervals, 
but  more  frequently  it  follows  absolutely  no  rule.  The  hemorrhage  is  seldom 
very  large,  so  that  the  loss  of  blood  is  in  itself  very  rarely  dangerous.     Still, 


HEMORRHOIDS  609 

the  rectal  hemorrhage  may  be  repeated  bo  often  as  to  cause  severe  and  per- 
sistent anaemia.    The  diminution  in  size  of  the  varices  after  the  hemorrha 
explains  why  the  hemorrhoidal  symptoms  are  apt  to  he  Less  marked  ae  Long 
as  there  are  hemorrhages  than  when  there  are  none.     Hence  the  old  term  of 
the  "  golden  vein  "  for  hemorrhoidal  bleeding. 

Besides  the  local  symptoms  mentioned  in  the  anus,  there  are  sometimes 
other  symptoms  which  are  due  to  an  implication  of  the  neighboring  venous 
plexuses,  the  vesical,  prostatic,  and  sacral  plexuses.  There  is  often  pain  in 
the  sacral  region,  difficulty  in  micturition,  and  in  women  vaginal  catarrh, 
anomalies  of  menstruation,  etc.  Since  the  symptoms  of  some  coexisting  mor- 
bid conditions,  such  as  abnormal  corpulency,  chronic  gastro-intestinal  catarrh, 
general  neurasthenia,  etc.,  may  be  added  to  the  general  picture,  we  can  com- 
prehend why  medical  superstition  has  found  in  hemorrhoids  an  excuse  for 
the  strangest  ideas,  like  that  of  "  aberrant  hemorrhoids  "  !  The  scientific  physi- 
cian should  be  careful  not  to  refer  such  manifold  symptoms  to  hemorrhoids 
without  due  consideration,  for  otherwise  important  diseases  may  be  readily 
overlooked. 

Treatment. — The  treatment  of  chronic  piles  is,  in  the  first  place,  mainly 
dietetic.  The  diet  to  be  prescribed  should  be  determined  by  the  constitution 
of  the  patient.  It  is  usually  advisable  to  limit  the  ingestion  of  meat,  and  to 
recommend  in  its  stead  a  larger  proportion  of  vegetables,  in  a  broad  sense, 
including  fruit,  such  vegetables  as  grow  below  the  surface  of  the  ground, 
simple  puddings,  and  buttered  bread.  It  is  usually  advantageous  to  prescribe 
a  sufficient  amount  of  physical  exercise.  In  addition  to  regular  walks,  gym- 
nastics, home  exercises,  rowing,  etc.,  are  to  be  considered,  while  riding  and 
bicycling,  on  the  other  hand,  are  not  well  borne  by  many  on  account  of  the 
local  irritation  they  occasion.  The  principal  requisite  is  to  insure  regular  and 
easy  evacuations  of  the  bowels.  In  addition  to  the  general  dietetic  measures 
just  mentioned,  cathartics  are  often  required.  The  bitter  waters  (Friedrichs- 
haller,  Ofner,  etc.),  sulphur  (the  principal  ingredient  of  most  "  pile  powders," 
— e.g.,  sulphur  depurati,  tartari  depurati),  aa  §ss.  (gm.  15),  elaeos,  menthae,1 
5ijss.  (gm.  10),  one  half  to  one  teaspoonful  s.o.s.,  and  compound  licorice  pow- 
der, are  preferred  as  particularly  reliable.  Enemata  are  to  be  employed  only 
with  care  on  account  of  the  local  irritation,  but  small  cold  injections,  or  oil  in- 
jections, may  occasionally  be  of  use.  A  favorable  combination  of  all  necessary 
dietetic  requirements  is  often  to  be  had  at  some  health  resort.  Of  these, 
Marienbad,  Carlsbad,  Tarasp,  Kissingen,  Homburg,  etc.,  are  to  be  principally 
recommended. 

The  local  treatment  consists  chiefly  in  protecting  the  piles  from  irritation. 
The  parts  are  best  cleaned  after  every  movement  of  the  bowels  with  cotton 
or  soft  linen,  and  the  region  of  the  anus  is  to  be  touched  with  oil,  vaselin,  or 
borated  vaselin.  Eegular  washings  of  the  anal  region  with  solutions  of  boric 
or  tannic  acid  are  also  to  be  recommended.  Hip  baths,  the  temperature  of 
which  may  be  regulated  according  to  the  subjective  experience  of  the  patients, 
have  also  a  favorable  action.  If  there  are  slight  inflammatory  symptoms  we 
apply  compresses  wet  with  a  solution  of  acetate  of  lead,  or  ice  water,  or  try 
suppositories    containing    morphin    or    cocain.      Certain    ointments     (e.  g., 


1  Powdered  sugar,  3j;  volatile  oil,  gtt.  ij.     M. 


610  DISEASES  OF  THE  DIGESTIVE  ORGANS 

chrysarobin,  extr.  belladonnas,  aa  gr.  xv.  [gm.  1],  iodoform,  gr.  vijss.  [gm. 
0.5],  vaselin,  5v  [gm.  20]),  are  also  highly  raised.  We  have  repeatedly  seen 
very  good  results  from  the  so-called  anusol  suppositories  (anusol-iodin-resor- 
cin-sulphonate  of  bismuth),  one  or  two  of  which  are  introduced  into  the  rectum 
daily.  The  so-called  noridal  suppositories  have  a  similar  action.  Ansesthesin 
or  cocain  ointments  are  recommended  for  severe  pains.  Constricted  piles  we 
should  endeavor  as  soon  as  possible  cautiously  to  replace  with  the  finger.  The 
pain  attending  this  operation  is  often  so  severe  that  chloroform  narcosis,  or 
at  least  the  local  application  of  cocain,  is  required.  If  there  is  suppurative 
phlebitis  an  incision  is  necessary.  In  some  cases  a  radical  operation  for  the 
piles  may  be  performed  at  the  same  time. 

The  bleeding  from  piles  is,  as  we  have  said,  seldom  severe  enough  to  de- 
mand special  treatment,  such  as  the  use  of  ice,  chlorid  of  iron,  or  packing 
the  rectum  (cotton  tampons  with  0.5-  to  l-per-1,000  adrenalin  solution).  In- 
ternal hemostatic  remedies  (particularly  the  fluid  extract  of  hamamelis,  a  tea- 
spoonful  three  times  daily,  and  hydrastis  canadensis,  ergotin,  etc. )  are  entirely 
unreliable  in  their  action.  If  the  hemorrhage  is  repeated  and  serious,  or  if 
the  inflammation  causes  persistent  and  extreme  discomfort,  we  should  urgently 
recommend  operative  removal  of  the  piles.  Particulars  as  to  the  methods  em- 
ployed for  this  purpose  will  be  found  in  the  text-books  on  surgery. 


CHAPTER    X 
HABITUAL    CONSTIPATION 

Persistent  tendency  to  constipation  is  a  frequent  symptom  in  many  dif- 
ferent acute  and  chronic  cases.  We  often  see  persistent  sluggishness  of  the 
bowels  in  all  sorts  of  conditions  of  weakness,  in  general  anaemia,  in  diseases 
of  the  stomach,  intestines,  liver,  lungs,  heart,  and  nervous  system,  and  it  is 
caused  by  a  great  variety  of  circumstances.  Often  the  weakness  of  the  peristal- 
sis of  the  intestine,  and  particularly  of  the  colon,  is  merely  one  manifestation 
of  a  general  debility ;  in  other  cases  the  activity  of  the  intestine  is  subnormal, 
because  of  the  insufficient  and  unstimulating  diet,  or  because  of  the  lack  of 
physical  exercise.  In  a  third  class  of  cases  there  is  disease  of  the  intestinal 
wall  itself,  such  as  catarrhal  conditions,  circulatory  disturbance,  atrophy  of 
the  muscular  coat,  or  constriction  of  the  lumen  of  the  intestine.  And,  finally, 
a  fourth  cause  is  disturbance  of  the  innervation  of  the  intestine,  because  of 
disease  of  the  brain  or  spinal  cord. 

The  above  are  examples  of  symptomatic  constipation,  but  in  this  chapter 
we  shall  not  discuss  these,  but  rather  cases  of  habitual  constipation  occurring 
as  an  apparently  independent  disease.  This  may  appear  alone  or  associated 
with  other  disturbances  likewise  purely  functional.  The  causes  of  this  fre- 
quent and  important  condition  are  by  no  means  invariable,  and  we  are  still 
far  from  a  clear  understanding  of  the  nature  of  all  the  disturbances  that 
belong  in  this  category.  Sometimes  habitual  costiveness  seems  to  be  associ- 
ated with  a  congenital  functional  weakness  of  the  muscular  coat,  or  perhaps 
of  the  nervous  apparatus  of  the  intestines.     At  any  rate,  it  is  often  possible 


HABITUAL   CONSTIPATION  611 

to  trace  the  symptoms  back  to  the  earliest  childhood.  In  other  cases  it  i- 
apparently  an  improper  mode  of  life  which  exercises  a  disturbing  effect  upon 
the  intestinal  activity;  lack  of  bodily  exercise  often  leads  to  disorders  of 
the  bowels,  and,  still  more,  irregularity  in  eating  and  an  improper  choice 
of  food.  In  young  girls,  especially,  false  modesty  may  primarily  lead  to  ir- 
regularity of  the  bowels. 

Sometimes  external  mechanical  influences  promote  constipation.  In 
women  unsuitable  apparel,  tight  bands  around  the  waist,  tightly  laced  cor- 
sets, and  the  like  certainly  produce  in  many  cases  a  permanent  malposition 
of  the  intestinal  organs  ("  enteroptosis,"  compare  the  chapter  on  Gastrop- 
tosis,  page  565),  and  particularly  of  the  large  intestine.  It  is  not  improb- 
able that  these  conditions  are  in  part  the  cause  of  the  chronic  constipation 
which  is  so  frequent  in  women  and  girls.  In  women  frequent  pregnancies 
may  also  exert  a  causative  influence  by  inducing  laxness  of  the  abdominal 
walls  and  a  tendency  to  enteroptosis. 

Habitual  constipation  is  associated  still  more  frequently  with  general 
neurasthenia  than  with  any  of  the  conditions  thus  far  enumerated  (compare 
the  chapter  on  Neurasthenia  in  Vol.  II).  The  nature  of  this  association  is 
probably  not  the  same  in  every  case.  Often,  neurasthenia  and  constipation 
seem  to  be  coordinate  symptoms;  sometimes  the  existing  constipation  has  an 
unfavorable  effect  upon  the  psychical  condition  of  patients,  rendering  them 
feeble,  fretful,  out  of  sorts,  and  nervous.  As  a  rule,  however,  neurasthenia  is 
the  primary  disease,  and  then  the  irregularity  of  the  bowels  appears  as  a 
result  of  abnormal  nervous  influences  or  of  secondary  conditions  (vide  infra). 
Often  the  two  states  act  in  a  vicious  circle,  each  sustaining  and  aggravating 
the  other.  The  most  essential  factor  is  often  the  hypochondriacal  tendency 
of  the  patients.  They  ascribe  an  excessive  importance  to  irregularity  of  the 
bowels,  and  regard  every  slight  disturbance  as  of  extreme  gravity.  Even  when 
the  movements  are  sufficient  they  cannot  free  themselves  from  a  disordered 
apprehension  that  they  are  not  really  adequate.  Such  patients  come  at  last 
to  devote  almost  all  their  thoughts  to  their  illness  and  make  the  most  pains- 
taking observations  and  investigations  of  their  dejections,  having  energy  for 
nothing  else  and  no  joy  in  life.  They  seek  aid  from  all  sorts  of  physicians 
and  quacks,  and  yet  they  have  no  actual  confidence  in  any  one  and  do 
not  follow  the  practitioner's  directions  with  the  requisite  persistence.  In 
many  of  these  cases  the  constipation  is  only  apparent  or  imaginary.  The 
patient  fears  to  eat  any  hearty  food  and  takes  little  nourishment,  and  con- 
sequently the  excreta  are  scanty.  In  other  instances,  however,  the  abnor- 
mal psychical  conditions  have  a  direct  inhibitory  influence  upon  the  in- 
testinal activity.  The  intestine  gets  out  of  the  habit  of  regular  action. 
Moreover,  the  unwise  use  of  internal  laxatives  may  entail  actual  disease  of 
the  intestine. 

Consequently,  if  the  physician  wishes  to  form  a  reliable  opinion  with  re- 
gard to  the  intestinal  function  in  a  case  of  chronic  constipation  from  actual 
observation,  the  first  requisite  is  that  he  should  himself  see  the  dejections  of 
the  patient  for  some  time,  while  the  diet  is  normal  and  all  laxatives  are  omit- 
ted. This  is  much  easier  in  a  hospital  or  sanitarium  than  in  ordinary  private 
practice.  When  a  patient  is  under  observation  in  this  way  it  should  be  no- 
ticed whether  the  abdomen  becomes  much  distended,  and  whether  hardened 


612  DISEASES   OF   THE   DIGESTIVE   ORGANS 

fecal  matter  can  be  felt  in  the  colon  or  the  sigmoid  flexure.  Furthermore, 
the  dejections  should  be  examined  as  to  their  amount  and  character.  They 
may  seem  nubby,  hard,  or  as  if  they  were  "  burned/'  or  of  abnormally  small 
diameter,  or  flattened,  or  covered  with  mucus.  If  we  find  that  the  evacuations 
are  distinctly  abnormal  we  infer  that  there  is  actual  disturbance  of  the  in- 
testinal functions;  while,  on  the  other  hand,  our  examinations  often  show 
that  the  complaints  are  exaggerated  or  imaginary. 

It  is  considered  very  important  by  many  physicians  to  distinguish  be- 
tween an  "  atonic  "  and  a  "  spastic  "  constipation.  In  the  former  case  the 
obstipation  is  due  to  peristaltic  weakness,  in  the  latter  to  conditions  of  tonic- 
spastic  contraction  of  the  intestines.  Dejections  that  are  thin,  pencil-like,  or 
resembling  sheep-dung,  a  retracted  abdomen,  palpable  contracted  intestinal 
coils,  etc.,  are  cited  as  the  symptoms  of  spastic  constipation.  This  distinction 
has  a  certain  theoretical  and  even  practical  importance,  but,  in  our  opinion, 
cannot  be  strictly  maintained. 

Treatment. — The  treatment  of  habitual  constipation  is  a  difficult  and  often 
a  thankless  task,  and  it  demands  patience  and  professional  tact.  It  goes  with- 
out saying  that  we  must  first  of  all  look  for  the  causal  factors.  If  we  succeed 
in  improving  the  underlying  disease — as,  for  instance,  the  chronic  gastro- 
intestinal catarrh,  the  chronic  affections  of  the  heart  or  lungs,  the  ansemic 
conditions,  or  certain  nervous  troubles — a  regulation  of  the  bowels  often  fol- 
lows of  itself.  In  ordinary  habitual  constipation  we  must  first  attend  to  the 
patient's  diet.  Since  most  of  these  patients  also  suffer  from  symptoms  of 
nervous  dyspepsia,  they  are  usually  very  careful  in  their  diet,  and  take  only 
a  little,  easily  digestible,  and  chiefly  liquid  food.  It  is  no  wonder  that  no 
good  dejections  follow  such  food.  Improvement  can  be  obtained  in  such 
cases  only  by  eating  plenty  of  food  which  can  mechanically  stimulate  the 
intestine.  Hence  we  must  try  to  bring  the  patient  back  to  ordinary  "  house- 
hold fare  " — to  take,*  besides  plenty  of  meat,  a  sufficient  amount  of  bread, 
vegetables,  etc.  It  is  a  very  good  thing  to  recommend  especially  certain 
kinds  of  bread,  such  as  Graham  bread  or  rye  bread,  and  also  larger  amounts 
of  butter,  besides  fruits,  prunes,  grapes,  apples,  pears,  dates,  and  figs,  either 
raw  or  boiled,  preserved  fruits,  and  honey. 

As  a  rule,  the  diet  most  suitable  for  each  individual  case  is  only  deter- 
mined by  repeated  trials.  A  coarse  diet  is  not  always  the  most  suitable.  In 
cases  with  susceptible  stomachs,  and  those  in  which  spastic  conditions  (vide 
supra)  of  the  intestines  must  be  thought  of,  results  are  occasionally  more 
readily  obtained  by  a  lighter  form  of  diet,  in  which,  however,  vegetables, 
stewed  fruit,  honey,  butter,  buttermilk,  etc.,  must  always  be  given  the  prefer- 
ence. It  is  often  efficacious  to  have  the  patient  drink  a  glass  of  cold  water 
in  the  morning  before  breakfast.  Of  true  laxatives  we  should  be  very  spar- 
ing, for  the  patient  readily  becomes  accustomed  to  them,  and  the  dose  has  to 
be  constantly  increased.  Among  the  milder  laxatives  the  various  waters 
which  contain  Epsom  salts,  such  as  Friedrichshall,  usually  one  or  two  wine- 
glassfuls  are  prescribed. 

In  general  practice  cathartic  teas  in  the  most  varied  combinations  are 
much  used  with  good  results.  We  have  personally  used  the  following  com- 
bination, e.  g. :  cort.  frangulas,  folior.  sennse,  herbae  millefolii,  rhizoma  gram, 
concis.  aa  §j  ov  (gm.  50),  a  teaspoonful  to  a  cup  of  tea. 


HABITUAL   CONSTIPATION  613 

For  more  continued  use  we  may  also  recommend  tamarinds,  rhubarb, 
podophyllin,  aloes,  jalap,  cascara  sagrada,  and  extract  of  frangula. 

The  purgen  tablets  (purgen  =  phenolphthalein)  often  produce  good  re- 
sults, likewise  California  fig  sirup  (Califig.).  In  cases  of  so-called  spastic 
constipation,  good  results  are  occasionally  seen  after  the  use  of  the  prepara- 
tions of  belladonna  (pills  or  powders  with  extr.  belladonnas,1  gr.  ^  to  ss. 
(gm.  0.02  to  0.03). 

It  is  not  possible  in  this  connection  to  give  a  minute  description  of  all 
these  remedies.  They  are  prescribed  in  the  most  varied  combinations  in  the 
shape  of  pills  and  powders.  It  is  often  necessary  to  make  repeated  changes 
in  the  medicine  and  its  dose  before  the  most  effectual  prescription  is  hit  upon, 
for  there  are  many  individual  peculiarities  in  this  regard.  Generally  the 
patients  themselves  decide  what  remedy  answers  their  purpose  best.  There 
are  patients  with  simple  habitual  constipation  who  for  years  take,  every 
evening,  some  powdered  rhubarb,  or  one  or  two  laxative  pills,  with  a  good 
result  and  feel  perfectly  well.  In  most  cases,  however,  the  efficiency  of  the 
internal  laxatives  gradually  fails,  the  patient  is  obliged  to  take  more  and 
more  powerful  remedies,  or  increasing  doses,  in  order  to  get  any  effect.  In 
such  instances  it  is  always  best  to  abandon  internal  laxatives  altogether,  and 
in  their  stead  to  employ  external  physical  agencies,  or  to  stimulate  the  rectum 
by  means  of  injections,  irrigations,  and  the  like. 

The  regular  use  of  injections,  if  carried  out  in  a  proper  manner,  may  be 
continued  for  a  long  time  without  harm.  The  practice  may  indeed  be  carried 
to  an  injurious  excess,  and  occasion  at  last  a  catarrh  of  the  rectal  mucous 
membrane,  because  of  the  constant  local  irritation,  or,  at  any  rate,  a  needless 
dependence  upon  local  stimulation.  The  simplest  way  of  making  an  injection 
is  by  means  of  an  irrigator.  There  are  also  various  shapes  of  injection  syringes 
used  by  many.  For  a  fluid  we  choose  simple  warm  water,  or,  what  is  often 
more  efficient,  cold  water.  We  can  strongly  recommend  the  employment  of 
soapsuds  (a  teaspoonful  of  powdered  soap  to  a  pint  or  two  of  water).  Lately, 
injections  of  oil  have  been  in  great  vogue.  The  patient  is  placed  on  his  left 
side,  and  by  the  means  of  a  fountain  syringe,  8  to  16  ounces  (gm.  250  to  500) 
of  fresh  poppy  oil  [or  fresh  cotton-seed  oil]  (olive  oil  is  much  dearer)  is  slowly 
introduced  into  the  rectum.  Small  injections  of  glycerin,  1  to  2  drachms 
(gm.  5  to  10),  are  also  effectual.  Still  more  convenient  and  often  satisfactory 
is  the  employment  of  glycerin  suppositories,  which  are  dissolved  in  the  rectum 
by  the  heat  of  the  body. 

The  external  physical  remedies  emplo3red  in  habitual  constipation  are  mas- 
sage, electricity,  and  hydrotherapy.  Eegular  massage  is  often  attended  with 
good  results.  The  patient  is  stroked  with  the  flat  of  the  hands  with  moderate 
or  even  with  considerable  pressure,  beginning  at  the  csecal  region,  and  pro- 
ceeding along  the  colon  to  the  sigmoid  flexure.  There  may  also  be  cau- 
tious kneading  of  the  abdomen.  A  ball  may  be  used  for  massage.  This  is 
very  convenient,  and  can  be  carried  out  by  the  patient  himself.  An  iron 
ball,  weighing  about  five  pounds  and  sewed  up  in  flannel,  is  rolled  for 
several  minutes  in  a  spiral  course  over  the  abdomen,  its  general  direction 
being  that  of  the  hands   of   a  watch.      Where   we   have   the   necessary   ap- 


1  [P.  G.     Ext.  belladonnse,  U.  S.  P.,  is  stronger.] 


614  DISEASES   OF   THE   DIGESTIVE   ORGANS 

pliances,  we  may  try  vibratory  massage,  which  often  produces  very  good 
results. 

The  electrical  treatment  consists  of  faradization  of  the  abdominal  walls, 
or  galvanization  of  the  intestine,  one  electrode  being  placed  upon  the  back. 
In  the  way  of  hydrotherapy,  cold  rubbing  and  sponging  are  employed,  cool 
and  "  Scotch "  (i.  e.,  alternating  warm  and  cold)  douches,  cold  and  warm 
compresses,  etc.  In  addition  to  these  methods  medical  gymnastics  may  be 
simultaneously  practiced.  The  well-known  books  on  indoor  gymnastics  (von 
Schreber  and  others)  give  detailed  directions  concerning  exercises  to  strengthen 
the  abdominal  muscles  and  for  the  stimulation  of  intestinal  peristalsis  (rais- 
ing the  upper  part  of  the  body  from  the  recumbent  position,  flexing  the 
thighs  on  the  abdomen,  etc.). 

In  the  treatment  of  habitual  constipation  associated  with  hypochondriasis, 
the  first  rule  is  to  treat  the  patient's  mental  condition.  We  should  not  make 
merry  over  his  trouble,  nor  should  we  rudely  let  him  feel  that  we  do  not 
consider  his  complaints  so  important  as  he  himself  imagines.  The  patient 
does  not  deserve  to  be  scoffed  at,  since  his  subjective  symptoms  are  to  him 
of  the  most  urgent  nature ;  but  it  is  extremely  important  to  divert  his  thoughts 
from  his  trouble.  As  in  many  other  reflex  processes,  so  in  defecation,  the 
voluntary  attention  abnormally  directed  to  it  has  an  inhibitory  action.  Hence 
we  admonish  the  patient  to  think  of  his  trouble  as  little  as  possible  and  tc- 
begin  his  regular  activities  again,  and  we  try  to  convince  him  of  the  ground- 
lessness of  his  fears.  The  cathartics,  which  most  patients  have  already  taken 
freely  without  the  desired  action,  are  usually  of  no  advantage  at  all.  On  the 
contrary,  it  is  almost  always  necessary  to  forbid  the  patient  to  use  cathartics 
at  all. 

We  should  not  only  employ  a  suitable  dietary  (vide  supra),  but  we  should 
seek  to  stimulate  the  intestinal  peristalsis  by  such  external  means  as  massage 
and  electricity  (vide  supra).  It  is  true  that  a  considerable  part  of  the  success 
of  these  methods  is  due  to  their  psychical  effect  upon  the  patient,  but  there  is- 
no  doubt,  also,  of  their  direct  invigorating  influence  upon  the  muscular 
coat  of  the  intestine.  We  must  not  omit  a  proper  general  treatment:  cold 
sponging,  baths,  a  country  residence,  and  sufficient  physical  exercise.  Finalty, 
it  is  often  very  useful  to  cause  the  patient  to  go  to  the  closet  at  a  fixed  hour 
daily,  even  if  there  be  no  special  desire  for  a  stool,  and  to  try  to  have  a  move- 
ment of  the  bowels.  Thus,  a  sort  of  training  and  education  of  the  bowels  is 
achieved,  even  when  the  patient  at  first  believes  it  impossible. 

By  these  means  only  do  we  succeed  in  giving  the  patient  renewed  courage, 
and  sometimes  finally  in  attaining  recovery  even  in  severe  and  persistent  cases. 
In  all  cases  of  habitual  constipation  we  should,  however,  not  only  endeavor  to 
hit  upon  the  proper  means  for  making  the  bowels  act,  but  if  it  is  in  any  wise 
possible  we  should  also  strive  to  arrange  the  patient's  life  so  sensibly  and 
suitably  that  he  will  have  regular  and  satisfactory  evacuations  without  any 
special  means.  To  accomplish  this,  it  is  often  requisite  that  we  should  per- 
suade the  patient  for  once  to  make  the  attempt  to  give  up  all  laxatives.  Such 
a  course  is  naturally  much  more  practicable  in  an  institution  than  in  a  private 
house.  The  author  has  himself  repeatedly  treated  patients  with  habitual  con- 
stipation simply  by  regimen — i.  e.,  by  proper  diet,  cold  sponging,  and  sufficient 
exercise  or  gymnastics,  without  any  other  remedies,  regardless  of  the  fact  that 


STRICTURE   AND   OBSTRUCTION   OF   THE   INTESTINES  615 

in  such  patients  the  stool  would  often  be  delayed  for  five,  eight,  or  ten  'lays, 
and  yet,  what  is  remarkable,  without  any  special  inconvenience.  'Finn  at 
last  the  bowels  would  move  spontaneously,  or  with  the  aid  of  a  small  injection 
of  cold  water,  and  would  gradually  assume  complete  normal  regularity. 


CHAPTER    XI 

STRICTURE    AND    OBSTRUCTION    OF    THE    INTESTINES 

iEtiology  and  Pathological  Anatomy. — The  anatomical  causes  of  stricture 
or  obstruction  of  the  intestines  are  as  follows : 

1.  Congenital  Closure. — Congenital  closure  of  the  intestines  is  found  at 
the  anus,  atresia  ani,  and  much  less  frequently  in  the  colon  or  small  intestines. 
The  form  first  mentioned  is  the  only  one  of  clinical  interest,  since  it  may  be 
relieved,  at  least  in  some  cases,  by  operation.  All  the  other  forms  of  con- 
genital closure  of  the  intestines  are  incompatible  with  a  long  duration  of  life. 

2.  Tumors  and  Cicatricial  Strictures. — Cancer  of  the  intestine  is  the  only 
tumor  that  has  any  clinical  significance.  We  have  already  described  its  most 
important  anatomical  relations  and  the  possibility  of  intestinal  stenosis  as  a 
result  of  it. 

We  see  cicatricial  strictures  most  frequently  after  recovery  from  tuber- 
cular ulcers.  They  are  located  principally  in  the  lower  part  of  the  small 
intestine  or  in  the  cascum.  Cases  have  been  observed  in  which  several  tuber- 
cular intestinal  strictures  were  present,  at  the  same  time,  while  there  was  no 
evidence  of  tuberculosis  in  other  parts  of  the  body.  Next  to  tubercular  ulcer, 
the  most  frequent  cause  of  cicatricial  stenosis  is  dysenteric  ulcer.  Strictures 
of  this  class  are  located  in  the  large  intestine.  Syphilis  leads  principally  to 
ulcerative  processes  in  the  rectum,  and  in  this  way  a  syphilitic  rectal  stenosis, 
which  has  already  been  discussed,  is  produced.  Syphilitic  ulcerations  with 
cicatricial  stenosis  may  also  occur  in  the  upper  portions  of  the  large  intestine, 
and,  exceptionally  perhaps,  also  in  the  small  intestine.  Typhoid  ulcers  only 
very  rarely  lead  to  cicatricial  stenosis.  Somewhat  more  frequent,  it  is  said, 
are  decubital  ulcers  that  arise  in  the  rectum  from  impacted  feces,  followed 
by  cicatrix  formation.  Lastly,  in  isolated  cases,  injuries  of  the  abdominal 
wall  have  been  held  responsible  for  causing  a  necrosis  of  a  circumscribed 
portion  of  the  intestine  with  subsequent  ulcerative  and  cicatricial  stenosis. 
Stenosis  of  the  duodenum  after  the  healing  of  a  duodenal  ulcer  {vide  supra) 
resembles,  in  its  clinical  symptoms,  stenosis  of  the  pylorus,  and  not  stenosis 
of  the  intestines. 

3.  Intestinal  Obstruction. — The  most  frequent  form  of  intestinal  obstruc- 
tion comes  from  the  impaction  of  feces.  From  the  different  conditions  which 
cause  enfeeblement  of  the  peristaltic  movements,  an  accumulation  of  feces 
(coprostasis)  may  arise,  especially  in  the  colon.  This  accumulation  gradually 
but  constantly  increases  until  it  leads  to  well-marked  symptoms  of  intestinal 
obstruction,  and  in  cases  of  obstruction  from  other  anatomical  causes,  fecal 
impaction  not  infrequently  aggravates  the  condition. 

We  see  obstruction  of  the  intestines  from  other  causes  much  less  frequently 
than  from  impaction  of  feces.     In  some  cases  impacted  gallstones  have  been 


616  DISEASES   OF  THE   DIGESTIVE   ORGANS 

found,  especially  in  the  lower  part  of  the  ileum  and  in  the  neighborhood  of 
the  ileocascal  valve,  almost  completely  stopping  up  the  lumen  of  the  intestine. 
Genuine  intestinal  calculi  (composed  of  phosphates)  may  exceptionally  lead 
to  obstruction.  Likewise,  occasionally  conglomerations  have  been  found, 
composed  of  indigestible  portions  of  food,  vegetable  fibers,  the  seeds  of  fruit, 
potato  skins,  grape  skins,  and  also  clumps  of  roundworms.  We  must  also 
mention  here  the  very  rare  cases  in  which  a  large  foreign  body  has  been  swal- 
lowed and  wedged  itself  into  some  part  of  the  intestine.  Such  a  thing  has 
been  seen,  especially  in  children  and  among  the  insane. 

4.  Intestinal  Constriction. — Although  the  mechanism  of  intestinal  con- 
striction in  external  hernias  lies  in  the  domain  of  surgery,  we  must  mention 
here  the  chief  causes  of  the  so-called  internal  intestinal  constriction  (internal 
incarceration  or  strangulation).  In  the  abdominal  cavity  pouches  and  diver- 
ticula of  the  peritoneum  are  found,  as  either  normal  or  abnormal  formations,  in 
which  single  loops  of  intestine  may  be  caught  and  constricted.  The  duodeno- 
jejunal hernia — the  so-called  Treitz's  retroperitoneal  hernia — is  worthy  of 
special  mention,  and  comes  from  the  entrance  of  a  loop  of  intestine  into  the 
duodeno-jejunal  fossa.  This  hernia  may  become  very  large.  It  is  sometimes 
found  by  accident  in  the  cadaver,  not  having  caused  any  symptoms  during 
life,  but  in  rare  cases  it  may  be  the  cause  of  acute  internal  constriction.  We 
must  also  mention  the  hernia  of  the  omental  bursa — where  a  loop  of  intestine 
passes  through  the  foramen  of  Winslow — the  intersigmoid  hernia,  the  sub- 
cecal hernia,  etc.  Diaphragmatic  hernia  is  of  greater  practical  significance 
because  it  is  somewhat  commoner.  By  this  name  we  designate  both  genuine 
protrusions  into  the  diaphragm  and  also  the  passage  of  abdominal  viscera 
through  congenital  or  acquired  (traumatic)  defects  in  the  diaphragm.  These 
hernias  may  exist  without  symptoms,  or  at  least  without  causing  any  signs 
of  severe  disease,  but  in  some  cases  they  cause  obstruction  by  constricting  or 
twisting  a  dislocated  loop  of  intestine. 

Those  cases  in  which  abnormal  slits  and  holes  in  the  omentum  or  mesen- 
tery give  rise  to  internal  constriction  are  to  be  added  to  the  list  of  the  internal 
hernias.  Finally,  abnormal  cords,  membranes,  and  false  ligaments  in  the 
abdominal  cavity  are  a  comparatively  frequent  cause  of  internal  constriction. 
Such  cords  and  bands  are  sometimes  left  as  the  results  of  a  former  perito- 
nitis, and  may  cause  constriction  or  kinks  of  single  loops  of  intestine.  Small 
diverticula  of  the  colon  sometimes  form  adhesions  due  to  localized  peritonitis, 
as  we  have  ourselves  seen,  and  thus  occasion  dangerous  intestinal  stenosis. 
One  such  false  ligament,  which  must  be  specially  mentioned,  is  found  as  a 
prolongation  of  Meckel's  diverticulum.  By  this  we  mean  that  diverticulum 
which  must  be  regarded  as  the  remains  of  the  omphalo-mesenteric  duct,  still 
persisting,  which  has  its  seat,  corresponding  to  the  duct,  from  half  a  meter 
to  a  meter  above  the  ileocascal  valve.  A  firm  cord  sometimes  arises  from 
the  free  end  of  this  diverticulum,  the  obliterated  omphalo-mesenteric  vein, 
which  adheres  to  some  part  of  the  internal  abdominal  wall  and  may  cause 
constriction  of  the  intestine.  Adhesion  of  the  free  end  of  the  vermiform 
appendix  has  been  the  cause  of  internal  constriction  in  some  cases. 

5.  Tivists  (Volvulus)  and  Knots  of  the  Intestine. — Twists  about  the 
mesenteric  axis  and  complete  constriction  of  a  portion  of  intestine  from  this 
cause  are  seen  most  frequently  in  the  sigmoid  flexure,  especially  if  the  mesen- 


STRICTURE  AND   OBSTRUCTION   OF  THE   INTESTINES  617 

tery.  of  the  flexure  is  unusually  narrow  congenitally.  The  spontaneous  cor- 
rection of  this  abnormal  condition  is  hindered  hy  the  weight  of  the  loops  of 
intestine  filled,  with  gas  and  masses  of  feces,  and  by  other  portions  of  intestine 
lying  on  the  place  of  twisting.  Sometimes  other  portions  of  intestine  wind 
themselves  several  times  about  the  pedicle  of  the  twisted  loop  so  as  to  form 
a  regular  knot.  Such  twistings  have  been  seen  especially  between  the  sig- 
moid flexure  and  a  portion  of  the  ileum.  External  injury  sometimes  gives 
rise  to  the  formation  of  a  knot.  In  some  cases  abnormally  great  peristalsis, 
severe  diarrhea,  precedes  the  appearance  of  obstruction.  Volvulus  of  the 
small  intestine  is  very  rare,  but  we  ourselves  have  observed  a  fatal  case  of 
volvulus  in  the  highest  part  of  the  small  intestine,  consequent  upon  violent 
vomiting,  excited  by  a  remedy  administered  by  a  quack  for  tapeworm. 

6.  Invagination  of  the  Intestine  (Intussusception). — If  a  portion  of  in- 
testine is  pushed  into  the  lumen  of  the  portion  that  lies  next  below,  we  term 
the  process  invagination.  The  cause  of  this  is  usually  assumed  to  be  a  diminu- 
tion or  a  complete  absence  of  peristalsis  in  a  circumscribed  portion  of  intes- 
tine. If  now  there  are  energetic  movements  in  the  portion  immediately 
above,  they  push  this  into  the  paralyzed  portion.  According  to  Xothnagel, 
the  beginning  of  the  invagination  is  a  spastic  contraction  of  a  limited  por- 
tion of  the  intestine,  in  the  shape  of  a  ring.  This  furnishes  a  fixed  point, 
and  the  contractions  of  the  longitudinal  muscles  of  the  intestine  below  the 
constricted  area  are  said  to  draw  the  lower  portion  of  the  intestine  upward 
over  this  ring. 

In  the  post-mortem  examinations  of  children  we  frequently  find  intussus- 
ception of  the  ileum  which  has  occurred  shortly  before  death,  and  so  is  of  no 
clinical  importance.  Sometimes  intussusception  has  occasioned  the  most 
severe  symptoms  of  intestinal  obstruction.  It  occurs  particularly  in  children 
up  to  the  tenth  year,  and  it  may  be  of  sudden  onset,  without  any  apparent 
cause.  Intussusception  of  this  sort,  which  often  involves  a  considerable  ex- 
tent of  the  intestine,  may  have  its  seat  at  almost  any  part  of  the  bowels. 
The  intussusception  most  frequently  involves  the  cascum  and  the  lowest  part 
of  the  ileum,  pushing  thence  into  the  colon  (invaginatio  ileoccecalis)  ;  intus- 
susception of  this  sort  may  be  so  extensive  in  children  that  the  invaginated 
ileum  reaches  into  the  rectum,  or  even  projects  from  the  anus.  There  are 
cases  in  which  the  ileum  alone  is  involved,  and  less  frequently  the  colon  alone. 
The  invaginated  portion  of  intestine  usually  suffers  compression  of  its  blood 
vessels,  particularly  the  veins.  This  is  followed  by  inflammation  of  the  con- 
stricted portion,  and  the  inflammation  often  extends  to  the  peritoneum.  Not 
infrequently  there  is  gangrene  of  the  inner  portion  of  the  intestine,  as  a 
result  of  strangulation  of  the  afferent  vessels.  The  necrotic  portions  may 
slough  off  and  be  discharged  at  stool.  Such  an  occurrence  has,  in  a  few  re- 
corded cases,  led  to  spontaneous  recovery  from  the  intussusception  and  from 
the  obstruction  which  it  had  caused. 

We  must  mention  intestinal  polypi  as  a  special  cause  of  intussusception,  as 
they  gradually  pull  that  portion  of  the  intestine  in  which  they  are  situated 
into  the  neighboring  portion  next  below  by  their  weight.  This  has  been  re- 
peatedly observed. 

7.  Compression  of  the  Intestine  from  Without. — Compression  of  the  in- 
testine, by  tumors  of  the  uterus,   ovarian   cysts,   pelvic   abscesses,   omental 


618  DISEASES  OF   THE   DIGESTIVE   ORGANS 

tumors,  etc.,  has  been  met  with  in  rare  cases  as  a  cause  of  intestinal  stenosis. 
The  symptoms  of  stricture  in  such  cases  develop  either  very  gradually  or 
sometimes  rather  suddenly. 

Some  general  pathological  and  pathologico-anatomical  conditions,  which 
must  be  considered  in  judging  all  the  different  varieties  of  intestinal  obstruc- 
tion, have  yet  to  be  discussed. 

We  desire  to  emphasize,  in  the  first  place,  that  not  every  interference  with 
the  propulsion  of  the  intestinal  contents  is  necessarily  due  to  some  mechanical 
obstruction.  Paralysis  of  the  intestinal  musculature  must  also  produce  the 
same  result,  and  thus  we  distinguish  between  "  a  mechanical  ileus  " — i.  e.,  in- 
testinal obstruction  due  to  an  organic  intestinal  constriction  and  a  "  paralytic 
or  dynamic  ileus."  Paralytic  ileus  is  observed  most  frequently  in  peritonitis 
(q.  v.).  By  an  extension  of  the  inflammatory  processes  from  the  serosa  to  the 
muscularis,  or  perhaps  also  through  the  toxic  action  of  the  chemical  products 
of  inflammation  on  the  muscle  fibers,  a  paralytic  condition  of  the  intestinal 
musculature,  with  all  its  sequelae,  is  not  infrequently  produced.  But  condi- 
tions of  this  kind,  which  cannot  be  readily  explained,  also  arise  from  severe 
injuries  of  the  abdominal  wall,  and  occasionally  after  laparotomies  and  her- 
niotomies, as  well  as  after  severe  gallstone  and  renal  colics.  The  natural 
thought  is  of  a  reflex  inhibition  of  the  intestinal  peristalsis.  The  rarer  cases 
of  paralytic  ileus  observed  after  embolism  of  the  mesenteric  artery  are  more 
easily  understood.  In  addition  to  the  paralytic  ileus,  we  also  speak  of  a 
spastic  ileus  (in  hysteria,  lead  poisoning)  ;  but  one  must  be  very  careful  in 
the  interpretation  of  such  conditions. 

True  mechanical  ileus  is  also  divided  into  two  important  groups — the 
simple  obturation,  or  occlusion  ileus,  and  the  strangulation  ileus.  The  im- 
portance of  this  distinction  depends  on  the  fact  that  the  condition  of  the 
intestinal  wall  is  entirely  different  in  these  two  forms  of  intestinal  obstruction. 
In  occlusion  of  the  intestine  (from  coprostasis,  gallstones,  etc.)  the  nutrition 
of  the  intestinal  wall  is  not  primarily  affected,  whereas  in  strangulation,  by 
•compression  of  the  afferent  and  efferent  blood  vessels,  an  arterial  anaemia,  or 
venous  hyperaemia,  is  produced  in  the  strangulated  (or  invaginated)  piece  of 
gut.  In  this  way  the  nutrition  of  the  intestine  is  disturbed.  The  intestine 
becomes  permeable  to  bacteria,  it  is  distended  with  gas,  and  may  finally  be- 
come necrotic  and  gangrenous  (vide  infra). 

The  condition  of  the  intestine  above  the  constricted  portion  deserves  par- 
ticular attention.  The  coils  of  intestine  above  this  part  are  generally  dis- 
tended with  gas  and  accumulation  of  feces.  But  it  should  be  noted  that 
the  abundant  fluid  found  above  the  narrow  part  of  the  intestine  is  by  no  means 
due  exclusively  to  the  ingesta,  but  is  largely  the  result  of  transudation  and  the 
secretion  of  intestinal  juices.  The  intestinal  contents  are  very  apt  to  undergo 
putrid  decomposition.  This  gives  rise  to  a  large  amount  of  gas  which  may 
not  be  reabsorbed,  so  that  above  the  obstruction  there  is  apt  to  be  a  very 
marked  tympanites. 

In  simple  obturation  stenosis  the  meteorism  extends  almost  over  the  en- 
tire portion  of  intestine  situated  above  the  constricted  part  (meteorism  due 
to  back  pressure). 

In  stenosis  due  to  strangulation  (vide  supra),  however,  the  meteorism  is 


STRICTURE   AND   OBSTRUCTION    OF   THE   INTESTLV  619 

-confined  at  first  to  the  constricted  loop  of  intestine  with  impaired  circulation 
(local  meteorism ) .  The  local  meteorism  is  followed  only  later  hy  a  general 
passive  tympanitic  distention  of  the  intestines.  All  intestinal  coils  which  are 
tympanitically  distended  soon  suffer  marked  lesions  of  their  walls.  In  pas- 
sive meteorism  the  distention  of  the  abdominal  wall  and  the  associated  dis- 
turbance in  circulation  must  be  considered,  but  in  addition,  also,  the  irrita- 
tion of  the  decomposing  intestinal  contents,  as  well  as  the  purely  mechanical 
pressure  of  the  stagnating  fecal  masses.  With  local  meteorism,  the  circu- 
lation of  the  constricted  loop  of  intestine  is  interfered  with  from  the  start. 
We  can  therefore  readily  understand  that  inflammatory  changes,  which  may 
progress  to  diphtheria  and  circumscribed  necrosis,  set  in  above  the  stenosed 
por+ion,  and  also,  with  great  rapidity,  in  the  constricted  loop  of  intestine. 
Diseased  intestinal  walls  of  this  kind  are  abnormally  permeable  to  bacteria 
and  toxins,  even  if  no  actual  tear  or  perforation  has  occurred.  Pyogenic  bac- 
teria or  putrified  intestinal  contents  thus  pass  readily  into  the  abdominal 
cavity,  and  the  onset  of  a  severe  purulent  or  gangrenous  peritonitis  is  un- 
avoidable. This  is  why  acute  peritonitis  is  so  frequent  a  lesion  in  persons  who 
die  of  intestinal  obstruction. 

If  the  intestinal  stenosis  has  lasted  a  long  time,  we  usually  find  in  the 
upper  portion  of  the  intestine,  besides  the  signs  of  inflammation,  a  manifest 
hypertrophy  of  the  muscular  coat,  the  result  of  the  abnormally  active  peri- 
stalsis by  which  the  muscle  has  tried  to  overcome  the  obstacle.  The  intestine 
helow  the  constriction,  in  contrast  to  the  part  just  described,  appears  narrow, 
contracted,  and  empty. 

Clinical  History. — We  must  distinguish  the  cases  with  a  rapid,  complete 
obstruction  of  the  intestine  from  those  in  which  the  condition  develops  gradu- 
ally, and  where  there  is,  therefore,  at  least  for  a  time,  merely  a  constriction 
of  the  intestine. 

1.  Intestinal  Constriction. — The  first  symptom  of  intestinal  constrictions 
that  occur,  particularly  in  cancer  of  the  intestines  and  cicatricial  strictures, 
and  more  rarely  in  constrictions  from  chronic  peritoneal  adhesions  and  bands, 
or  from  compression  of  the  gut  from  without,  etc.,  are  disturbances  of  defeca- 
tion. The  bowels  are  costive,  they  move  only  at  long  intervals,  and  their 
motion  is  often  associated  with  pain  and  tenesmus.  In  the  description  of 
cancer  of  the  intestines  we  have  already  mentioned  that  the  feces  passed 
sometimes  have  a  peculiar,  flat,  compressed,  or  scybalous  form. 

But  since  stools  of  this  nature  also  occur  under  other  conditions  (obstinate 
chronic  constipation,  insufficient  nourishment),  and  may  occasionally  be  ab- 
sent in  cases  of  existing  stenosis,  their  diagnostic  significance  should  not  be 
overestimated. 

Blood  and  mucus  are  often  mixed  with  the  dejections  and  are  due  to 
the  character  of  the  primary  disease.  In  some  cases  there  is  no  constipa- 
tion, and  there  may  be  even  constant  diarrhea,  due  to  a  catarrh  of  the  in- 
testinal mucous  membrane  above  the  stenosis  (vide  supra).  We  can  easily 
understand  from  the  physiological  conditions  that  in  stenosis  of  the  small 
intestines,  whose  contents  have  an  approximately  fluid  consistence,  disturb- 
ances of  defecation  are  less  apt  to  take  place  than  in  stenosis  of  the  large  in- 
testine, where  the  fecal  masses  have  already  assumed  a  more  firm  consistence. 

Physical  examination  of  the  abdomen  often  gives  important  and  valuable 


620  DISEASES   OF  THE   DIGESTIVE   ORGANS 

information.  The  abdomen  is  usually  swollen  by  meteorism  (vide  supra). 
The  intensity  of  the  meteorism  varies  very  much  in  different  eases  and  at 
different  times  in  the  same  patient.  Meteorism  is  sometimes  absent,  especially 
in  stenosis  at  the  beginning  of  the  intestine.  There  may  then  be  gastrectasis. 
The  marked  peristaltic  movements,  plainly  visible  through  the  abdominal 
walls,  are  very  characteristic  of  most  intestinal  contractions.  The  contour 
of  single  loops  of  intestine  is  often  marked,  at  times  quite  sharply,  and  then 
we  can  sometimes  feel  the  thickened  intestinal  walls  through  the  lax  abdom- 
inal wall  (the  so-called  "intestinal  erection"  of  Nothnagel).  We  may  often 
decide  upon  the  seat  of  the  stenosis  from  the  location  and  course  of  the 
visible  peristaltic  movements.  In  general,  it  is  true  that  peristalsis  is  much 
more  noticeable  when  the  stenosis  is  in  the  small  intestine  than  when  it  is  in 
the  colon. 

In  most  cases  of  intestinal  stenosis  severe  colic  attacks  frequently  accom- 
pany the  visible  intestinal  contractions.  The  point  of  origin  of  the  pains,, 
at  least  in  many  cases,  corresponds  approximately  to  the  site  of  the  stenosis. 

If  we  put  our  ear  to  the  anterior  abdominal  wall  we  can  often  hear  many 
gurgling  and  splashing  noises,  which  sometimes  have  a  distinct  metallic  qual- 
ity. Eructations  are  frequent,  and  in  some  cases  there  is  occasional  vomiting. 
We  must  finally  state  that  we  have  been  repeatedly  struck  by  the  great  ex- 
tent and  strength  with  which  we  could  feel  the  pulsation  of  the  aorta  through 
the  swollen  loops  of  intestine. 

The  duration  of  all  these  symptoms  varies  with  the  nature  of  the  primary 
lesion.  Of  course  the  greatest  importance  attaches  to  the  condition  of  the 
muscular  layer  of  the  intestine  above  the  constricted  spot.  For  a  time  the 
muscle  may  overcome  the  obstruction  because  of  its  gradual  hypertrophy,  but 
at  last  the  muscular  coat  becomes  insufficient,  and  consequently  the  symp- 
toms become  more  severe.  This  explains  why  the  symptoms  of  intestinal 
stenosis  change  gradually  or  suddeiily  into  those  of  complete  intestinal  ob- 
struction. With  this  change  we  have  grave  symptoms.  Sometimes,  in  cases 
of  chronic  stenosis  of  the  intestine,  some  temporary  causes  may  occasion  re- 
peated attacks  of  intestinal  obstruction,  which,  however,  are  relieved  and  give 
place  again  to  the  milder  symptoms  of  mere  stenosis. 

2.  Intestinal  Obstruction. — The  symptoms  of  intestinal  obstruction  (ileus 
miserere)  either  develop  gradually  from  the  preceding  symptoms  of  intestinal 
constriction,  or  occur  at  the  outset  in  all  their  menacing  severity.  But  here, 
also,  there  are  many  variations,  according  to  the  nature  of  the  morbid  process 
which  is  the  cause  of  the  intestinal  obstruction.  For  the  present  we  will  dis- 
regard ileus  following  a  preceding  peritonitis  (paralytic  ileus,  vide  supra)  ;  we 
can  then  divide  the  remaining  varieties,  as  previously  stated,  into  two  main 
groups.  In  the  one  group  (obturation  or  occlusion  ileus)  we  have  to  deal  at 
first  more  with  a  mechanical  obstruction  of  the  lumen  of  the  intestines  and  its 
consequences,  while  at  first  the  intestinal  wall  itself  is  not  damaged  (at  least 
not  in  its  entirety ) .  To  this  category  belong  intestinal  occlusions  from  copros- 
tasis,  from  gallstones,  and  as  a  sequel  to  preceding  stenosis  caused  by  tumors 
and  cicatrized  ulcers,  from  compression  from  without,  etc.  The  second  group, 
on  the  other  hand,  is  designated  as  strangulation  ileus;  here  the  loop  of  intes- 
tine, which  is  either  squeezed,  twisted  about  its  pedicle,  or  incarcerated,  suffers 
a  grave  disturbance  in  its  circulation  from  the  very  start,  and,  in  consequence, 


STRICTURE  AND  OBSTRUCTION   OF  THE  INTESTINES  621 

soon  becomes  inflamed  and  permeable  to  bacteria  ami  their  toxins.  These  are 
the  cases  in  which  the  purely  mechanical  symptoms  of  intestinal  obstruction  arc- 
soon  followed  by  diffuse  septic  peritonitis. 

The  fully  developed  clinical  picture  of  ileus  generally  permits  us  to  recog- 
nize the  gravity  of  the  condition  at  a  glance.  The  face  of  the  patient  shoA 
well-marked  "  facies  abdominalis,"  the  eyes  and  cheeks  are  sunken,  the  nose  is 
pointed,  and  the  entire  face,  as  well  as  the  extremities,  cool  and  cyanosed.  The 
voice  is  feeble  and  weak,  but  the  intellect  is  perfectly  clear.  The  tongue  is  dry, 
respiration  is  difficult,  as  the  diaphragm  is  displaced  upward  the  pulse  becomes 
rapid  and  small,  and,  finally,  scarcely  perceptible.  The  temperature  is  usually 
subnormal,  but  elevations  of  temperature  may  occur  if  peritonitis  has  set  in. 
Movements  of  the  bowel  and  expulsion  of  gas  cease  entirely,  often  in  spite  of  a 
desire  to  defecate.  On  the  other  hand,  eructations  and  vomiting  soon  set  in. 
The  latter  may,  at  first,  be  a  simple  reflex  vomiting,  such  as  is  observed  particu- 
larly in  acute  strangulation.  If,  however,  the  intestinal  occlusion  lasts  for 
some  time,  the  vomiting  soon  assumes  a  fecal  character  ("  stercoraceous  vom- 
iting "),  which  is  quite  characteristic  of  ileus.  The  odor  of  the  vomitus  becomes 
more  and  more  foul  and  distinctly  fecal,  and  finally  completely  resembles  diar- 
rheal movements.  As  has  been  previously  mentioned,  we  are  dealing  here  with 
a  putrefaction  of  stagnating  intestinal  contents  above  the  site  of  obstruction. 
It  is  possible  that  these  masses  are  conveyed  upward  into  the  stomach  by  anti- 
peristalsis,  but  this  statement  is  disputed  by  many  observers.  In  the  main,  it 
appears  to  be  simply  a  damming  back  and  regurgitation,  practically  an  "  over- 
flow," of  the  filled  intestinal  loops,  into  the  stomach,  since  the  pylorus  grad- 
ually gives  way  to  the  increasing  distention  of  the  small  intestines. 

The  examination  of  the  abdomen  is  of  the  greatest  importance.  There  is 
generally  tympanitic  distention  of  the  abdomen,  but  the  meteorism  varies  some- 
what in  the  different  cases.  If  the  stenosis  is  situated  low  down  in  the  large 
intestine,  the  colon  becomes  distended  first.  Corresponding  to  its  anatomical 
position,  it  becomes  more  or  less  clearly  defined  as  a  thick,  long,  rounded 
prominence.  In  obstruction  of  the  small  intestine,  on  the  other  hand,  the 
meteorism  is  more  pronounced  in  the  middle  part  of  the  abdomen.  The  dis- 
tinction above  drawn  between  general  meteorism  from  stagnation  and  local- 
ized meteorism  is  of  especial  importance.  By  exact  comparative  palpation  dur- 
ing the  initial  stage  in  acute  strangulation  we  can  occasionally  locate  the  cir- 
cumscribed distention  of  the  strangulated  intestinal  loop.  This  inflated  and 
fixed  strangulated  coil  shows  no  peristalsis,  and  remains  entirely  immobile. 
Occasionally,  not  the  strangulated  loop,  but  the  one  situated  above  the  site  of 
strangulation,  becomes  prominent  through  a  damming  back  of  the  tympanitic 
distention.  Moderate  peristaltic  motions  and  "  erections "  can  be  produced 
in  it  by  slight  mechanical  stimuli.  The  distention  becomes  more  general  and 
more  pronounced  with  the  increase  in  the  symptoms,  until  finally,  with  the  on- 
set of  peritonitis,  general  paralysis  of  the  intestines  sets  in.  The  percutory  con- 
ditions depend  on  the  degree  of  gaseous  distention  of  the  intestines  and  the 
amount  of  exudation  that,  under  certain  conditions,  forms  in  the  abdominal 
cavity.  An  initial  severe  abdominal  pain  occurs  especially  in  acute  strangu- 
lation of  the  intestines.  Later  on  there  is  a  more  continuous  pain  or  else  acute 
exacerbations,  which  can  rarely  be  sharply  localized.  In  fatal  cases  the  pains 
frequently  cease  entirely  with  the  onset  of  general  intestinal  paralysis.     Pres- 


622  DISEASES   OF  THE   DIGESTIVE   ORGANS 

sure  on  the  abdomen  in  intestinal  obstruction  is,  as  a  rule,  not  painful;  it 
may  even  slightly  diminish  the  pain.  The  abdomen  becomes  very  tender  only 
after  peritonitis  has  set  in. 

The  excretion  of  urine,  especially  in  cases  of  obstruction  in  the  small  intes- 
tine, is  generally  diminished,  on  account  of  the  decreased  absorption  and  the 
general  desiccation  of  the  body,  through  the  exudation  into  the  intestine  or 
.  the  peritoneum.  Not  infrequently  the  scanty  urine  contains  albumen,  casts, 
and  blood  corpuscles.  The  increase  of  indican  x  in  the  urine  is  also  important. 
In  the  stagnating  intestinal  contents  above  the  stenosis  large  quantities  of 
indol,  phenol,  etc.,  are  produced  by  putrefaction  of  the  proteid  materials. 
Indol  is  excreted  as  indican.  Marked  indicanuria  is  found  principally  in  steno- 
sis of  the  small  intestine,  because  proteid  bodies,  capable  of  decomposition, 
generally  occur  only  in  small  amounts  in  the  large  intestine.  The  so-called 
Eosenbach's  reaction  (a  deep-red  coloration  with  a  violet  foam,  on  adding  nitric 
acid  drop  by  drop  to  the  boiling  urine)  is  also  occasionally  found  in  severe  cases 
of  intestinal  strangulation. 

The  general  course  and  duration  of  intestinal  obstruction  naturally  varies 
greatly  with  the  nature  of  the  underlying  morbid  process.  We  have  already 
emphasized  the  practically  important  distinction  between  intestinal  occlusion, 
which  generally  takes  a  slower  course,  and  only  later  on  gives  rise  to  the  grave 
clinical  picture  of  ileus  with  general  collapse  and  peritoneal  symptoms,  and  the 
clinical  picture  of  intestinal  strangulation,  which  much  more  rapidly  reaches  an 
alarming  degree  of  severity.  The  gravest  cases  may  end  fatally  in  two  to  three 
days.  The  duration  of  the  disease  is  generally  about  a  week.  In  cases  of  sim- 
ple obstruction,  or  those  which  develop  only  gradually  from  a  stenosis,  the 
duration  of  the  illness  may  be  very  much  more  prolonged.  The  danger  con- 
sists, above  all,  in  a  poisoning  of  the  body  through  absorption  of  the  products 
of  putrefaction  and  a  consequent  vasomotor  and  cardiac  paralysis,  and,  further- 
more, in  the  onset  of  secondary  peritonitis.  The  majority  of  the  serious  cases 
end  fatally. 

Aside  from  operative  interference,  recovery  may  ensue  even  after  the 
gravest  symptoms,  but  it  is  rare.  Cases  of  intestinal  obstruction  by  obturation 
.are  the  most  likely  to  recover.  Incarcerated  gallstones,  impacted  feces,  etc., 
may  be  discharged  with  a  subsidence  of  the  grave  symptoms.  The  possibility  of 
recovery  by  sloughing  off  of  the  gangrenous  internal  portion  of  intestine  in 
cases  of  invagination  has  already  been  alluded  to  above.  But  it  is  undoubtedly 
possible  that  cases  of  internal  strangulation  also  may  be  spontaneously  relieved 
so  long  as  no  serious  nutritive  disturbances  have  occurred  in  the  strangulated 
loop. 

As  soon  as  general  peritonitis  has  set  in  recovery  is  impossible.  However, 
on  account  of  the  difficulty  of  an  accurate  diagnosis,  the  prognosis  of  the  indi- 
vidual case  is  often  uncertain. 

Diagnosis.  Varieties  of  Intestinal  Obstruction. — To  go  into  details  as  to 
the  clinical  symptoms  of  all  the  separate  forms  of  intestinal  constriction  and 
obstruction  would  lead  merely  to  repetitions.     Our  judgment  of  each  case  is 

1  The  indican  test  is  performed  in  the  following  way:  We  mix  equal  volumes  of  urine  and 
officinal  hydrochloric  acid  (P.  G.),  and  then  add,  drop  by  drop,  a  concentrated  solution  of 
chlorid  of  lime.  If,  now,  chloroform  is  added,  upon  shaking  carefully  the  chloroform  will  take 
on  a  very  distinct  blue  color  if  the  urine  contains  any  considerable  amount  of  indican. 


STRICTURE   AND   OBSTRUCTION   OF  THE   INTESTINES  623 

based,  in  the  first  place,  on  a  very  careful  history,  which  often  furnishes  ma- 
terial diagnostic  aid  (gallstones  and  other  previous  diseases,  rapid  or  slow 
onset,  etc.).  In  the  objective  examination  that  then  follows,  all  external 
hernial  canals  are  examined  first  (inguinal  and  femoral  canals,  umbilicus). 
Thereupon  there  should  be  a  careful  inspection  and  palpation  of  the  abdomen, 
in  which  particular  attention  must  be  paid  to  a  circumscribed  distention  of 
individual  loops  of  intestine,  visible  peristalsis,  localized  points  of  tenderness, 
etc.    Finally,  rectal  and  vaginal  examination  should  never  be  omitted. 

Schematically  arranged,  the  distinction  between  obstruction  and  strangu- 
lation is  based  principally  on  the  following  points : 

OBSTRUCTION  STRANGULATION 

No  symptoms  of  collapse  at  first.  At  the  onset  grave  symptoms  of 

These    develop    only    later    on,    and      collapse  and  facies  abdominalis. 
gradually.     Pulse  remains  strong  for  Small  rapid  pulse, 

a  long  time.     Marked  pain  is  rare  at  Frequently    violent    initial    pain, 

the  onset.  which  continues. 

Vomiting    occurs    late     (overflow  Initial    (reflex)   vomiting.     Later 

vomiting).  on,  also  overflow  vomiting. 

Meteorism    becomes    rapidly    dif-  Localized  meteorism  at  first  in  the 

fuse.  strangulated  loop  of  intestine.    Later 

on,    also    meteorism    due    to    back 
pressure. 
Exudation    into    the    abdominal  Slight    exudation    into    the    ab- 

cavity  is  generally  absent.  dominal     cavity     frequently     occurs 

from   the   strangulated   piece   of   in- 
testine. 

With  regard  to  distinguishing  between  stenosis  of  the  colon  and  of  the 
small  intestine,  stenosis  of  the  small  intestine  is  indicated  by  a  special  prom- 
inence of  the  central  portion  of  the  abdomen,  by  the  visible  and  active  peristal- 
tic motion  of  many  coils  of  intestine,  by  the  occurrence  of  fecal  vomiting,  and 
by  the  presence  of  a  strong  reaction  of  indican  in  the  urine;  while  stenosis 
of  the  large  intestine  is  characterized  by  a  distention  which  corresponds  more 
with  the  course  of  the  colon,  without  much  visible  peristalsis,  and  a  slow  de- 
velopment of  severe  constitutional  symptoms.  In  a  few  cases,  inflation  of  the 
large  intestine  with  air  is  said  to  have  cleared  up  the  diagnosis  where  the 
stenosis  was  situated  low  down.  Important  data  are  occasionally  obtained  by 
X-ray  examination.  Certain  deductions  may  occasionally  be  made  from  the 
amount  of  fluid  which  can  be  introduced  into  the  rectum.  We  shall  recur  later 
to  the  differential  diagnosis  between  intestinal  obstruction  and  diffuse  peri- 
tonitis, when  considering  the  latter. 

Of  the  special  varieties  of  intestinal  obstruction,  we  will  call  attention  to 
three  as  of  practical  importance — viz.,  intussusception  in  children,  volvulus  of 
the  sigmoid  flexure,  and  fecal  impaction. 

Intussusception  appears,  as  we  have  indicated,  mainly  in  children  under 
ten  years.  Its  symptoms  usually  begin  rather  suddenly  with  violent  colicky, 
abdominal  pain.     There  soon  appear,  also,  liquid  dejections  of  bloody  mucus 


624 


DISEASES   OF   THE   DIGESTIVE   ORGANS 


ACUTE   INTESTINAL   OBSTRUCTION 

Chief  Common  Symptoms. — Sudden  pain,  intermittent  or  constant,  with  exacerbations;  tends 
to  become  constant  with  time.  Vomiting,  early,  severe,  becoming  feculent.  Constipation, 
more  or  less  absolute.     Abdominal  distention.     Shock. 


Strangulation  by  Bands  or 

through  Apertures    (25 
per    cent    of    all    cases    of 

Volvulus  of  Colon. 

Acute  Intussusception. 

acute  obstruction). 

Age  and  Sex.  .  . 

Young  adults;  rare  after 

Males  at  4  :  1 :  40  to  60. 

More    than    50    per  cent 

40. 

under  10  years. 

Previous  peritonitis  in  68 
per  cent;    previous   at- 
tacks of  obstruction  in 
12  per  cent. 

Previous  constipation. 

Usually  negative. 

Sudden  in  70  per  cent. 

Sudden. 

Sudden  in  75  per  cent. 

Pain 

Early,  severe,  continuous, 

Early,  less  severe,  inter- 

Early    and     severe;     in- 

mittent at  first,  becom- 

creasing and  later  sub- 

ing constant  with  ex- 

siding;   at    first    parox- 

Local Ten- 

acerbations. 

ysmal. 

DEBNESS 

Absent  at  first,  appears 

Early     over     distended 

Common  about  a  tumor. 

later. 

coil,  and  constant. 

Early,  marked;  in  60  per 

Less  early,   severe  and 

Still  less  early  and  severe ; 

cent  becomes  feculent; 

constant ;  often  affords 

in  25  per  cent  becomes 

affords  no  relief. 

relief. 

feculent. 

Constipation.  . 

Continuous  and  absolute  ; 

Early  and  absolute;  no 

Seldom     absolute ;     diar- 

no blood. 

blood. 

rhea  not  uncommon ; 
blood  in  80  per  cent. 

Prostkation.  .  . 

Marked. 

Rather  less  marked ;  may 
be  dyspnoea. 

Marked. 

Tenesmus 

Absent. 

In  15  per  cent. 

In  55  per  cent  and  often 

Abdominal 

early. 

Wall 

Flaccid  unless  peritonitis. 

Rigid   from   early  peri- 
tonitis. 

Flaccid  unless  peritonitis. 

Tumor 

Very  rare. 

Absent. 

In  50  per  cent;  invagina- 
tion sometimes  felt  in 
rectum. 

Meteorism.  .  .  . 

Slight,      appears     about 

Early,  rapid,  increases, 

Rare,  unless  marked  con- 

third day. 

and  is  extreme. 

stipation. 

N.  B. — No  trustworthy  conclusions  can  be  drawn  from  the  seat  of  the  pain  as  to  the  seat  of 
the  obstruction  unless  local  peritonitis  comes  on.  The  pain  is  usually  referred  in  all  forms  to 
the  region  of  the  navel.  In  complete  obstruction  the  pain  is  constant  though  with  exacerba- 
tions; intermittent  pain  shows  that  the  obstruction  is  partial.  Coils  of  intestine  are  not  visible 
through  the  abdominal  wall  in  acute  cases. 

or  almost  clear  blood,  originating  from  the  constricted  portion  of  the  intestine. 
Often  there  is  great  tenesmus  and  protrusion  of  the  anus.  We  have  already 
mentioned  that  sometimes  the  invaginated  portion  of  intestine  may  be  felt  in 
the  rectum.  The  sausage-like  tumor  of  the  invaginated  portion  of  intestine 
can  occasionally  be  felt  on  external  palpation  along  the  course  of  the  colon. 

The  further  course  corresponds  with  that  of  intestinal  obstruction,  except 
that  it  should  be  said  that  fecal  vomiting  generally  occurs  in  the  most  fre- 
quently observed  ileocecal  intussusception  only  comparatively  late  in  the  attack. 

Volvulus  of  the  sigmoid  flexure  generally  occurs  in  older  people  who  have 
previously  suffered  from  chronic  constipation.  The  onset  of  these  grave 
symptoms  is  very  sudden.  A  severe  pain  is  felt  in  the  left  iliac  fossa.  The 
visible  and  palpable  distended  intestinal  loop  extends  from  this  region  up- 
ward toward  the  diaphragm.  General  meteorism  soon  supervenes.  Small 
quantities  of  blood  are  occasionally  passed  by  rectum.  Stercoraceous  vomiting 
occurs  only  late,  if  at  all.  The  amount  of  fluid  which  can  be  introduced  into 
the  rectum  is  small.  The  remaining  symptoms  correspond  to  the  general 
picture  of  an  internal  strangulated  hernia. 


STRICTURE   AND   OBSTRUCTION   OF  THE   INTESTINES 


025 


CHRONIC    INTESTINAL   OBSTRUCTION 


Stricture  of  the  Small 

Stricture  of  the  Large 

Fecal  Accumulation. 

Gut. 

Gut. 

Age  and  Sex.  .  . 

Adults. 

Adults. 

Adults;  more  common  in 
females,  the  hysterical, 
the  insane,  hypochon- 
driacs. 

Cancer,  trauma,  tubercu- 

Cancer, trauma,  tuber- 

Previous constipation. 

losis;     disordered,     im- 

culosis, dysentery;  dis- 

perfect, irregular  action 

ordered,  imperfect,  ir- 

of bowels  from  time  to 

regular  action  of  bow- 

time, with  intervals  of 

els  from  time  to  time, 

comparative  ease. 

with  intervals  of  com- 
parative ease. 

Onset 

Gradual. 

Gradual. 

Gradual. 

Pain 

Intermittent. 

Intermittent. 

Less  prominent. 

Vomiting 

Late,     scanty,     feculent 

Less  prominent,   rarely 

Late,  scanty,  rarely  fecu- 

only    toward     end     of 

feculent    or    provoked 

lent,  often  absent. 

acute   attack;   may   be 

by  food. 

provoked  by  food. 

Constipation.  . 

May  alternate  with  diar- 

Form of  feces  may  be 

Gradually  increasing ;  may 

rhea;    blood    points  to 

altered;    blood   points 

be     spurious     diarrhea; 

cancer. 

to  cancer. 

no  blood. 

Tenesmus 

Absent. 

Often  present. 

Absent. 

Meteorism.  .  .  . 

Not  marked,  unless  acute 

Often  marked. 

Late;  generally  increases 

attack. 

with  obstruction. 

Tumor 

Only  in  cancer,  and  then 

Only  in  cancer,  and  then 

Common  and  distinctive; 

in  30  per  cent. 

in  40    per    cent;  may 

most  easily  felt  in   cae- 

be felt  in  rectum. 

cum;  little  or  no  ten- 
derness; sometimes 
movable,    and    can    be 

Coils  of  In- 

changed in  shape. 

testine  

Marked  in  proportion  to 

Marked  in  proportion  to 

Rarely  seen. 

emaciation. 

emaciation. 

N.  B. — In  any  form  of  chronic  obstruction,  the  symptoms  of  acute  occlusion  may  suddenly 
supervene. 

Lastly,  we  desire  to  mention,  as  of  practical  importance,  that  form  of  in- 
testinal obstruction  which  is  produced  by  the  accumulation  of  large  quantities 
of  old  fecal  masses  in  the  rectum.  We  sometimes  find  monstrous  accumula- 
tions of  feces  in  the  rectum,  especially  in  old  women  who  have  previously  suf- 
fered from  habitual  constipation,  or  in  whom  constipation  is  due  to  some  other 
affection.  Severe  symptoms  usually  come  on  quite  suddenly,  after  long-con- 
tinued mild  prodromal  symptoms,  and  these  severe  symptoms  are  much  like 
the  picture  of  internal  strangulation — severe,  sometimes  colicky,  abdominal 
pain,  great  tenderness  of  the  abdomen,  which  is  usually  swollen,  marked  gen- 
eral collapse,  loss  of  strength,  a  small  pulse,  an  outbreak  of  cold  sweat,  vomit- 
ing, etc.  If  we  try  to  give  an  enema  in  such  cases,  very  little  fluid  runs  into 
the  rectum.  On  introducing  the  finger,  it  usually  strikes  solidly  oh  old,  hard,' 
fecal  masses  above  the  sphincter,  and  there  is  often  nothing  left  but  to  under- 
take the  dirty  task  of  removing  at  least  a  part  of  the  scybala  with  our  own 
hands.  We  may  then  succeed,  by  repeated  enemata  and  by  giving  cathartics 
internally,  in  removing  sometimes  quite  an  incredible  amount  of  accumulated 
feces,  and  in  obtaining  thus  a  rapid  recovery  from  the  condition. 

The  diagnosis  of  the  nature  of  an  intestinal  obstruction  is  so  difficult  in 
many  cases,  and  yet  so  important  with  reference  to  treatment,  that  the  editor 
ventures  to  introduce  tables  of  differential  diagnosis  of  the  more  common  forms 
of  the  condition.  These  tables  are  based  upon  the  masterly  prize  essay  of 
Treves  of  London. 


626  DISEASES   OF  THE   DIGESTIVE   ORGANS 

Treatment. — As  soon  as  the  dangerous  signs  of  intestinal  obstruction  are 
recognized  by  the  physician,  his  first  duty  is  to  make  as  careful  an  examination 
(vide  supra)  as  possible,  so  as  to  determine  whether  the  obstruction  may  not 
be  within  the  reach  of  direct  treatment.  If  there  is  an  incarcerated  external 
hernia,  it  demands  special  surgical  treatment.  If  there  is  an  impaction  of 
gallstones,  or  intestinal  calculi,  or  foreign  bodies,  we  may  in  some  cases 
furnish  appropriate  assistance  by  the  cautious  use  of  laxatives.  The  treatment 
of  fecal  impaction  is  of  special  importance.  We  have  described  the  most 
frequent  form  of  this  in  detail  above.  As  has  already  been  said,  it  is  usually 
necessary  to  remove  at  least  a  part  of  the  feces  with  the  fingers,  or  some 
instrument  like  a  dressing  forceps  or  a  spoon.  In  the  second  place,  we  may 
use  large  enemata  of  pure  water,  or  soapsuds,  or  oil,  which  must  often  be 
repeated  four  or  five  times  a  day,  until  they  have  a  satisfactory  result.  These 
are  best  given  by  a  funnel  and  an  oesophageal  tube  ("  intestinal  tube  ")  intro- 
duced as  high  as  possible  into  the  intestine.  Cathartics  administered  inter- 
nally serve  as  aids,  especially  castor  oil,  senna,  saline  cathartics,  etc. 

In  stenosis  of  the  rectum  from  cicatrices  and  new  growths  we  can  also 
sometimes  employ  local  surgical  treatment.  The  treatment  of  fecal  accumu- 
lations usually  plays  an  important  part  here.  Finally,  the  cases  of  ileocecal 
invagination,  in  which  the  lower  end  of  the  invaginated  ileum  reaches  the 
rectum,  may  receive  local  treatment.  We  may  try  a  partial  replacement  by 
a  "  sponge  sound  "  (an  elastic  oesophageal  tube  to  the  end  of  which  a  sponge  is 
fastened).  Blowing  in  air  by  the  bellows  was  also  recommended  for  this 
purpose  by  the  old  physicians.  As  a  rule,  however,  we  use  here  large  enemata 
of  warm  water,  which  sometimes  seem  to  exert  a  favorable  meehanical  action. 

If  the  symptoms  of  a  more  or  less  chronic  constriction  of  the  intestinal 
lumen  exist,  the  treatment  consists,  at  first,  only  of  a  regulation  of  the  diet 
(a  fluid  or  soft  diet,  which  produces  only  little  fecal  matter),  mild  cathartics, 
and  the  occasional  administration  of  opium,  perhaps  with  belladonna,  where 
the  peristalsis  is  increased  and  painful.  Externally,  cold  packs  or  warm 
applications  are  generally  iised.  Above  all,  it  is  important  to  decide  the 
question  whether  an  operative  removal  of  the  obstruction,  or  at  least  pallia- 
tive surgical  treatment  (an  artificial  anus),  is  possible. 

In  acute  intestinal  obstruction  we  must  also,  first  of  all,  consider  whether 
timely  surgical  intervention  may  still  bring  relief.  The  more  the  symptoms, 
grave  from  the  onset,  point  to  an  acute  intestinal  obstruction,  the  more 
urgently  should  early  laparotomy  be  advocated.  If  the  symptoms  are  less 
fulminant,  and  the  general  condition  good,  expectant  treatment  may  be  pur- 
sued at  first.    But  here,  also,  we  must  caution  against  delaying  too  long. 

If  we  cannot  decide  on  an  operation,  or  if  the  latter  is  impossible,  internal 
symptomatic  treatment  of  the  ileus  is  then  in  order.  It  goes  without  saying 
that  the  patient  should  have  complete  physical  rest.  All  food  should,  if  pos- 
sible, be  entirely  forbidden.  The  torturing  thirst  may  be  relieved  by  bits  of  ice 
or  sips  of  cold  bitter  tea.  Formerly  when  there  was  obstruction  of  the  bowels, 
it  was  the  custom  to  make  trial  of  laxatives,  first  employing  milder  remedies, 
then  more  vigorous  drugs,  and  finally,  as  a  "  last  resort/'  metallic  mercury 
in  single  doses  of  from  5  to  10  ounces  (gm.  150  to  300),  which  is  sometimes 
claimed  to  act  mechanically  in  "  desperate  cases "  by  its  weight.  Except 
among  some  champions  of  mercury,  the  present  opinion  among  physicians 


STRICTURE   AND   OBSTRUCTION   OF  THE   INTESTIN]  627 

tends  far  more  to  the  belief  that  cathartics  are  usually  of  tin  service,  but  are 
often  directly  injurious  by  increasing  the  resistance.  Hence  we  have  at 
present  gone  over  to  the  treatment  of  severe  internal  incarcerations  with  large 
doses  of  opium  (20  drops  of  laudanum  or  2  to  3  gr.  [gm.  0.1  to  0.2]  of 
opium,  several  times  a  day).  It  is  often  very  advantageous  to  administer 
opium  in  suppositories  (ext.  opii,  gr.  j  to  ij  =  gm.  0.05  to  0.1).  Opium  acts 
favorably  on  the  patient's  pain,  the  vomiting  is  diminished,  and,  by  quieting 
the  peristalsis,  the  danger  of  increasing  the  stenosis  and  tearing  the  intestine 
is  also  lessened.  Sometimes  the  first  dejection  appears  during  the  adminis- 
tration of  opium.  Morphin  subcutaneously  injected  has  much  less  effect  upon 
the  intestine  than  opium;  its  employment  is  therefore  limited  to  cases  in 
which  pain  is  so  violent  as  to  demand  relief.  Objection  is  made  to  the  opium 
treatment,  not  without  some  justice,  that  by  lessening  the  pains  it  obscures 
the  gravity  of  the  disease.  This  objection  is,  however,  justified  only  if  opium 
is  used  without  strict  indications  and  haphazard.  Besides  opium,  atropin 
has  recently  been  repeatedly  strongly  recommended.  It  seems  doubtful  if  it 
is  efficacious  in  true  strangulative  ileus.  In  intestinal  obstruction,  and  per- 
haps also  in  the  paralytic  form  of  ileus,  its  usefulness  appears  to  be  more 
probable,  since  in  small  doses  (gr.  y|^-  to  -gV^  gm.  0.0005  to  0.001)  it  stimu- 
lates intestinal  peristalsis.  In  some  cases,  good  results  are  said  to  have  been 
obtained  only  after  larger  doses  (gr.  -^V^o   ^„  =  gm.  0.001  to  0.002). 

Although,  as  already  mentioned,  there  are  a  number  of  objections  to  the 
internal  use  of  cathartics,  we  may  try  large  enemata  in  many  cases.  The 
injections  must  be  given  cautiously  but  persistently,  and  they  must  be  often 
repeated.     They  sometimes  give  good  results  even  in  severe  cases. 

Instead  of  plain  water,  we  generally  use  soapsuds,  and  occasionally,  also, 
oil  injections.  Unpleasant  effects  have  been  reported  by  other  observers,  but 
we  ourselves  have  never  seen  any.  The  introduction  of  air  into  the  rectum, 
instead  of  water,  has  been  recommended  and  has  been  useful,  particularly 
when  the  obstruction  was  situated  low  down  and  was  the  result  of  a  kink  or 
some  similar  trouble.  The  employment  of  regular  gastric  lavage  (Kussmaul, 
Calm,  and  others)  is  very  beneficial  in  many  cases  of  fecal  vomiting;  if  this 
is  a  prominent  symptom,  the  stomach  should  be  washed  out  in  every  case. 
Large  amounts  of  feculent  liquid  are  frequently  removed  through  the  stomach 
tube,  and  it  is  easy  to  see  that  freeing  the  stomach  of  its  accumulations  may 
favor  a  more  vigorous  peristalsis.  Even  when  the  nature  of  the  intestinal 
obstruction  precludes  definitive  recovery,  lavage  usually  gives  no  inconsider- 
able relief. 

We  need  not  enter  into  details  as  to  the  general  treatment.  It  goes  without 
saying  that  the  patient's  strength  must  be  kept  up  as  much  as  possible,  and 
that  in  severe  stages  of  collapse  all  possible  stimulants  must  be  used,  such  as 
strophanthus,  camphor,  and  ether.  Local  applications  to  the  abdomen  are 
usually  ill  borne  on  account  of  the  tenderness.  Wet  compresses  may  be  tried, 
or,  what  is  still  better,  hot  moist  packs  applied  to  the  entire  abdomen.  Opium 
is  the  best  remedy  for  pain  and  vomiting,  as  already  stated,  but  it  must  often 
be  replaced  by  subcutaneous  injections  of  morphin.  In  cases  of  extreme 
gaseous  distention,  the  attempt  has  occasionally  been  made  to  puncture  the 
distended  intestinal  coils  with  a  Pravaz  syringe,  in  order  to  partially  evacuate 
the  gas.    This  method  appears,  however,  to  be  not  entirely  devoid  of  danger. 


628 


DISEASES   OF   THE   DIGESTIVE  ORGANS 


[The  safety  with  which  laparotomy  is  now  performed  has  stimulated  the 
study  of  all  affections  on  which  the  operation  has  any  bearing.  Internal 
strangulations  and  invaginations  may  be  relieved,  and  the  portion  of  intestine 
containing  a  noncancerous  stricture  can  be  excised.  An  early  operation  offers 
much  better  chances,  of  course.  In  these  da3rs  persons  should  not  be  allowed 
to  die  directly  from  intestinal  occlusion  without  an  attempt  being  made  to 
restore  the  permeability  of  the  canal  by  surgical  means.] 


CHAPTER    XII 

INTESTINAL    PARASITES 

(Helminthiasis) 


1.     TAPEWORMS 

Natural  History  of  the  Tapeworm. — Three  of  the  tapeworms  (cestodes) 
which  are  found  in  the  intestines  have  a  clinical  significance :  the  tcenia  solium, 
the  tcenia  mediocanellata,  and  the  bothriocephalus  latus. 

1.  The  tcenia  solium  is,  when  fully  developed,  2  or  3  meters  long.  Its 
head  (Figs.  74  and  75)  is  about  the  size  of  that  of  a  pin,  and  has  four 
projecting  cup-like  suckers,  and  in  front  a  beak  with  about  twenty-six  hooks. 
The  top  of  the  head  is,  as'  a  rule,  plainly  pigmented.  A  small  neck,  about 
an  inch  (2  to  3  cm.)  long,  is  attached  to  the  head,  and  then  follow  the  single 


Pig.  74.  —  (From  Hel- 
ler.) Head  of  tsenia 
solium. 


Fig.  75.— (From  Helleb.)      Head  of 
cysticereus  of  the  brain. 


Fig.  76.  —  (From  Hel- 
ler.) Taenia  solium. 
Mature  segment. 


"segments"  (proglottides)  of  the  tapeworm,  of  Avhich  the  youngest,  lying 
near  the  head,  are  still  very  small  and  short.  They  gradually  increase  in 
length  and  breadth,  and  at  about  a  meter  from  the  head  they  have  an  approx- 
imately quadrilateral  shape.  The  segments,  which  lie  farther  down,  and  which 
have  already  reached  puberty,  have  the  form  of  pumpkin  seeds,  and  are  -J  to  § 
of  an  inch  [9  or  10  mm.]  long  and  6  or  7  wide.  The  matrix  or  uterus  runs 
through  the  middle  of  each  mature  segment  (see  Fig.  76),  and  from  it,  on  each 
side,  go  seven  or  eight  side  branches,  which  ramify  like  a  tree.    On  one  side,  a 


INTESTINAL   PARASITES 


629 


little  below  the  middle,  lies  the  sexual  orifice  (Fig.  76,  a).  The  male  sexual 
organs  consist  of  a  number  of  little  clear  vesicles  in  the  anterior  portion  of  the 
segments.  The  thick-shelled  eggs  (Fig-  Vi,  '•'>)  develop  in  the  uterus,  and 
contain  an  embryo  with  six  booklets. 

The  taenia  solium  inhabits  the  small  intestines  of  man.     Its  head  clings  to 
the  mucous  membrane  so  tightly,  usually  at  some  point  in  the  upper  third 


1.  8.  7. 

Fig.  77. — Comparative  view  of  the  eggs  of  some  of  the  commoner  intestinal  parasites.  1.  Egg 
of  distoma  hepaticum.  2.  Distoma  laneeolatum.  3.  Taenia  solium.  4.  Taenia  medio- 
eanellata.  5.  Bothriocephalus  latus.  6.  Oxyuris  vermicularis.  7.  Trichocephalus  dis- 
par.    8.  Asearis  lumbricoides. 


of  the  small  intestine,  that  the  neck  is  often  torn  off  in  trying  to  loosen  the 
worm  from  the  intestinal  wall.  The  rest  of  the  worm,  which  is  in  part  in 
many  coils,  extends  to  the  lower  part  of  the  ileum,  but  only  exceptionally 
into  the  caecum.  From  the  lower  end  long  chains,  only  rarely  single  mature 
segments,  are  detached,  mix  with  the  contents  of  the  intestine,  and  are  passed 
with  the  feces,  together  with  some  of  the  eggs  from  the  uterus. 

The  further  development  of  the  eggs  of  the  taenia  solium  takes  place  in 
another  "  host,"  almost  alwa}rs  in  the  hog.  Hogs  are  infected  by  eating  feces, 
offal,  etc.,  containing  taenia  eggs.  The  thick  shell  of  the  eggs  is  dissolved 
in  the  hog's  stomach,  and  the  free  embryos  pierce  the  walls  of  the  stomach 
and  intestines  and  travel  with  the  blood  current,  or  through  the  tissues,  into 
the  different  organs,  especially  into  the  muscles.  Here  they  develop,  in  two 
or  three  months,  into  cysts  something  larger  than  a  pea,  from  whose  walls  a 
newly  developed  taenia  head  arises,  a  so-called  scolex  (nurse).  These  cysts 
are  termed  worm  cysts,  measles,  or  cysticerci  cellulosce.  They  live  from  three 
to  six  years;  then  they  die  and  become  calcified.  If  a  cysticercus  gets  into  a 
man's  stomach  from  his  eating  raw  or  imperfectly  cooked  ham  or  pork,  a  new 
and  complete  taenia  sprouts  from  the  scolex,  which  forms  mature  segments  in 
three  or  four  months. 

We  usually  find  only  one  tapeworm  in  a  man,  but  several  specimens 
have  been  seen  (as  many  as  seventeen)  at  the  same  time  in  the  same  intes- 
40 


630 


DISEASES  OF  THE  DIGESTIVE  ORGANS 


tine.  The  length  of  a  tapeworm's  life  is  not  certainly  known,  but  it  has 
happened  that  some  persons  have  lodged  the  same  tapeworm  for  ten  or  fif- 
teen years. 

Although  the  fully  developed  taenia  solium  is  seen  only  in  man,  as  we  have 
said,  the  cysticercus  cellulosae  has  been  found,  in  rare  cases,  in  dogs,  rats,  and 
monkeys,  etc.,  as  well  as  in  hogs.  It  is  a  particularly  important  fact  that  the 
cysticercus  cellulosse  itself  may  also  occur,  as  such,  in  man.  If  tapeworms  or 
mature  segments  get  into  a  man's  stomach  in  any  way,  probably  by  autoinfec- 
tion  by  the  finger,  etc.,  the  embryos  travel  into  other  organs.  Cysticerci  are 
often  found  in  men,  singly  or  in  groups,  especially  in  the  skin,  the  brain,  the 
eye,  and  the  muscles.  There  is  a  special  form  of  cysticercus  of  the  brain,  in 
which  we  find  a  whole  chain  of  cysts,  like  a  cluster  of  grapes,  but  sterile,  the 
so-called  cysticercus  racemosus. 

2.  The  taenia  mediocanellata,  or  taenia  sagnata  (from  saginare,  to  fatten),  is 
far  more  common  than  the  taenia  solium  in  many  parts  of  Germany.    It  is  longer 

than  the  taenia  solium,  being  about  10  to  13  feet  [3  or  4 
meters]  long,  and  its  individual  segments  are,  on  the 
whole,  broader  and  thicker.  The  head  (Fig.  78)  has  also 
four  prominent  cup-like  suckers,  but 
it  has  no  crown  of  hooklets.  The 
mature  segments  differ  from  the  pro- 
glottides of  taenia  solium,  in  that  the 
central  uterus  sends  off  many  more 
(twenty  to  thirty)  side  branches, 
which  divide  dichotomously,  and  not 
like  a  tree.  The  sexual  opening  is 
also  on  the  side  (Tig.  79,  a). 

The  life-history  of  the  taenia 
mediocanellata  is,  on  the  whole,  like 
that  of  the  taenia  solium.  The 
taenia  mediocanellata,  however, 
throws  off  single  mature  segments 
much  more  frequently  than  the 
taenia  solium.  These  segments  are 
found  in  the  feces,  and  here  they  often  exhibit  a  crawling  motion.  A  kindred 
fact  is  that  it  is  always  easy  to  find  large  numbers  of  tapeworm  eggs  in  the  feces 
of  individuals  who  harbor  the  taenia  mediocanellata.  This  is  usually  diffi- 
cult in  the  case  of  taenia  solium.  The  eggs  of  taenia  mediocanellata  and 
taenia  solium  are  very  similar  (vide  Fig.  77).  They  have  a  tough,  radially 
striated  shell,  and  in  both  varieties  the  six  hooks  of  the  embryo  can  be  seen 
in  the  interior.  The  cysticercus  of  taenia  mediocanellata  does  not  inhabit 
pork,  but  beef,  so  that  the  infection  of  man  by  this  tapeworm  comes  from 
eating  raw  beef.  In  man  the  cysticercus  of  taenia  mediocanellata,  which  is 
somewhat  smaller  than  the  cysticercus  cellulosae,  has  never  yet  been  observed. 

3.  The  bothriocephalus  latus  occurs  in  Holland,  Switzerland  (Geneva), 
Pomerania,  East  Prussia,  Hamburg,  and  Eussia  (the  German  Baltic  provinces). 
It  has  been  observed  in  middle  Germany  only  in  isolated  cases.  It  is  the  largest 
tapeworm ;  it  may  be  6  or  8  meters  long,  and  sometimes  has  over  4,000  joints. 
The  head  of  the  bothriocephalus   (Fig.  80)   consists  of  a  little  club-shaped 


Figs.  78  and  79. — (From  Heller.) 
Fig.  78. — Head  of  taenia  mediocanellata. 
Fig.  79. — Taenia  mediocanellata.     Mature  seg 
ment. 


INTESTINAL   PARASITES 


031 


Figs.  80  and  81. — (From  Heller.) 
Fig.  80. — Head  of  bothrioccphalus  latus. 

a.  Lateral  view,  enlarged.    6.  Natural 

size. 
Fig.  81. — Bothriocephalus  latus.    Mature 

segment. 


swelling,  with  two  slit-like  depressed  suckers  on  the  sides.  A  long,  thread-like 
neck  joins  the  head  to  the  youngest  segments.  The  full-grown  segments  (  Fig. 
81)  are  short,  but  are  distinguished  by  their  great  breadth.  The  largest 
segments  measure  in  length  about  £  to  £ 
in.  [3  or  4  mm.],  and  in  breadth  §  to  \ 
in.  [10  or  12  mm.],  but  the  last  joints 
are  longer  and  are  not  so  broad,  so 
that  they  have  an  approximately  quadri- 
lateral form.  The  uterus  consists  of  a 
very  tortuous  canal  in  the  center.  The 
sexual  orifice  does  not  lie  on  one  side,  as 
in  the  taenia,  but  in  the  middle  of  the  ab- 
dominal surface,  nearer  the  anterior  bor- 
der of  the  segment  than  the  posterior. 
The  eggs  (vide  supra,  Fig.  77,  5)  are  of 
an  oval  form,  and  have  a  hood-shaped  lid 
at  one  end.  They  are  to  be  found  in  al- 
most every  dejection  of  persons  affected 
with  a  bothriocephalus.  Single  joints  of 
the   tapeworm   are   not   passed   with   the 

stools,  but  portions  of  the  worm,  several  feet  long,  come  away  from  time  to 
time,  especially  in  the  spring  and  autumn. 

The  eggs  develop  only  in  fresh  water.  The  embryo  (Fig.  82),  which  is 
formed  in  them  in  a  few  months,  and  is  provided  with  six  hooklets  and  with 
vibrating  cilia,  is  swallowed  by  fishes  (chiefly  pike  and  eel-pouts,  according  to 

Braun,  salmon,  according  to  Kuchennieister), 
and  develops  in  their  muscles  and  internal 
organs  into  cysticerci.  The  infection  of  man 
with  bothriocephalus  comes  from  eating  such 
fish  containing  cysticerci. 

[In  the  United  States,  the  taenia  solium  is 
sometimes  seen,  the  taenia  mediocanellata  is 
common,  and  the  bothriocephalus  is  practically 
confined  to  immigrants.] 

4.  These  three  kinds  of  tapeworms  that 
have  been  enumerated  are  the  most  important, 
but  we  will  briefly  mention  the  tcenia  nana  and 
the  tarnia  cucumerina  (taenia  elliptica).  The 
first  of  these,  the  taenia  nana  [dwarf],  is  the 
smallest  tapeworm,  being  only  §  to  §  in.  [1  to 
1.5  cm.]  long.  The  long  head  is  provided  with  four  suckers  and  a  circlet 
of  hooks  which  can  be  extended  far  out.  The  anterior  joints  are  very  narrow 
and  short,  those  farther  back  broadening  not  inconsiderably.  The  taenia  nana 
is  very  frequent  in  Italy  and  also  in  Sicily.  In  Germany  it  has  been  seen 
only  exceptionally.  Its  cysticercus  is  said  to  inhabit  snails.  It  is  seen  es- 
pecially in  children,  and  in  them  sometimes  in  very  great  numbers.  Single 
joints  are  difficult  to  find  in  the  dejecta,  but  the  discovery  of  its  eggs  with 
the  microscope  is  very  easy.  The  expulsion  of  the  worm  by  means  of  san- 
tonin and  thymol  (vide  infra)  is  usually  a  simple  matter. 


Fig.  82. —  Embryo  of  bothrio- 
cephalus latus,  with  its  ciliated 
coat.     (Leuckakt.) 


632  DISEASES   OF  THE   DIGESTIVE   ORGANS 

The  taenia  cucumerina  is  8  to  10  in.  [20  to  25  cm.]  long.  Its  posterior 
joints  are  6  to  8  mm.  long,  but  have  a  width  of  only  1  mm.  The  head  is  pro- 
vided with  many  hooklets ;  the  beak  can  be  extended  and  retracted.  The  taenia 
cucumerina  occurs  especially  in  children.    Its  cysticercus  is  found  in  the  dog. 

Symptoms  and  Diagnosis. — In  many  cases  tapeworms  are  lodged  in  the  in- 
testines without  causing  any  morbid  symptoms.  We  can  recognize  their  pres- 
ence only  by  occasionally  finding  the  segments  in  the  dejections. 

In  other  cases,  however,  tapeworms  cause  a  list  of  disturbances  which  are 
often  exaggerated  by  anxious,  hypochondriacal,  and  nervous  persons,  but  which 
ought  not  to  be  too  little  regarded.  The  symptoms  are  referred  chiefly  to  the 
intestinal  canal.  Sometimes  there  is  quite  severe  abdominal  pain,  which  may 
assume  a  colicky  character.  The  patient  also  frequently  complains  of  irregu- 
larity of  the  bowels,  and  of  occasional  diarrhea,  which  alternates  with  consti- 
pation. Many  general  symptoms  are  also  added  to  those  mentioned — loss  of 
appetite,  or  at  times  marked  veracity,  general  languor,  disinclination  to  work, 
mental  disturbance,  depression,  etc.  Often  the  general  nutrition  is  considerably 
impaired. 

There  are  also  certain  symptoms  to  be  mentioned  which  were  formerly  ex- 
plained as  "  reflex."  Still,  it  is  much  more  probable  that  poisonous  matter  may 
be  produced  by  the  tapeworms  under  certain  circumstances,  about  which  we  do 
not  yet  have  accurate  knowledge,  and  that  these  poisons  occasion  some  of  the 
symptoms  of  tapeworm  (vide  infra).  Among  these  we  sometimes  see  marked 
salivation,  tickling  in  the  nose,  dilatation  of  the  pupils,  palpitation,  vomiting, 
headache  (migraine),  etc.  In  some  cases  even  severe  spasms  and  choreic  condi- 
tions have  been  referred  to  the  presence  of  tapeworms  (particularly  the  taenia 
nana)  in  the  intestinal  canal,  but  it  is  hard  to  decide  how  far  such  a  supposed 
connection  can  really  be  regarded  as  justified. 

The  peculiar  fact  that  nearly  all  cases  of  helminthiasis  lead  to  a  marked 
eosinophilia  (increase  of  the  eosinophil  leucocytes)  of  the  blood,  must  also  be 
referred  to  the  production  of  certain  substances. 

Thus,  in  most  cases  tapeworms  cause  comparatively  little  disturbance,  but 
they  may  occasion  severe  illness.  It  must  especially  be  pointed  out  that  when 
the  bothricephalus  latus,  or  exceptionally  a  taenia,  is  present  in  the  intestines 
there  will  often  be  an  extremely  severe  anaemia,  quite  like  pernicious  anaemia 
(q.  v.).  The  patient  becomes  excessively  pale  and  feeble,  the  blood  shows 
marked  oligocythemia  and  poikilocytosis ;  there  are  anaemic  cardiac  murmurs 
and  similar  symptoms.  This  condition  also  is  probably  referable  to  poisonous 
matter  produced  by  the  bothriocephalus  latus,  absorbed,  by  the  intestines,  and 
fatal  to  the  red  blood  corpuscles.  If  the  tapeworm  is  promptly  expelled  there 
is  rapid  and  complete  recovery. 

Although  many  of  the  symptoms  mentioned  may  arouse  suspicion  as  to  the 
presence  of  a  tapeworm,  the  diagnosis  can  be  made  only  by  finding  the  joints 
or  eggs  of  the  tapeworm  in  the  dejections.  In  many  cases  the  patient  himself 
brings  some  of  the  segments  found  by  him  in  the  dejections  to  the  physician, 
but  in  judging  of  them  a  certain  caution  is  always  necessary,  since  shreds  of 
mucus,  remains  of  food,  etc.,  are  quite  frequently  presented  to  the  physician, 
under  the  idea  that  they  are  segments  of  tapeworm.  But,  on  the  other  hand, 
it  is  also  very  important  that  the  physician  himself  should  not  forget  the  pos- 
sibility of  a  tapeworm  and  should  himself  direct  attention  in  suspicious,  cases 


INTESTINAL  PARASITES  633 

to  the  dejections  of  the  patient.  If  there  is  a  taenia  mediocanellata  or  a  bothrio- 
cephalus  latus,  it  is  usually  easy  to  find  the  eggs  in  the  feces,  but  in  the  case 
of  taenia  solium  this  is  more  difficult.  With  taenia  solium  we  usually  have  to 
search  for  segments  of  the  tapeworm  in  the  stools.  Many  patients  with  all 
sorts  of  indefinite,  mild,  gastric  and  intestinal  symptoms,  or  such  general  symp- 
toms as  headache  or  languor,  or  even  graver  disturbances,  such  as  apparent 
pernicious  anaemia,  are  finally  cured  when  the  true  cause  of  the  disease  is  found 
to  be  a  tapeworm. 

If  we  obtain  a  few  joints  of  the  tapeworm  we  should  endeavor  to  determine 
from  them  the  species.  If  we  spread  out  the  pieces  of  tapeworm  between  two 
microscopic  slides,  the  thicker,  fatter  segments  of  the  taenia  mediocanellatu, 
with  its  many-branched  uterus,  may  usually  be  distinguished  without  difficulty 
from  the  more  tender  and  more  translucent  segments  of  the  taenia  solium,  with 
a  smaller  number  of  lateral  branches  to  its  sexual  apparatus.  The  statement  of 
many  patients  that  single  segments  of  tapeworm  come  from  them  at  other  times 
than  when  at  stool,  and  that  they  find  them  on  their  underclothing,  almost 
always  points  to  the  presence  of  a  taenia  mediocanellata  in  the  intestine.  The 
eggs  of  taenia  solium  and  taenia  saginata  are,  as  has  been  already  stated,  very 
similar  to  each  other,  while  it  is  easy  to  diagnosticate  the  bothriocephalus  latus 
by  its  eggs,  as  they  are  so  characteristic  (vide  supra,  Fig.  77). 

If  we  suspect  a  tapeworm,  without  having  secured  the  certain  evidence  of 
segments  or  eggs  in  the  dejection,  it  is  a  good  plan  to  give  the  patient  a  mild 
cathartic,  such  as  castor  oil,  or  a  dose  of  boiled  pumpkin  seeds,  since  after  this, 
if  the  intestine  harbors  a  tapeworm,  single  portions  of  it  often  come  away. 

Treatment. — The  "  tapeworm  cures,"  which  are  recommended  in  so  great 
a  number  that  we  can  by  no  means  mention  all  of  them  here,  but  only  the  most 
important  and  the  most  serviceable,  aim  at  killing  or  benumbing  the  worm, 
and  then  at  removing  it  from  the  intestine  in  toto  by  cathartics. 

We  usually  begin  with  a  so-called  "  preparatory  treatment."  This  is  to 
cleanse  the  intestine,  especially  the  large  intestine,  from  old  fecal  masses,  in 
order  to  prepare  as  free  a  passage  as  possible  for  the  worm.  For  this  purpose 
we  give  the  patient  a  mild  laxative,  or,  better  still,  a  large  enema  of  cold 
water.  Many  physicians  recommend  that  there  should  first  be  given  some 
active  purge,  such  as  calomel  or  castor  oil,  but  this  is  exhausting  to  the  patient, 
and  we  believe  it  is  not  usually  necessary.  We  also  forbid  for  a  day  or  two  the 
use  of  vegetables,  black  bread,  etc.,  and  prescribe  instead  a  limited  diet  of 
white  bread,  some  meat,  milk,  and  coffee.  It  is  a  widespread  practice  to  take 
during  the  preparatory  treatment  certain  articles  of  food  to  "  make  the  worm 
ill."  Among  these  a  salad  of  finely  chopped  and  very  salt  herring  with  onions 
and  garlic  is  especially  recommended.  A  similar  action  is  also  ascribed  to 
strawberries,  cranberries,  and  bilberries.  Hence,  on  the  day,  and  especially  on 
the  afternoon,  before  treatment,  we  have  the  patient  take  a  large  amount  of  the 
articles  of  food  mentioned,  such  as  herring  salad. 

On  the  next  morning,  after  everything  has  been  prepared,  after  the  bowels 
have  moved  the  night  before,  etc.,  the  patient  takes  no  breakfast,  or  only  some 
strong  sweet  black  coffee,  and  then  he  takes  the  special  anthelmintic.  The 
number  of  taenicides  recommended  is,  as  we  have  said,  very  great.  At  present 
the  following  are  most  in  use:  Many  experienced  physicians  and  we  ourselves 
now  employ  almost  exclusively  the  ethereal  extract  of  male  fern  (oleoresina 


634  DISEASES  OF  THE  DIGESTIVE  ORGANS 

aspiclii).  It  is  true  that  the  reliability  of  this  drug  as  dispensed  by  different 
apothecaries  varies,  but  in  most  cases,  if  we  can  obtain  a  good  fresh  preparation, 
the  result  is  perfectly  satisfactory.  It  should  be  said,  however,  that  the  drug 
is  not  entirely  free  from  danger;  in  exceptional  cases  large  doses  have  caused 
symptoms  of  poisoning,  particularly  amaurosis,  also  jaundice;  and  even  death 
has  occurred.  We  should,  therefore,  hold  firmly  to  the  rule  of  never  exceeding 
a  dose  of  2.5  to  3  drachms  (gm.  10  to  12).  We  have  never  seen  unfortunate 
results  from  this  amount.  The  best  way  of  administering  the  drug  is  in  the 
gelatin  capsules  which  are  for  sale,  of  which  each  contains  15  to  30  gr.  (gm.  1 
to  2)  of  the  extract.  The  so-called  "  gelodurat  capsules"  (gelatin  capsules 
hardened  in  formalin),  suggested  by  the  chemist  H.  Eumpel,  which  contain 
gr.  xv  (gm.  1)  of  the  extract  of  male  fern,  and  only  dissolve  in  the  small 
intestine,  being  therefore  well  tolerated  by  the  stomach,  are  very  practical. 
As  a  rule,  eight  of  these  capsules  are  sufficient  for  a  complete  cure.  We  gen- 
erally refrain  from  administering  any  further  cathartic  (castor  oil).  It  is 
much  better  to  wait  quietly  and  see  whether  the  worm  is  not  passed  spontane- 
ously, or,  at  most,  after  a  few  hours  to  give  a  careful  rectal  irrigation,  which 
generally  brings  out  the  complete  worm  (i.  e.,  with  the  head) . 

The  other  tapeworm  remedies  which  were  formerly  used  are  at  present 
almost  entirely  displaced  by  the  extract  of  male  fern.  We  will  mention  also 
the  bark  of  the  pomegranate  root  (cortex  radicis  punicse  granati),  which  is 
given  after  maceration  of  120  to  150  parts  in  1,000  of  water,  subsequently 
reduced  to  150  parts  by  boiling),  the  very  efficacious  pelletierinum  tannicum 
(in  doses  of  gr.  vijss.  to  gr.  xxij  =  gm.  0.5  to  1.5)  obtained  from  pomegranate 
root,  the  flores  koso  (3  to  4  powders  of  gr.  Ixxv  =  gm.  5  in  white  wine), 
kamala,  etc.  Pumpkin  seeds  (semina  cucurbitse  maxima?),  which,  as  has  been 
previously  mentioned,  are  much  in  vogue  as  a  popular  remedy,  have  been  re- 
peatedly recommended  by  physicians,  particularly  as  they  do  not  share  the  bad 
taste  of  nearly  all  the  other  tapeworm  remedies.  About  120  seeds,  or  for  chil- 
dren half  as  many,  are  peeled,  pounded  up,  and  mixed  with  sugar,  or  else 
made  into  an  emulsion,  and  administered. 

The  treatment  is  to  be  regarded  as  absolutely  successful  only  when  we  find 
the  head  of  the  tapeworm,  as  well  as  its  segments,  in  the  patient's  dejections. 
We  may  best  search  for  the  head  in  the  feces  by  diluting  the  dejection  repeatedly 
with  water,  and  pouring  off  the  water.  The  tapeworm  then  remains  at  the 
bottom  of  the  vessel.  As  it  may  be  that  the  head  has  been  dislodged  even 
if  it  has  not  been  found,  we  should  not  repeat  the  treatment  for  tapeworm 
until,  some  months  later,  there  are  indubitable  signs  that  the  tapeworm  still 
exists. 

Every  tapeworm  treatment  is  rather  drastic,  and  hence  it  is  well,  after  the 
treatment  is  over,  to  recommend  the  patient  to  be  prudent  in  his  diet,  and  to 
be  careful  about  his  digestive  tract  for  some  time.  In  persons  who  are  very 
weak,  or  who  have  some  other  disease,  we  do  not  willingly  undertake  to  remove 
a  tapeworm  without  urgent  reasons ;  but  in  people  who  are  otherwise  healthy  it 
is  always  well  to  get  rid  of  a  tapeworm,  even  if  it  causes  no  severe  symptoms. 
The  chief  reason  for  this  is  that  taenia  solium  might  occasion  cysticerci  in  the 
brain.  The  best  time  for  undertaking  a  treatment  is  when  segments  or  large 
pieces  of  the  worm  come  away  quite  frequently  of  their  own  accord.  We  should 
never  prescribe  a  treatment  on  the  mere  statements  or  suspicions  of  the  patient. 


INTESTINAL   PARASITES 


035 


We  must  always  convince  ourselves  with  complete  certainty  of  the  presence  of  a 

tapeworm  in  the  intestine;. 

We  must  finally  mention  that  the  only  efficient  prophylaxis  against  acquir- 
ing a  tapeworm  lies  in  entirely  avoiding  the  use  of  raw  or  half-cooked  beef  or 
pork.  The  more  widely  spread  the  taking  of  raw  moat  is,  as  in  Abyssinia,  the 
more  common  are  tapeworms  in  man.  Certain  callings,  like  those  of  the 
cook  or  the  butcher,  are  also  especially  exposed 
to  infection. 


2.     ROUNDWORMS 

{Ascaris  lumbricoides) 

Natural  History. — Ascaridcs  are  pale  red- 
dish, cylindrical  worms,  pointed  at  both  ends, 
with  the  sexes  in  different  individuals.  The  fe- 
males are  12  to  16  in.  [30  or  40  cm.]  long,  the 
males  about  25.  At  the  cephalic  end  of  the  worm 
are  found  three  lips  furnished  with  fine  teeth. 
The  tail  is  straight  in  the  females 'and  curved  in 
the  males.  In  the  female  sexual  organs  (Fig.  83) 
60,000,000  of  eggs  may  develop,  at  a  rough  esti- 
mate. These  eggs  are  often  found  in  the  feces  of 
persons  who  have  roundworms  in  their  intestines 
(see  Fig.  77,  8).  They  have  a  great  capacity  of 
resisting  external  influences,  and  a  worm-like 
embryo  develops  in  them  in  about  nine  weeks. 
The  further  dissemination  of  roundworms  takes 
place  without  any  intermediate  host  in  this  man- 
ner: the  eggs  containing  the  embryo  worms  are, 
through  some  chance,  swallowed  and  then  grow 
in  the  intestines  into  sexually  mature  worms. 
Experimental  infection  with  the  eggs  of  round- 
worms gives  distinctly  positive  results  (Lutz, 
Epstein). 

The  roundworms  inhabit  chiefly  the  small  in- 
testine. In  severe  vomiting  they  often  reach 
the  stomach  and  are  vomited  up.  In  individual 
cases  they  have  been  found  in  the  bile  ducts,  in 
the  air-passages,  and,  after  perforation  of  the  in- 
testine, in  the  abdominal  cavity.  The  number  of 
roundworms  existing  at  the  same  time  in  the 
intestine  may  be  very  considerable.  We  find 
them  most  commonly  in  children  and  in  adults 
from  the  lower  classes.  Eound worms  have  been 
repeatedly  observed  to  crawl  out  of  the  anus, 
the  mouth,  or  the  nose  of  children  during 
sleep. 

The  roundworm  is  also  common  in  hogs  and 
cattle  as  well  as  in  man. 


Fig.  83. — (From  Heller.)  As- 
caris lumbricoides.  Female,  6 
in.  [143  mm.]  long.  a.  Vagina. 
b.  Intestine,  c.  Boundary  be- 
tween the  uterus  and  oviducts. 
d.  Longitudinal  bands,  e.  Coil 
of  oviducts  and  ovaries. 


636  DISEASES  OF   THE   DIGESTIVE   ORGANS 

Symptoms. — In  general,  roundworms  are  innocent  parasites,  which  may 
exist  in  large  numbers  in  the  intestines  without  any  bad  results.  In  other  cases 
they  cause  symptoms  similar  to  those  ascribed  to  taeniae — abdominal  pain,  lan- 
guor, itching  of  the  nose  and  skin,  urticaria,  burning  in  the  eyes,  salivation,  etc. 
— symptoms  which  are  all  ambiguous,  and  whose  definite  connection  with  the 
presence  of  roundworms  it  is  hard  to  make  out.  Occasionally  they  excite  long- 
continued  and  persistent  vomiting,  or  violent  diarrhea,  these  symptoms  persist- 
ing until  the  worms  are  expelled,  when  they  promptly  cease.  Leichtenstern 
found  that  it  was  not  very  exceptional  for  children  to  be  noticeably  anaemic  when 
harboring  ascarides,  and  to  improve  remarkably  when  the  worms  were  expelled. 

The  cases  recorded  in  literature  are  quite  numerous  in  which  severe  nervous 
symptoms  have  been  caused  by  roundworms  and  have  disappeared  after  the 
removal  of  the  parasites.  However  cautious  we  may  be  in  accepting  such  state- 
ments, nevertheless  their  credibility  cannot  be  wholly  denied.  We  would  men- 
tion especially  convulsions,  epileptiform  seizures,  choreic  and  cataleptic  condi- 
tions, contractures,  and  temporary  mental  disturbances,  which  are  claimed  to 
be  excited  by  ascarides.  It  is  said  that  children  with  ascarides  not  infrequently 
exhibit  mild  nervous  disturbances,  such  as  headache,  vertigo,  mydriasis,  and 
chills.  All  these  symptoms,  and  in  part  also  those  above  enumerated,  are  per- 
haps not  so  immediately  dependent  upon  the  presence  of  the  worms  in  the  intes- 
tinal canal,  but  are  due  rather  to  toxins  developed  under  certain  circumstances. 

In  some  cases  the  presence  of  ascarides  may  excite  much  more  severe  symp- 
toms by  unfortunate  accidents,  as,  for  example,  sudden  suffocation  from  the 
entrance  of  a  roundworm  into  the  larynx.  When  a  very  large  number  of  round- 
worms have  been  present  in  the  intestine,  severe  symptoms  of  intestinal  stenosis 
have  been  observed  from  their  rolling  together  into  a  ball.  If  a  roundworm 
crawls  into  the  bile  ducts,  it  may  give  rise  to  jaundice,  and  even  to  the  develop- 
ment of  an  abscess  of  the  liver.  In  the  abscesses  of  the  anterior  abdominal  wall, 
usually  termed  "  worm  abscesses,"  the  roundworms  probably  play  a  purely  acci- 
dental part.  We  have  to  do  in  such  cases  with  perityphlitic  abscesses  or  with 
inflamed  hernise,  which  have  perforated  externally,  by  which  the  roundworms 
which  are  accidentally  found  in  the  intestines  pass  out,  without  having  any 
causal  relation  to  the  abscess. 

Diagnosis. — The  diagnosis  of  roundworms  is  not  usually  difficult.  Often 
a  few  worms  appear  of  themselves,  or  as  the  result  of  a  simple  laxative.  If 
not,  search  must  be  made  in  the  dejections  for  the  eggs  of  the  ascarides. 
These  are  always  easily  found.  It  is  advisable  to  obtain  a  particle  of  the  con- 
tents of  the  rectum  for  the  purpose  of  microscopic  examination  by  introducing 
an  elastic  catheter. 

Treatment. — The  oldest  remedy  for  ascarides  is  wormseed — santonica. 
This  is  best  given  in  the  form  of  an  electuary — santonica,  1  drachm  (gm.  5)  ; 
jalap,  15  gr.  (gm.  1)  ;  and  sirup,  1  ounce  (gm.  30),  to  be  taken  in  three  doses 
— in  combination  with  a  cathartic.  Of  late,  wormseed,  on  account  of  its  bad 
taste,  has  been  almost  wholly  replaced  by  santonin,  which  is  derived  from  it. 
This  is  prescribed  in  1-  or  2-gr.  (gm.  0.05  to  0.10)  powders,  or  still  more  fre- 
quently in  the  form  of  santonin  troches  ("worm  tablets"),  which  may  be  had 
of  any  apothecary.  It  is  well  to  give  santonin  also  in  connection  with  a  cathar- 
tic, such  as  calomel.  We  give  the  patient  one  or  two  doses  of  santonin  in  the 
morning  for  three  days,  and  on  the  fourth  we  give  a  cathartic.     Severe  symp- 


INTESTINAL   PARASITES 


637 


toms  of  poisoning  (vomiting,  dilated  pupils,  apathy,  convulsions,  psychical 
disturbances)  have  been  seen  only  occasionally  from  the  careless  use  of  it. 
Milder  symptoms,  such  as  a  yellowness  of  the  urine  and  conjunctivae,  and 
xanthopsia,  or  seeing  everything  yellow,  arc  somewhat  more  frequent. 

In  exceptional  cases  santonin  fails  to  expel  the  ascarides.  We  may  then  try 
male  fern  or  thymol  (gr.  viij  to  xxiv,  gm.  0.5  to  1.50)  in  two  or  three  doses 
given  in  the  course  of  the  day. 


3.     OXYURIS   VERMICULARIS 

(Seatworms.     Pinworms) 

Natural  History. — The  oxyures  are  little  roundworms,  the  females  §  to  \  in. 
[10  or  12  mm.]  long,  the  males  only  3  or  4  (see  Figs.  84  and  85).  The  eggs, 
when  they  reach  the  human  stomach,  develop  very       ^  c 

rapidly.     The  embryos,  set  free,  collect  in  the  small 
intestine  and  later  mainly  in  the  caecum.    As  soon 
as  they  become  sexually  mature  they  pair,   and 
then   wander   gradually    down   into    the    rectum, 
where  they  collect  in  great  numbers.     When  the 
eggs  inside  the  female  become  ripe,  the  female 
leaves  the  rectum  and  lays  its  eggs  outside,  where 
they   are   soon   destroyed    (Leichtenstern).      The 
eggs  may  easily,  however,  be  conveyed  by  fingers 
or  by  articles  of  diet,  or  by  similar  means,  to  the 
stomach  of  the  same  host  or  directly,  without  in- 
termediate host,  to  some  other  person,  whereupon 
the  development  of  the  worm  begins  afresh.     As 
will  be  readily  understood,  children,  with  their 
untidy  habits,  are  much  more  exposed  to  infection 
with  the  oxyuris  than  adults.     The  fact  that  the 
female  oxyuris  never  lays  its  eggs  in  the  intestine 
explains  why  the  eggs  of  the  oxyuris  are  rarely  if 
ever  found  in  the  stools.     The  female  crawls  out 
of  the  anus  to  deposit  its  eggs. 
Male  as  well   as   female  worms 
are   discharged  with  the  stools. 
The    entire    cycle    of    develop- 
ment   of    the    oxyuris    occupies 
about  fourteen  days.    The  num- 
ber of  these  worms  which  may 
be  present  at  the  same  time  in 
the   intestine    is    very   consider- 
able,  so   that   "  the   entire   mu- 


1.  Fe- 


FiG.  84,  Fig.  85. 

Fig.  84. — Oxyuris  vermicularis.     Natural  size, 
male.     2.  Two  males. 

COUS  membrane  of  the  colon  Fig.  85. — Oxyuris  vermicularis,  enlarged,  a.  Mature 
is  covered  with  them  like  a  female'  not  yet  impregnated,  b.  Male.  c.  Female 
n       „  containing  eggs. 

Symptoms  and  Treatment. — The  oxyures  found  in  the  upper  portions  of 
the  intestine  and  in  the  caecum  cause  no  symptoms  whatever,  but  in  the  lower 
part  of  the  rectum  their  presence  causes  local  symptoms,  especially  a  very 


638 


DISEASES   OF  THE   DIGESTIVE   ORGANS 


severe  feeling  of  itching  and  burning  in  the  anus,  which  makes  the  child  con- 
stantly scratch  and  dig  with  his  fingers.  This  itching  of  the  anus  is  most 
severe  at  night  in  bed.  In  girls  the  oxyures  frequently  travel  into  the  vagina, 
by  which  an  intense  itching  is  also  set  up  there,  which  sometimes  leads  to 
masturbation.  In  some  cases  in  boys  and  men,  oxyures  have  been  found  to 
be  the  cause  of  abnormal  sexual  irritation.  Other  clinical  symptoms  are  rare, 
but  sometimes  there  may  be  anaemia  or  nervous  disturbances,  and  in  rare  cases 
marked  intestinal  catarrh,  or  inflammation  of  the  vulva. 

The  diagnosis  of  oxyures  is  not  difficult.  Our  attention  is  called  to  the 
itching  of  the  anus,  etc.,  and  we  look  for  worms.  Single  worms  are  easily 
found  in  the  dejections,  and  often  on  the  skin  about  the  anus. 

Treatment  is  directed  first  to  the  expulsion  of  the  threadworms  from  the 
rectum,  and  the  prevention  of  any  fresh  self-infection.  For  this  purpose  the 
chief  means  are  large  injections,  which  must  be  employed  persistently,  once 
or  twice  a  day,  for  weeks;  for  fluid  we  may  choose  simple  warm  water,  a  one- 
per-cent  solution  of  tannic  acid,  or  water  containing  vinegar,  salt,  or  glycerin. 
Injections  of  1  or  1.25  drachms  (gm.  4  to  5)  [for  children  gr.  xxx  to  xl  =  gm. 
2  to  2.5])  of  guiasanol  (a  guaiacol  preparation  made  by  the  Hochster  dye 
works)  are  claimed  to  be  particularly  efficacious.  Injections  containing  corro- 
sive sublimate  or  carbolic  acid  should  never  be  employed  because  of  the  danger 
of  poisoning.  It  is  difficult  to  remove  completely  the  oxyuris  from  the  upper 
part  of  the  intestine,  particularly  from  the  csecum.  For  this  purpose  the  most 
efficient  remedy  seems  to  be  santonin,  perhaps  combined  with  calomel  or  castor 
oil.  The  itching  at  the  anus  is  alleviated  by  cold  compresses  or  by  the  in- 
unction of  small  amounts  of  unguentum  hydrargyria 

Extreme  cleanliness  is  very  important.  The  anus  should  be  frequently 
washed,  and  also  the  fingers,  particularly  the  finger  nails,  to  prevent  the  spread 
of  the  parasites. 

4.     ANCHYLOSTOMA   DUODENALE 

(Dochmius  seu  Strongylus  duodenalis.     Uncinariasis.     Hookworm  Disease) 

The  anchylostoma  duodenale  is  a  worm  first  observed  in  upper  Italy  and  in 
Egypt  in  large  numbers,  of  which  many  inhabit  the  upper  portion  of  the  small 
intestine,  especially  the  duodenum,  but  also  the  jejunum  and  ileum.  The  male 
is  1  to  §  in.  [6  to  10  mm.]  long,  the 
female  10  to  18.  At  the  cephalic  end 
(Figs.  86  and  87)  is  found  a  bell- 
shaped  mouth  capsule,  which  is  pro- 
vided with  two  small  teeth  on  its  dor- 


Fig.    86. — Anchylostoma   duodenale,  natural 
size.     a.  Male.     b.  Female. 


Fig.  87.  —  (From  Heller.)  Anchylostoma 
duodenale,  enlarged.  Head  with  bell-like 
mouth. 


INTESTINAL   PARASITES  639 

sal  erlge,  and  four  larger  curved  teeth  on  its  ventral  edge.  With  this  suck- 
ing and  hiting  apparatus  the  worm  fixes  itself  firmly,  like  a  wel  cup,  on 
the  intestinal  mucous  membrane,  and  is  nourished  by  the  blood  which  it 
sucks  out.  The  place  in  the  intestine  to  which  an  anchylostoma  has  fastened 
may  be  recognized  in  the  cadaver  as  a  little  ecchymosis.  The  worms  sometimes 
bore  completely  into  the  inner  part  of  the  mucous  coat. 

The  eggs  of  the  anchylostoma  are  discharged  in  great  numbers  with  the 
feces  (vide  infra).  From  these  the  larvae  develop  and  thrive,  particularly  in 
the  dirty  water  of  mud  puddles  and  ditches;  and  by  means  of  water  that  is 
spattered,  or  more  often  by  dirty  hands,  they  reach  the  mouth  and  the  intes- 
tinal canal  of  man  again,  and  then  rapidly  develop  to  sexual  maturity.  Ee- 
cently  several  investigators  (Loos,  Schaudinn,  and  others)  have  shown  ex- 
perimentally that  the  anchylostoma  larvae  can  also  enter  the  body  through  the 
skin  and  reach  the  intestinal  tract  (presumably  through  the  lung  capillaries 
into  the  bronchial  tubes  and  from  there  the  oesophagus  and  stomach).  Prob- 
ably this  method  of  infection  actually  plays  a  great  role. 

If  the  intestine  harbors  many  anchylostomata,  the  small  but  constant  loss 
of  blood  caused  by  them  is  not  without  influence  on  the  organism.  In  addi- 
tion, there  are  probably  specific  toxic  influences  which  have  an  injurious 
effect  upon  the  red  blood  corpuscles.  The  symptoms  of  a  severe  anaemia 
gradually  develop.  Griesinger  first  made  the  discovery,  in  the  year  1854, 
that  the  disease  long  known  by  the  name  of  "  Egyptian  chlorosis  "  was  caused 
by  the  anchylostoma  duodenale.  Since  then  confirmatory  observations  have 
been  made  in  many  parts  of  the  tropics. 

The  disease  caused  by  the  anchylostoma  has  become  particularly  known 
in  Europe  because  of  the  great  frequency  with  which  it  occurred  among  the 
Italian  laborers  who  were  employed  in  building  the  Saint  Gothard  Tunnel. 
Since  then  many  well-established  cases  have  been  found  in  other  lands ;  e.  g., 
Hungary;  Germany,  particularly  in  the  brickmakers  of  the  Ehine;  also  re- 
peatedly in  miners  and  laborers  in  tunnels. 

The  symptoms  of  the  disease  consist,  as  we  have  said,  of  a  gradually  in- 
creasing general  anaemia,  for  which  no  special  organic  lesion  can  be  made  out 
objectively  as  a  cause.  The  patient  also  suffers  from  very  great  general 
weakness  and  languor,  dyspnoea,  palpitation,  headache,  oedema,  etc.  The 
changes  in  the  blood  (oligocythasmia,  poikilocytosis)  are  precisely  similar  to 
those  seen  in  pernicious  anaemia.  The  disease  may  last  for  months,  or  even 
years,  and  it  often  ends  fatally,  if  it  be  not  recognized  and  treated  in  time. 

Leichtenstern  has  made'  numerous  and  accurate  observations  with  regard 
to  the  brickmakers  of  Cologne.  He  states  that  no  symptoms  are  observed 
for  three  or  four  weeks  after  infection  with  the  embryos  of  the  anchylostoma. 
Some  five  or  six  weeks  after  infection,  when  the  parasites  become  sexually 
mature  and  breed,  there  appear  bloody  diarrhea,  intestinal  colic,  and  accom- 
panying progressive  anaemia.  At  this  time  there  is  probably  more  shifting 
ahout  of  the  parasites  in  the  intestine,  while  they  later  become  more  fixed. 
This  explains  why  the  disease  evinces  a  more  acute  and  severe  character  at  first, 
and  then  takes  on  the  form  of  a  chronic  anaemia,  with  great  diminution  or 
cessation  of  the  bloody  stools. 

The  diagnosis  is  easy  if  we  only  think  of  the  possibility  of  anchylostoma. 
It  is  not  very  difficult  to  find  an  abundance  of  eggs  in  the  feces.    They  are  of 


640 


DISEASES  OF  THE  DIGESTIVE  ORGANS 


oval  shape  and  characterized  by  the  frequent  presence  in  them  of  two  or  more 
spherules  due  to  subdivision  (see  Fig.  88).  The  worms  themselves  are  not 
usually   found  in   the   stools   unless   anthelmintics   have   been   administered. 

Charcot's  crystals  are  often  found  in 
the  dejections  previous  to  the  appear- 
ance of  the  anchylostoma  eggs  (Leich- 
tenstern).  There  is  always  an  increase 
of  the  eosinophile  leucocytes  in  the  blood. 
If  the  disease  is  recognized,  treat- 
ment is  usually  satisfactory.  We  pre- 
scribe the  same  anthelmintics  as  for  the 
other  intestinal  parasites,  particularly 
extract  of  male  fern  in  suitable  doses  (2 
to  3  drachms  [gm.  10  to  12]),  besides 
laxatives  and  injections.  In  this  way  it 
is  often  possible  to  banish  the  parasites 
entirely  from  the  intestinal  canal,  and 
thus  to  induce,  even  in  severe  cases,  a 
complete  and  often  surprisingly  rapid  recovery.  Besides  extract  of  male  fern, 
thymol  has  been  found  an  effectual  remedy.  Of  this,  about  2.5  to  3.5  drachms 
(gm.  10  to  14)  are  given  daily  in  doses  of  30  gr.  (gm.  2)  each.  For  children 
the  dose  is  proportionately  less.  Leichtenstern  recommends  that  a  few  doses 
of  calomel  and  one  or  two  injections  should  be  administered  on  the  day  pre- 
ceding the  specific  treatment  with  male  fern  or  thymol. 

The  prophylaxis  from  infection  with  anchylostoma  is  an  important  matter 
in  industrial  hygiene.  The  points  chiefly  to  be  considered  are  to  enjoin  the 
greatest  cleanliness  upon  the  workmen,  to  arrange  properly  for  the  reception 
and  removal  of  the  excreta,  and  to  provide  good  drinking  water.  [The 
type  seen  in  the  United  States  is  the  Uncinaria  americce  (or  Necator 
americanus),  and  has  been  shown  by  Stiles  to  be  prevalent  and.  important 
in  the  South.  Besides  the  anaemia,  eosinophilia  is  an  important  sign.  Thymol 
is  the  favorite  remedy — 30  gr.,  repeated  in  two  hours,  and  followed  two  hours 
later  by  a  purge,  preferably  not  castor  oil,  as  this  may  dissolve  the  thymol  and 
cause  toxic  symptoms.] 


i  e 

Fig.  88. — Egg  of  anchylostoma  duodenale. 
a  to  d,  various  stages  of  segmentation; 
e,  with  embryo.  (From  Pereoncito 
and  Schulthess.) 


5.     TRICHOCEPHALUS   DISPAR 

(Whipworm) 

The  trichocephalus  dispar  is  a  worm  1.3  to 
2  in.  [4  or  5  cm.]  long,  whose  anterior  part  is 
very  thin,  but  whose  posterior  part  is  decided- 
ly thick  (Fig.  89).  It  resides  chiefly  in  the 
cascum,  but  also  in  the  colon,  where  it  is  often 
found  in  small  numbers,  and  sometimes  in 
abundance.  The  yellow  or  reddish-brown  eggs 
of  the  parasite  are  characteristic,  and  they 
may  be  easily  found  in  the  feces  upon  microscopic  examination,  but  the  para- 
sites themselves  scarcely  ever  come  away  spontaneously  with  the  dejections. 
As  a  rule,  the  trichocephalus  has  no  clinical  significance,  but  lately  Moss- 


Fig.  89. — (From  Heller.) 
Trichocephalus  dispar. 


ACUTE   PERITONITIS  641 

brugger  has  reported  a  few  cases  of  severe  trouble  in  children,  due  to  this 
parasite.  The  infection  was  supposed  to  be  due  to  eating  earth.  The  symp- 
toms consisted  in  great  anaemia  and  in  long-continued  and  violent  diarrhea, 
with  watery  movements  containing  mucus  and  blood.  The  dejections  also 
showed  many  eggs  of  the  trichocephalus  and  Charcot's  crystals.  Treatment 
was  very  difficult  and  tedious,  for  the  ordinary  anthelmintics  seemed  to  have 
slight  effect.  The  most  promising  remedies  in  such  cases  would  probably  be 
extract  of  male  fern  and  thymol. 


SECTION   VI 
Diseases  of  the  Peritoneum 

CHAPTEE    I 

ACUTE    PERITONITIS 

(Inflammation  of  the  Peritoneum) 

JEtiology. — There  are  two  ways  by  which  inflammatory  agents  most  fre- 
quently reach  the  peritoneum :  one  is  from  the  gastro-intestinal  tract,  and  the 
other — in  women — is  from  the  genitals. 

All  the  diverse  forms  of  ulceration  which  attack  the  digestive  canal  may 
involve  the  serous  layer.  In  such  a  case  an  inflammation  arises  which  is  at 
first  limited,  but  which  may  under  certain  circumstances  become  more  exten- 
sive. This  inflammation  may  be  regarded  as  analogous  to  that  of  the  pleura 
in  pneumonia;  but  the  anatomy  of  the  stomach  and  intestine  is  such  that 
very  often  an  ulcer  in  their  walls  ends  in  a  complete  perforation.  If  this 
occurs,  the  inflammatory  germs  contained  in  the  prima?  via?  at  once  escape 
into  the  peritoneal  cavity  and  there  excite  an  inflammation,  which,  from  the 
specific  character  of  its  cause,  is  invariably  purulent,  and  very  frequently  is  at 
the  same  time  septic  or  ichorous.  The  possibility  of  a  peritonitis  due  to  per- 
foration, as  a  result  of  the  various  ulcerative  processes  of  the  stomach  and 
the  intestines,  has  been  frequently  referred  to  in  the  previous  sections  of  this 
work.  Thus  it  may  occur  in  simple  ulcer  and  in  ulcerating  cancer  of  the 
stomach;  in  typhoid,  tubercular,  or  dysenteric  ulceration  of  the  intestine;  in 
ulceration  of  the  intestine  above  intestinal  stenoses  of  many  varieties;  and 
in  the  small  ulcers  of  the  vermiform  appendix  due  to  the  pressure  of  hard 
substances. 

The  female  organs  of  generation  are  the  other  important  source  of  peri- 
tonitis. In  labor  and  premature  delivery  the  genital  tract  was  formerly  often 
directly  infected.  At  the  present  time  this  complication  has  fortunately  be- 
come infrequent,  thanks  to  the  advances  in  asepsis.  The  various  forms  of 
inflammation  which  are  thus  set  up,  including  endometritis,  metritis,  and 
parametritis,  may  in  several  different  ways  reach  the  peritoneum.  A  septic 
inflammation  of  the  endometrium  may  involve  the  peritoneum  by  direct  ex- 
tension up  the  Fallopian  tubes.    In  other  cases  it  is  through  the  lymph  vessels 


642  DISEASES  OF  THE   DIGESTIVE   ORGANS 

that  a  purulent  metritis  or  parametritis  spreads  to  the  peritoneum.  The 
larger  parametritic  abscesses  may  break  into  the  peritoneal  cavity.  It  is  to 
be  particularly  noticed,  however,  that  in  many  cases  of  septic  puerperal  peri- 
tonitis the  uterus  and  its  appendages  are  in  a  perfectly  normal  condition, 
having  served  merely  as  a  gateway  to  the  inflammatory  agents  without  suf- 
fering any  harm  themselves. 

Besides  these  two  chief  sources  of  peritonitis,  numerous  others  are  pos- 
sible, although  much  less  frequent. 

Sometimes  peritonitis  is  due  to  an  extension  of  inflammation  from  other 
abdominal  viscera.  Hepatic  abscess,  suppurating  hydatid  cysts  of  the  liver, 
ulcer  of  the  biliary  ducts,  splenic  abscess  or  infarction,  purulent  nephritis 
or  pyelitis,  abscess  near  the  bladder  or  in  the  prostate,  suppurating  ovariarr 
cysts,  tubal  pregnancy,  psoas  abscess,  and  Pott's  disease — all  these  may  pro- 
duce peritonitis,  either  by  direct  extension  or  by  perforation. 

It  is  worthy  of  note  that  peritonitis  may  occur  as  a  sequel  of  pleurisy. 
The  pleural  and  peritoneal  cavities  are  directly  connected  by  the  lymph-vessels 
of  the  diaphragm;  and  empyema,  as  well  as  tuberculous  pleurisy  (see  next 
chapter),  may  spread  to  the  peritoneum. 

Penetrating  wounds  of  the  abdomen  are  a  fruitful  source  of  acute  peri- 
tonitis. Surgical  operations  upon  abdominal  organs  come  under  the  same 
head.  A  large  number  of  laparotomies  proved  fatal  before  antisepsis  was  in- 
troduced, because  the  inflammatory  germs  thus  admitted  excited  a  diffuse 
septic  peritonitis.  Even  tapping  the  abdomen  for  ascites  may  cause  acute 
peritonitis  if  the  trocar  is  not  aseptic.  Abdominal  injuries,  in  which  the  walls 
are  not  penetrated,  very  rarely,  if  ever,  give  rise  to  peritonitis.  One  way  in 
which  they  have  been  said  to  produce  it  is  by  exciting  internal  hemorrhage. 
In  the  newborn,  peritonitis  exceptionally  results  from  infection  through  the 
navel. 

Far  less  frequent  are  those  cases  of  acute  peritonitis  which  occur  as  a  part 
of  certain  general  diseases.  In  this  class  belong  the  suppurative  peritonitis 
sometimes  developing  by  a  hematogenous  route  in  general  sepsis  and  the  peri- 
tonitis of  acute  articular  rheumatism  (q.  v.).  The  latter  is  rare  and  usually 
benign.  It  must  be  regarded  as  analogous  to  the  "  rheumatic  "  inflammation 
which  occurs  in  other  serous  membranes,  including  the  endocardium,  peri- 
cardium, and  pleura.  It  is  possible  that  rheumatic  peritonitis  of  this  sort  may 
exceptionally  occur  as  an  apparently  primary  disease.  It  is  a  well-established 
fact  that  peritonitis  may  also  develop  in  the  course  of  acute  or  chronic  ne- 
phritis. This  we  have  ourselves  observed.  It  is,  of  course,  comparable  with 
the  inflammation  which  not  infrequently  attacks  the  pericardium  and  pleura 
in  the  course  of  nephritis,  which  probably  depends  upon  the  retention  in  the 
blood  of  the  solids  which  ought  to  be  excreted  with  the  urine.  We  must  also 
mention  that  in  very  rare  instances  a  specific  gonorrheal  peritonitis  occurs, 
either  in  connection  with  a  constitutional  infection  from  gonorrhea,  perhaps 
associated  with  gonorrheal  synovitis  or  endocarditis,  or  from  the  direct  exten- 
sion of  gonorrheal  inflammation  from  other  parts  to  the  peritoneum. 

From  all  that  has  been  said,  it  is  evident  that,  from  a  purely  serological 
standpoint,  peritonitis  is  by  no  means  a  stereotyped  and  uniform  disease. 
The  actual  pathogenic  agents,  exclusive  of  the  rare  cases  of  mere  intoxication, 
are  always  bacteria,  but  bacteria  of  diverse  kinds.    In  the  cases  of  peritonitis 


ACUTE   PERITONITIS  643 

due  to  perforation,  the  bacterium  coli  seems  to  play  an  important  part,  and 
often  also  streptococci  are  influential.  The  cases  of  septic  or  puerperal  peri- 
tonitis are  mostly  occasioned  by  streptococci;  rarely  the  peritonitic  exudation 
has  been  found  to  contain  pneumococci,  staphylococci,  gonococci,  proteus 
forms,  and  other  germs.  Not  infrequently  there  seems  to  be  a  mixed  infection 
from  the  start. 

Pathology. — Like  the  analogous  inflammations  of  the  pleura  and  peri- 
cardium, peritonitis  is  divided  into  different  varieties,  according  to  the  char- 
acter of  the  inflammatory  exudation.  The  nature  of  the  exciting  cause  of 
most  cases  of  peritonitis  is  such  that  by  far  the  most  frequent  variety  is  the 
fibrinopurulent.  If  the  process  involves  the  entire  peritoneum — that  is,  if 
there  is  a  "  diffuse  general  peritonitis  " — we  generally  find  upon  opening  the 
abdomen  that  the  parietal  layer  of  the  peritoneum  and  the  outer  surface  of 
the  intestinal  coils  are  distinctly  reddened  from  marked  vascular  injection. 
There  may  even  be  small  ecchymoses  here  and  there.  The  serous  membrane 
is  clouded,  a  result  partly  of  desquamation  of  its  endothelium,  and  partly  of 
the  more  or  less  abundant  fibrinous  exudation  which  covers  the  peritoneum 
with  a  sheet  of  coagulated  fibrin.  Very  often  the  coils  of  intestine  have 
formed  numerous  adhesions  with  one  another  (compare  pleuritic  adhesions). 
In  cases  of  brief  duration  these  can  still  be  easily  broken  up,  but  after  a  pro- 
longed illness  they  are  extremely  firm.  There  is  usually  also  some  free,  fluid, 
fibrinopurulent  exudation  in  the  abdominal  cavity.  Its  amount  varies  greatly. 
Sometimes  there  is  only  a  small  quantity  of  opaque  fluid  in  the  dependent 
portions  of  the  cavity;  sometimes  there  are  many  quarts,  causing  great  disten- 
tion of  the  abdomen.  The  exudation  seldom  inclines  to  a  seropurulent 
character.  It  is  usually  predominantly  purulent.  Very  often  the  purulent 
exudation  undergoes  decomposition  into  the  offensive  sanious  fluid  of  septic 
peritonitis.  This  is  particularly  apt  to  occur  when  the  disease  originates 
from  an  intestinal  perforation  or  from  puerperal  poisoning.  The  perforation 
through  the  walls  of  the  intestine  is  sometimes  so  large  as  to  admit  consid- 
erable amounts  of  intestinal  gases  and  feces  into  the  peritoneal  cavity.  It 
is  also  possible  that  the  putrefaction  of  peritoneal  exudations  may  generate 
offensive  gases.  In  rare  instances  the  exudation  is  hemorrhagic;  but  most 
cases  of  hemorrhagic  peritonitis  do  not  belong  here,  but  come  rather  under 
the  tubercular  or  cancerous  forms  (vide  infra). 

In  severe  and  protracted  cases  of  peritonitis  the  intestine  is  involved  to  a 
certain  extent.  There  is  a  collateral  inflammatory  oedema  of  its  walls,  causing 
a  considerable  increase  in  thickness,  while  at  the  same  time  they  are  often 
friable  and  easily  torn.  The  weakness  of  the  muscular  layer  of  the  intestine 
may  amount  to  complete  paralysis,  and  thus  permit  excessive  intestinal  tym- 
panites, either  diffuse  or  local. 

Milder  forms  of  general  peritonitis  with  serofibrinous,  or  chiefly  serous, 
exudation  are  relatively  infrequent.  Under  this  head  would  come  certain  ap- 
parently primary  and  usually  chronic  cases  with  favorable  issue,  and  also  the 
peritonitis  which  sometimes  occurs  as  a  sequel  of  an  ascites  which  has  existed 
for  some  time  (see  next  chapter).  Probably  also  in  those  rare  cases  of  peri- 
tonitis arising  in  the  course  of  acute  rheumatism  and  ending  in  recovery,  the 
exudation  has  been  serofibrinous. 

We  have  spoken  thus  far  of  diffuse  general  peritonitis,  but  cases  are  not 


644  DISEASES   OF  THE   DIGESTIVE   ORGANS 

rarely  seen  of  circumscribed  or  "  encapsulated  "  peritonitis.  Here,  also,  we 
have  mild  varieties  with  fibrinous  exudations  on  the  one  hand,  and  on  the 
other  purulent  inflammation.  The  milder  inflammation  is  a  result  of  the  ex- 
tension of  the  most  varied  forms  of  inflammation  from  neighboring  organs. 
Thus,  deep  intestinal  ulcers,  for  example,  give  rise  to  a  mild  circumscribed 
inflammation  of  the  corresponding  portion  of  the  serous  layer.  A  similar 
condition  results  from  superficial  splenic  infarctions;  from  various  hepatic 
diseases,  when  they  reach  the  surface  of  the  liver,  and  from  numerous  patholog- 
ical conditions  of  the  female  genitals.  In  many  of  these  cases  the  peritonitis 
takes  a  chronic  course  and  leads  to  adhesions,  and  hence  is  called  adhesive 
peritonitis. 

Circumscribed  purulent  peritonitis  has  precisely  the  same  aetiology  as  the 
general  form,  with  this  single  difference,  that  firm  adhesions  are  quickly 
formed  around  the  spot  whence  the  inflammation  proceeds,  limiting  it  and 
preventing  it  from  involving  the  entire  peritoneum.  It  occurs  most  frequently 
as  a  purulent  perityphlitis  (q.  v.),  consequent  upon  perforation  of  the  vermi- 
form appendix,  and  also  as  pelvic  peritonitis,  which  is  a  possible  sequel  of 
most  of  the  forms  of  puerperal  inflammation  to  which  the  uterus  and  its  ap- 
pendages are  liable.  But  we  may  also  have  encapsulated  purulent  peritonitis 
after  the  perforation  of  gastric  and  intestinal  ulcers,  or  of  suppurative  proc- 
esses in  the  biliary  passages,  and  from  similar  causes.  If  the  abscess  is  situated 
directly  below  the  diaphragm  it  is  termed  subphrenic. 

Histologically  considered,  acute  peritonitis  is  perfectly  analogous  to  the 
inflammatory  processes  which  attack  other  serous  membranes.  The  endo- 
thelium becomes  degenerated,  and,  for  the  most  part,  is  cast  off.  There  is  an 
exudation  from  the  blood  vessels  of  a  fibrinous  fluid,  which  is  partly  coagulable, 
and  with  this  exudation  round  cells  escape  in  greater  or  less  abundance.  In 
the  further  progress  of  the  disease  there  is  an  inflammatory  new  growth  of 
vascular  connective  tissue,  which  probably  originates  chiefly  from  the  endo- 
thelium and  the  permanent  tissue  cells,  but,  according  to  some,  starts  in  part 
also  from  the  wandering  cells.  The  new  formation  of  blood  vessels  certainly 
seems  to  be  due  chiefly  to  budding  from  the  capillaries  of  the  serosa.  Thus 
arise  the  adhesions  of  connective  tissue  and  the  false  membranes  found  in 
chronic  cases  between  the  different  coils  of  intestine.  They  lead  in  process  of 
time  to  marked  thickening  and  retraction  of  the  omentum  and  mesentery 
(peritonitis  deformans) .  Most  cases  of  purulent  peritonitis  prove  fatal  in  the 
early  acute  stage.  If  a  case  recovers,  the  exudation  undergoes  fatty  degenera- 
tion, and  its  cellular  constituents  are  thus  disintegrated  and  then  are  absorbed. 

The  results  of  circumscribed  purulent  peritonitis  are  detailed  in  connec- 
tion with  the  clinical  history. 

Clinical  History. — 1.  Acute  General  Peritonitis. — The  following  descrip- 
tion applies  chiefly  to  the  severe  purulent  form,  the  one  by  far  most  frequently 
met  with.  It  occurs  in  most  instances  after  perforation,  in  puerperal  cases, 
and  after  external  injuries,  such  as  surgical  operations.  In  most  of  these 
cases  the  peritonitis  is  a  secondary  disease,  so  that  it  must  obviously  be  greatly 
modified  in  its  general  characteristics  and  behavior  by  the  original  trouble. 
In  the  first  place,  the  onset  is  modified.  Many  cases  of  peritonitis  due  to 
perforation  begin  almost  abruptly,  the  patient  having  been  previously  in  per- 
fect health.     Thus,  as  already  mentioned,  the  first  indication  of  a  gastric  or 


ACUTE   PERITONITIS  645 

duodenal  ulcer  may  be  given  by  perforation.  Some  eases  of  perforation  of  the 
vermiform  appendix  present  equally  sudden  and  unexpected  symptoms. 

There  are  many  other  cases  in  which  the  symptoms  of  peritonitis  supervene 
upon  those  of  some  grave  disease  already  existing.  For  example,  typhoid 
fever,  intestinal  tuberculosis  or  intestinal  stenosis,  may,  by  causing  perfora- 
tion, excite  a  peritonitis.  Here  the  symptoms  of  this  secondary  disease  may 
be  more  or  less  completely  veiled  by  the  other  grave  local  and  constitutional 
disturbances. 

Again,  an  acute  general  peritonitis  may,  as  we  have  already  said,  be  the 
sequel  to  a  local  and  circumscribed  inflammation  of  the  peritoneum.  Thus,  a 
purulent  perityphlitis,  or  a  purulent  puerperal  pelvic  peritonitis,  may  finally 
become  universal.  In  such  unfortunate  cases  the  change  in  symptoms  is  often 
gradual,  and  is  not  clearly  pronounced. 

We  have  now  indicated  certain  variations  from  the  general  course  of  the 
disease;  but,  nevertheless,  almost  every  case  of  acute  general  peritonitis,  what- 
ever its  aetiology,  presents  clinical  symptoms  which  are  so  characteristic  and 
typical  that  a  general  description  of  the  disease  will  be  both  easy  and  advan- 
tageous. 

The  symptoms  of  acute  peritonitis  form  two  groups,  the  local  and  the  con- 
stitutional. The  latter  are  the  result  of  the  local  disturbance  acting  upon  the 
general  condition  of  the  patient. 

Of  the  local  symptoms,  pain  deserves  to  be  named  first.  It  is  usually  the 
earliest  symptom,  and,  as  the  disease  progresses,  it  is  generally  the  excruciating 
abdominal  pain  which  attracts  most  attention.  The  localization  of  the  pain 
in  the  beginning  of  the  illness  may  be  of  diagnostic  value  in  doubtful  cases,  if 
such  as  to  indicate  the  possible  starting  point  of  the  inflammation;  for  ex- 
ample, the  vermiform  appendix  or  a  gastric  ulcer.  Later,  the  pain  extends 
over  the  whole  abdomen.  As  a  rule,  there  are  brief  remissions  followed  by 
fresh  exacerbations.  The  pain  is  aggravated  by  voluntary  movements,  by  deep 
inspirations,  and  probably  by  intestinal  peristalsis.  The  abdominal  tenderness 
is  often  extreme  in  peritonitis,  and  is  very  characteristic.  The  gentlest  palpa- 
tion is  torture,  and  often  the  slightest  pressure  of  the  bedclothes  is  almost 
unbearable.     Frequently  the  greatest  tenderness  is  in  the  umbilical  region. 

Acute  peritonitis  seldom  exists  without  pain.  The  exceptions  to  this  rule 
are  seen  chiefly  in  patients  who  are  extremely  prostrated,  and  whose  sensibility 
and  intelligence  are  much  impaired.  Here  the  peritonitis  may  escape  notice — 
as  in  severe  typhoid  or  in  the  last  stage  of  tuberculosis.  Comparatively  slight 
pain  is  supposed  to  occur  in  those  cases  in  which  the  parietal  peritoneum  is 
not  markedly  involved  in  the  inflammation. 

On  physical  examination,  the  abdomen,  as  a  rule,  is  found  to  be  dis- 
tended. This  is  an  early  symptom,  and  gradually  becomes  more  and  more 
pronounced.  It  is  due  mainly  to  the  intestinal  tympanites  which  we  have  al- 
ready mentioned,  which  sometimes  becomes  very  great  if  the  muscular  fibers 
of  the  intestine  are  paralyzed.  In  the  later  stages  the  liquid  effusion  into  the 
peritoneal  cavity  of  course  contributes  to  the  prominence  of  the  abdomen,  but 
even  then  the  distention  is  seldom  so  uniform  or  so  broad  as  in  ascites.  In 
peritonitis,  coils  of  distended  intestine  can  often  be  recognized  by  their  char- 
acteristic contour  through  the  abdominal  wall.  On  palpation  usually  the  most 
striking  fact  is  the  general  increased  rigidity  of  the  abdominal  walls  dependent 
41 


646  DISEASES  OF  THE  DIGESTIVE  ORGANS 

upon  a  reflexly  increased  tonicity  of  the  abdominal  muscles.  This  increased 
resistance,  the  "  defense  musculaire  "  of  the  French,  is  explained  as  being  a 
protection  against  painful  pressure.  It  also  accounts  for  the  frequent  disap- 
pearance of  the  abdominal  reflexes. 

Palpation  also  often  shows  a  very  characteristic  diversity  in  the  sense  of 
resistance  in  different  portions  of  the  abdomen,  occasioned  by  variations  in  the 
amount  of  exudation,  by  adhesions,  or  by  the  dilatation  of  some  of  the  in- 
testinal coils,  and  similar  causes. 

In  general,  if  the  abdominal  wall  is  yielding  and  thin,  the  peritonitic  dis- 
tention will  be  greater,  so  that  it  is  most  marked  in  puerperal  cases,  where 
the  preceding  pregnancy  has  rendered  the  walls  lax.  In  a  person  with  power- 
ful muscles  and  tense  abdominal  walls  the  convexity  of  the  abdomen  is  seldom 
great.  In  some  cases  there  is  no  convexity  whatever.  The  walls  may  be  as 
hard  as  a  board,  and  the  abdomen  flat  or  slightly  concave.  In  such  cases  the 
diagnosis  may  be  difficult.  Sometimes,  again,  the  original  retraction  of  the 
abdominal  walls  is  succeeded  by  more  or  less  distention  of  the  abdomen. 

Percussion  over  the  distended  intestinal  coils  yields  a  resonant  and  usually 
tympanitic  sound.  It  is  not  till  a  considerable  amount  of  liquid  effusion  has 
collected  that  there  is  dullness,  most  marked  in  the  dependent  portions  of  the 
abdomen.  If  there  is  much  tympanites,  however,  quite  a  large  effusion  may 
exist  without  being  detected  on  percussion.  Percussion  also  gives  results 
analogous  to  those  of  palpation,  in  that  there  is  often  a  diversity  in  the  quality 
of  the  resonance  of  different  portions  of  the  abdomen  in  peritonitis. 

Usually  there  is  too  much  pain  to  permit  a  careful  examination  of  the 
change  of  dullness  consequent  upon  change  of  decubitus.  In  general  the 
numerous  adhesions  between  the  separate  coils  of  intestine  also  interfere  with 
the  free  motion  of  the  peritonitic  exudations. 

Percussion  not  only  gives  information  about  the  existence  of  a  liquid,  puru- 
lent effusion,  but  is  also  of  value  in  determining  the  level  of  the  diaphragm, 
as  affected  by  abnormal  abdominal  distention.  The  upper  limit  of  hepatic 
dullness  is  raised  to  the  fifth  or  even  the  fourth  rib.  The  heart  is  also  pushed 
up.  There  is  a  tympanitic  resonance  above  the  margin  of  the  ribs  on  the 
right  side. 

The  diaphragmatic  movements  in  respiration  are  very  slight,  partly  on 
account  of  the  increased  intra-abdominal  pressure,  and  partly  on  account  of 
the  sensitiveness  of  the  abdomen.  For  this  reason  peritonitis  patients  almost 
always  show  a  pronounced  costal  type  of  respiration. 

The  area  of  hepatic  dullness  is  not  only  displaced  upward,  but  is  also  evi- 
dently diminished.  This  is  due  in  part  to  coils  of  distended  intestine  overlap- 
ping the  anterior  edge  of  the  liver,  and  in  part  to  the  organ  being  tilted  up- 
ward in  such  a  way  that  its  area  of  contact  with  the  anterior  wall  of  the  body 
is  less  than  normal.  Formerly  the  total  disappearance  of  hepatic  dullness  was 
regarded  as  a  sure  sign  that  gas  has  escaped  from  the  intestine  into  the  ab- 
dominal cavity.  The  inference  is  not  always  correct.  The  liver  may  be  dis- 
placed backward  by  coils  of  intestine,  and  hepatic  dullness  be  thus  abolished, 
although  there  is  no  air  free  in  the  peritoneal  cavity. 

If  there  is  a  considerable  effusion,  it  is  possible,  as  in  ascites  (q.  v.),  to 
get  a  sensation  of  fluctuation  by  gentle,  quick  palpation.  If,  after  the  phys- 
ical examination,  the  existence  of  a  peritonitic  exudate  is  still  doubtful,  posi- 


ACUTE   PERITONITIS  647 

tive  evidence  is  furnished  by  an  exploratory  puncture  which,  at  the  same  time, 
permits  us  definitely  to  determine  the  character  of  the  exudate. 

As  a  rule,  auscultation  of  the  abdomen  does  not  throw  much  light  on  a 
case  of  peritonitis.  In  the  distended  coils  of  intestine,  not  infrequently  at 
the  beginning  of  the  disease,  we  hear  all  sorts  of  gurgling  sounds.  In  the 
later  stages  the  intestinal  paralysis  which  is  present  causes  a  cessation  of  all 
peristalsis.  Sometimes  we  hear  a  peritonitic  friction  sound,  due  to  the  move- 
ments of  respiration,  causing  two  rough  surfaces  to  rub  against  each  other. 
In  particular,  perihepatic  friction  is  heard  not  very  infrequently. 

If  the  results  of  physical  examination  leave  us  still  in  doubt  as  to  the 
presence  of  a  peritonitic  exudation,  we  may  attain  certainty  by  an  exploratory 
puncture,  and  at  the  same  time,  if  there  be  any  exudation,  determine  its 
character. 

The  digestive  apparatus  is  almost  always  disturbed  by  any  severe  case  of 
peritonitis.  In  all  severe  cases  the  tongue  is  dry,  fissured,  and  often  thickly 
coated.  A  moist  tongue  is  regarded  prognostically  as  a  good  sign.  The 
appetite  disappears  entirely.  On  the  other  hand,  there  is  usually  a  torturing 
thirst. 

As  to  the  stomach,  vomiting  is  the  most  important  symptom.  Vomiting  is 
often  seen  early  in  the  disease,  and  recurs  frequently  as  the  illness  progresses. 
It  sometimes  is  spontaneous,  and  sometimes  follows  the  ingestion  of  food. 
If  spontaneous,  the  vomitus  consists  of  watery  mucus,  usually  of  a  greenish 
tinge.  We  do  not  know  absolutely  the  cause  of  the  vomiting  in  peritonitis. 
Apparently  it  is  in  part  a  reflex  action,  excited  by  the  inflammation  of  the 
serous  membrane.  Possibly  the  external  pressure  of  the  exudation  also  affects 
the  stomach,  and  it  may  be  that  absorbed  toxins  also  excite  vomiting.  It  must 
be  added  that  vomiting  may  be  absent  in  acute  peritonitis.  This  is  seen 
when  the  patient  is  comatose,  and  sometimes  also  when  the  peritonitis  has 
developed  upon  perforation  of  a  gastric  ulcer,  because  the  contents  of  the 
stomach  are  thus  emptied  out  through  the  hole  in  its  walls.  The  vomiting 
is  usually  accompanied  by  frequent  eructations. 

Of  the  intestinal  symptoms,  the  reader  has  already  become  acquainted  with 
the  tympanites,  and  also  with  the  fact  that  it  is  due  mainly  to  a  paresis  of  the 
muscular  fibers  of  the  intestine.  This  same  muscular  weakness  furnishes  an 
obvious  reason  for  the  persistent  constipation  usually  observed  in  peritonitis. 
If  the  intestinal  paralysis  progresses,  so-called  paralytic  ileus  (vide  supra) 
may  finally  develop.  On  the  other  hand,  we  may  have  diarrhea  instead,  from 
increased  peristalsis  and  secondary  intestinal  catarrh.  Especially  in  some 
forms  of  septic  puerperal  peritonitis,  diarrhea  is  frequently  observed.  Mic- 
turition is  usually  scant  and  often  painful.  This  is  probably  dependent  upon 
an  involvement  of  the  peritoneal  covering  of  the  bladder.  Not  infrequently 
the  urine  contains  some  albumen,  and  occasionally  also  indican. 

The  pushing  up  of  the  diaphragm  has  a  noteworthy  effect  upon  the  thoracic 
organs.  The  lower  lobes  of  the  lungs  are  compressed,  so  that  considerable 
dyspnoea  results.  The  heart  is  likewise  crowded  upward,  so  that  the  apex  beat 
is  usually  to  be  felt  in  the  fourth  intercostal  space. 

Every  case  of  acute  peritonitis  that  is  at  all  extensive  has  marked  constitu- 
tional effects.  These  are  in  part  the  result  of  the  wakefulness  due  to  pain, 
and  the  restlessness  and  fever.     But  perhaps  there  are  also  reflex  inhibitory 


648  DISEASES   OF   THE   DIGESTIVE   ORGANS 

influences,  originating  in  the  irritation  of  the  peritoneal  nerves  and  affecting 
chiefly  the  heart,  just  as  Goltz  in  his  well-known  experiment  killed  a  frog  by 
blows  upon  the  abdomen.  The  chief  factor,  however,  is  in  all  probability  the 
toxins  which  are  readily  absorbed  from  the  peritonitic  exudation  by  the  peri- 
toneum, and  thus  enter  the  circulation.  They  produce  a  vasomotor  paralysis 
of  the  splanchnic  area,  so  that  all  the  other  vascular  regions  are  emptied. 

There  is  no  other  disease,  except  internal  strangulated  hernia — and  the 
effect  of  that  is  perfectly  analogous — which  produces  general  collapse  and 
weakness  so  quickly  as  does  peritonitis.  The  imperfectly  nourished  and  poorly 
filled  heart  acts  progressively  weaker.  The  countenance  ("fades  abdom- 
inalis")  is  rapidly  altered,  the  cheeks  fall  in,  and  the  eyes  become  hollow. 
The  nose  grows  sharp  and  cool,  the  lips  and  tongue  dry.  The  skin  of  the 
extremities  is  also  cool  and  bluish,  as  a  result  of  impaired  circulation.  The 
peritonitis  has  hardly  begun  before  we  find  the  pulse  small  and  soft.  In  many 
severe  cases  the  pulse  finally  becomes  almost  imperceptible.  At  the  same 
time  the  pulse  rate  increases,  as  is  usual  in  collapse  from  any  cause,  so  that 
120  to  140  beats  per  minute  is  not  an  exceptional  rapidity.  Only  in  excep- 
tional instances  is  there  no  increased  rapidity  of  the  pulse. 

The  temperature  varies  greatly  in  different  cases.  It  may  be  high  in  the 
rectum,  although  the  skin  feels  cool.  Still,  very  high  fever  is  not  usual;  and 
there  are  often  considerable  remissions.  We  even  frequently  observe  the  sub- 
normal temperature  of  collapse.  In  general,  streptococcic  peritonitis  runs  its 
course  with  higher  temperature  than  that  caused  by  the  colon  bacillus.  In 
the  latter,  fever  may  even  be  almost  entirely  absent.  The  number  of  respira- 
tions per  minute  is  usually  30  to  40.  This  increased  rate  is  due  not  only  to 
the  compression  of  the  lower  lobes  of  the  lungs,  but  also  to  the  pain  caused 
by  full  inspirations  and  to  the  impeded  circulation. 

The  intellect  usually  remains  unimpaired  to  the  end.  Not  infrequently 
just  before  death,  a  striking  euphoria  appears.  Sometimes  there  may  be  mild 
delirium,  or  an  approach  to  stupor,  toward  the  close  of  the  disease. 

The  course  of  acute  general  peritonitis  in  the  great  majority  of  cases  is 
unfavorable.  With  the  appearance  of  the  grave  symptoms  just  depicted  the 
prognosis  becomes  almost  hopeless.  The  course  of  the  disease  is  also  compara- 
tively rapid.  Marked  variations  in  the  intensity  of  the  symptoms  are  infre- 
quent. The  grave  local  and  constitutional  symptoms  persist,  and,  as  a  rule, 
the  patient  dies  at  the  end  of  a  few  (two  to  six)  days.  Still,  it  is  not  well  to 
make  general  dogmatic  statements  as  to  the  clinical  history,  for  the  aetiology 
of  each  individual  case  impresses  upon  it  individual  characteristics.  A  peri- 
tonitis resulting  from  gastric  or  intestinal  perforation  is  usually  quickly  fatal. 
The  same  is  true  of  almost  all  cases  of  puerperal  septic  peritonitis.  In  a  few 
cases,  however,  the  inflammation  is  limited,  by  the  encapsulation  of  the  exu- 
dation. These  may  finally  end  in  recovery  through  perforation  of  the  abdom- 
inal walls  or  perforation  into  the  intestinal  canal.  Now  and  then  an  acute 
general  peritonitis  may  assume  a  chronic  form.  The  effusion  is  mostly  reab- 
sorbed, and  the  newly  formed  adhesions  and  false  membranes  contract  into 
firm  bands  of  connective  tissue.  The  liver,  spleen,  and  other  abdominal 
viscera  acquire  a  tough  coating  of  connective  tissue.  The  omentum  and 
mesentery  are  shortened  and  thickened.  Indeed,  the  omentum  may  roll  itself 
almost  completely  up.     Although  the  clinical  symptoms  become  less  severe, 


ACUTE  PERITONITIS  049 

weakness  usually  persists,  with  gradual  exhaustion  and  death.  Often  the 
intestine  is  so  bent  or  pinched  as  to  give  rise  to  grave  symptoms  from  stenosis. 
Recovery  from  acute  general  peritonitis  is  very  exceptional.  IT  seen,  it  is 
usually  in  mild  cases,  such  as  sometimes  occur  after  menstruation,  abortion, 
or  labor.  A  favorable  outcome  is  the  rule,  also,  in  those  very  rare  eases  that 
develop  in  the  course  of  an  acute  articular  rheumatism,  as  well  as  in  certain 
forms  of  gonococcus  peritonitis,  especially  those  that  occur  in  women  subse- 
quent to  a  gonorrheal  endometritis  and  salpingitis,  and  also  in  pneumococcus 
peritonitis.  This  last  is  usually  observed  in  children;  it  has  a  sudden  onsel 
with  simultaneous  gastrointestinal  symptoms  and  a  tendency  to  encapsulated 
abscess  formation  below  the  umbilicus.  In  these  groups  of  cases  the  inflam- 
mation is  either  of  a  serofibrinous  nature  and  is  finally  absorbed,  or  it  is  sup- 
purative, and  becomes  limited  early  in  the  disease  with  the  formation  of  a 
circumscribed  abscess,  which  ruptures  spontaneously  either  into  the  intestinal 
lumen  or  externally  (as  through  the  umbilicus  in  pneumococcus  peritonitis), 
or  else  can  be  opened  by  operation. 

2.  Acute  Circumscribed  Peritonitis. — The  local  symptoms  of  this  are  essen- 
tially the  same  as  we  have  just  ascribed  to  the  general  form ;  except  that,  a 
smaller  extent  of  tissue  being  involved,  they  are  correspondingly  limited.  The 
pain  and  tenderness  are  confined  mainly  to  one  region,  but  its  boundaries 
are  rarely  sharply  defined.  On  palpation  of  this  region,  we  find  an  increased 
resistance  which  is  sometimes  almost  like  that  produced  by  a  tumor.  If  there 
is  an  encapsulated  effusion,  we  may  detect  fluctuation,  particularly  if  the 
abscess  is  going  to  point  outward.  On  percussion  over  the  affected  spot,  there 
is  either  dullness  or  a  muffled  tympanitic  resonance. 

The  constitutional  symptoms  are  likewise  those  of  general  peritonitis,  only 
usually  less  severe.  Beflex  vomiting  does  occur,  but  is  seldom  so  persistent 
as  in  the  diffuse  inflammation.  The  physical  weakness  and  symptoms  of  col- 
lapse are  decided,  but  do  not  usually  become  extreme.  There  is  generally  an 
irregular  fever,  which  may  now  and  then  assume  an  intermittent,  pysemic 
character.  Most  cases  run  a  chronic  course.  If  the  illness  be  very  much 
prolonged,  death  may  finally  ensue  from  general  debility.  Eeoovery  is  possi- 
ble if  the  pus  can  be  let  out.  This  may  be  accomplished  either  by  the  surgeon 
or  by  Nature.  Spontaneous  discharge  of  the  abscess  may  take  place  through 
the  abdominal  walls,  into  the  intestine,  or  even,  in  rare  instances,  through 
the  pleura  into  the  lungs.  But  if  the  pus  finds  its  way  into  the  general  peri- 
toneal cavity,  the  peritonitis  becomes  diffuse  and  causes  death. 

To  describe  in  detail  each  separate  variety  of  circumscribed  peritonitis 
would  occupy  too  much  space,  and  would  also  lead  to  useless  repetitions.  We 
have  already  spoken  at  some  length  of  one  especially  important  form — namely, 
perityphlitis.  Perimetritis  and  pelvic  peritonitis  are  chiefly  puerperal  affec- 
tions, and  are  fully  discussed  by  writers  on  gynaecology. 

The  so-called  subphrenic  abscesses  deserve  a  more  exhaustive  discussion  at 
this  point.  They  develop  below  the  diaphragm,  between  it  and  the  liver  on 
the  right  side,  and  between  it  and  the  stomach,  colon,  and  spleen  on  the  left. 
Right-sided  subphrenic  abscesses  usually  originate  from  suppurative  processes 
in  the  liver,  bile  passages,  the  right  kidney,  the  appendix,  etc.  Left-sided 
subphrenic  abscesses  most  frequently  develop  from  perforated  gastric  ulcers 
and  much  more  rarely  from  the  left  kidney,  the  spleen,  the  left  lobe  of  the 


650  DISEASES  OF   THE   DIGESTIVE   ORGANS 

liver,  etc.  In  individual  cases,  caries  of  the  lower  ribs  and  suppurative  proc- 
esses in  the  lungs  and  the  pleura  that  extend  through  the  diaphragm,  also 
lead  to  subphrenic  abscesses.  If,  in  a  stomach  or  colon  perforation,  the 
abscess  contains  air,  or  gases  have  developed  in  it  as  a  result  of  decomposition, 
this  type  of  abscess  is  designated  as  a  subphrenic  pyopneumothorax.  The 
symptoms  of  subphrenic  abscess  are  local  pain,  fever,  and,  depending  upbn 
the  position  and  size  of  the  abscess,  dullness  and  other  physical  signs.  The 
differentiation  from  empyema  and  pneumothorax  is  not  always  easy.  The 
most  important  differential  point  in  favor  of  subphrenic  abscess  is  the  demon- 
stration of  the  presence  of  the  respiratory  mobility  of  the  lower  boundary 
of  the  lung.  Sometimes  the  irregularity  of  the  upper  boundary  of  dullness 
is  striking,  especially  in  those  cases  where  the  abscess  develops  on  the  right 
side,  anteriorly,  between  the  liver  and  diaphragm.  If  the  abscess  contains 
air,  metallic  auscultatory  phenomena  are  present,  as  in  pneumothorax  (coin 
sound  and  metallic  splashing  sounds  on  succussion).  If  vesicular  breathing 
can  be  demonstrated  above  the  tympanitic  area,  then  it  is  certain  that  the 
cavity  lies  below  the  diaphragm.  Still,  it  should  be  noted  that  pleuritic 
exudates,  at  first  serous,  but  later  also  purulent,  frequently  develop  secondarily 
to  a  subphrenic  abscess.  This  and  other  complications  (pericarditis,  perfora- 
tions, etc.)  often  cause  the  physical  condition  to  become  still  more  involved 
and  difficult  of  interpretation.  The  X-ray  examination  frequently  gives  im- 
portant information.  Practically,  the  chief  point  is  to  recognize  the  presence 
of  pus  in  time.  For  this  purpose  exploratory  puncture  is  of  the  utmost 
importance,  and  must  never  be  neglected  in  these  cases.  As  soon  as  suppura- 
tion has  been  demonstrated,  proper  surgical  treatment  with  sufficiently  free 
opening  of  the  abscess  cavity  must  be  instituted.  Almost  all  cases  of  sub- 
phrenic abscess  that  are  not  treated  surgically  run  an  unfavorable  course. 

Of  the  other  forms  of  circumscribed  suppuration  in  the  abdominal  cavity, 
perinephritic  abscess  will  be  considered  more  in  detail  later.  I  would  refer 
here,  briefly,  to  a  form  of  localized  suppurative  peritonitis,  observed  particu- 
larly in  children,  in  which  a  painful  fluctuating  tumor  develops  above  the 
left  inguinal  fold,  and  which  usually  ends  favorably  by  perforation  of  the 
abscess  into  the  rectum.  The  infection  of  the  peritoneum  in  these  cases  prob- 
ably comes  from  the  descending  colon  or  the  sigmoid  flexure. 

Diagnosis. — The  diagnosis  of  peritonitis  is  in  many  cases  an  easy  matter, 
when  we  have  the  characteristic  symptoms  of  tenderness  and  tympanites,  vom- 
iting, and  collapse.  Often  the  starting  point  of  the  inflammation  is  equally 
obvious  in  cases  of  secondary  peritonitis  supervening  upon  some  disease 
which  we  have  already  clearly  recognized,  such  as  typhoid  fever,  gastric  ulcer, 
or  puerperal  diseases.  But  where  the  peritonitis  is  apparently  primary,  we 
must  inquire  carefully  into  the  previous  history  and  the  earliest  symptoms  of 
the  attack,  in  order  to  form  even  a  surmise  as  to  aetiology. 

The  diagnosis  is  sometimes  greatly  obscured  by  the  fact  that  under  certain 
circumstances  very  similar  symptoms  may  be  excited  by  other  disorders  af- 
fecting the  intestines.  Thus,  in  typhoid  fever  there  may  be  great  tympanites 
and  grave  constitutional  symptoms,  with  abdominal  pain,  so  that  peritonitis 
may  be  diagnosticated,  while  the  autopsy,  if  there  be  one,  discloses  no  signs 
of  it.  Deep  ulcers  of  the  intestine,  however  produced,  may  give  rise  to  such 
great  abdominal  tenderness  as  likewise  to  simulate  peritonitis.     The  differen- 


ACUTE   PERITONITIS  051 

tial  diagnosis  between  peritonitis  due  to  perforation  and  acute  intestinal 
obstruction  (q.  v.)  is  often  very  difficult.  In  both,  when  there  is  severe  con- 
stitutional infection,  the  symptoms  are  almost  the  same,  and,  furthermore, 
diffuse  peritonitis  may  occasion  such  a  paralysis  of  the  intestine  or  such  ex- 
cessive tympanites  as  to  prevent  any  motion  of  the  bowels,  and  even  to  cause 
fecal  vomiting  (the  so-called  paralytic  ileus).  On  the  other  hand,  intestinal 
obstruction  is  not  infrequently  complicated  by  general  peritonitis,  so  that  the 
two  conditions  may  both  exist  simultaneously.  The  following  are  the  chief 
points  of  distinction  between  them,  although  even  these  are  not  infallible : 

PERITONITIS  INTESTINAL   OBSTRUCTION 

1.  Begins  with  fever  and  with  ab-  1.  Begins  without  fever.  Pain 
dominal  pain,  often  localized.  absent  in  obturation  (vide  supra). 

2.  Abdomen  very  sensitive  to  2.  Abdomen  at  first  soft  and  not 
pressure,  hard,  and  tense.  especially  tender  upon  pressure. 

3.  Pain  tends  to  abate  as  the  dis-  3.  Abdominal  pain  gradually  and 
ease  goes  on.  constantly  increasing. 

4.  No  visible  peristalsis  of  the  in-  4.  Sometimes  visible  peristalsis; 
testines.  intestinal  coils  can  be  felt  like  rolls. 

5.  Seldom  fecal  vomiting,  fre-  5.  Distinct  fecal  vomiting,  hic- 
quently  hiccough  and  simple  vomit-  cough  rare. 

ing. 

6.  Exudation  demonstrable  in  the  6.  No  free  exudation  in  the  peri- 
peritoneal  cavity.                                         toneal  cavity,  or  only  slight,  later. 

7.  Passage    of    gas    not    entirely  7.  Complete  obstruction, 
stopped. 

Another  diagnostic  error,  which  we  have  already  mentioned,  is  not  infre- 
quent— that  is,  the  occurrence  of  peritonitis  may  be  entirely  overlooked.  This 
is  especially  likely  to  happen  when  the  localized  symptoms,  such  as  pain  and 
tympanites,  are  very  slight.  Sometimes  the  only  things  which  call  attention 
to  the  onset  of  peritonitis  are  the  rapid  change  in  the  general  condition  of  the 
patient  and  in  his  pulse  and  temperature. 

The  diagnosis  of  localized  peritonitis  also  is  often  difficult.  Many  obscure, 
6evere,  febrile  conditions  are  shown  by  the  autopsy  to  be  deep-seated  suppura- 
tions in  the  abdominal  cavity.  We  should  never  neglect  taking  a  careful  his- 
tory and  making  a  thorough  examination,  including  rectal  and  vaginal  palpa- 
tion and  exploratory  puncture. 

It  is  well  to  remember  that  even  a  pregnant  uterus  and  a  distended  and 
therefore  painful  bladder  have  been  mistaken  for  peritonitis !  Hysterical 
meteorism  (see  the  chapter  on  Hysteria)  may  also  be  erroneously  ascribed  to 
peritonitis. 

Treatment. — Although  severe  cases  are  generally  almost  hopeless,  yet  we 
must  try  to  meet  the  symptomatic  indications,  and  must  do  all  in  our  power 
to  promote  a  limitation  of  the  process,  if  it  be  possible. 

External  counterirritants  or  "  revulsants  "  are  seldom  of  much  use.  Paint- 
ing with  tincture  of  iodin  and  mercurial  inunctions  seem  so  utterly  purpose- 
less that  they  should  be  discarded.  The  local  abstraction  of  blood  cannot  be 
employed  in  an  extensive  peritonitis  with  constitutional  prostration.     It  is 


652  DISEASES  OF  THE  DIGESTIVE   ORGANS 

only  in  a  circumscribed  peritonitis  which  is  very  painful^  and  when  the  gen- 
eral condition  of  the  patient  remains  comparatively  favorable,  that  bleeding 
is  to  be  considered.  Under  these  circumstances  the  application  of  eight  to 
fifteen  leeches  sometimes  causes  decided  abatement  of  the  pain.  The  local 
application  of  ice  to  the  abdomen  is  universally  in  vogue.  It  moderates  the 
pain,  and  it  may  also  have  a  beneficial  influence  in  quieting  peristalsis.  Still, 
some  patients  cannot  bear  ice,  and  sometimes  hot  cloths  and  poultices  give 
great  relief. 

Of  all  internal  remedies,  there  is  but  one  of  great  value,  namely,  opium. 
This  in  large  doses  (15  to  20  drops  of  laudanum  or  1  gr.  [gm.  0.05]  of  ex- 
tract of  opium  every  one  or  two  hours)  almost  always  proves  beneficial.  It 
moderates  both  the  pain  and  the  vomiting  or  eructations ;  and  also,  by  dimin- 
ishing the  peristaltic  movements  of  the  intestine,  opium  contributes  in  another 
way  to  assuage  the  suffering  and  possibly  to  limit  the  spread  of  the  inflam- 
mation. Experience  shows  that  almost  all  patients  bear  large  doses  of  opium 
remarkably  well  in  peritonitis.  Perhaps  this  is  because  the  drug  is  only 
slowly  absorbed.  To  substitute  injections  of  morphin  for  opium  is  wise  only 
in  cases  where  we  wish  to  produce  narcosis  as  rapidly  as  possible,  or  when  the 
vomiting  or  pain  does  not  prove  amenable  to  the  ordinary  treatment.  In 
such  cases  we  may  also  prescribe  laudanum  by  enema  or  the  extract  in  a 
suppository. 

Sometimes  particular  symptoms  demand  special  attention.  For  vomiting 
we  may  employ,  besides  opium,  bits  of  ice,  small  quantities  of  sherbet,  and  per- 
haps chloroform  or  cocain.  If  tympanites  is  excessive,  we  may  try  to  remove 
some  of  the  gas  through  a  rectal  tube  passed  as  high  up  as  possible.  Turpentine 
enemata,  containing  1  teaspoonful  of  turpentine  to  7  ounces  (200  c.c.)  of  a  thin 
gum-arabic  solution,  are  also  recommended.  Some  physicians  also  puncture 
the  distended  intestinal  coils  with  a  fine  trocar.  Collapse  and  cardiac  failure 
require  the  exhibition  of  stimulants,  such  as  camphor  oil  subcutaneously, 
ether,  champagne,  etc.  A  hypodermoclysis  of  normal  (0.6  per  cent)  saline  so- 
lution is  also  of  service.  It  is  generally  very  difficult  to  nourish  the  patient. 
As  a  rule,  small  quantities  of  ice-cold  milk  are  the  best  of  anything  as  food. 

The  surgical  treatment  of  acute  peritonitis  is  constantly  growing  in  im- 
portance. It  is  self-evident  that  in  the  case  of  a  circumscribed  abscess  in  the 
abdominal  cavity  the  only  way  of  giving  prompt  relief  is  by  operative  inter- 
ference; but  even  in  acute  diffuse  peritonitis  the  results  obtained  by  laparot- 
omy, while  not  brilliant,  are  encouraging,  and  further  trials  are  the  more 
imperative,  because  otherwise  the  prognosis  of  such  cases  is  almost  absolutely 
hopeless.  The  more  promptly  the  inflammatory  germs  and  septic  matter  are 
removed  from  the  abdominal  cavity,  the  greater  is  the  possibility  of  perma- 
nent cure.  The  details  of  the  surgical  treatment  of  peritonitis  must  be  sought 
elsewhere. 


CHAPTER    II 

CHRONIC    AND    TUBERCULOUS    PERITONITIS 

etiology. — Chronic  nontuberculous  peritonitis  is  a  rather  rare  disease.    It 
is  found  most  frequently  in  post-mortem  examinations  of  patients  who  have 


CHRONIC  AND  TUBERCULOUS  PERITONITIS  653 

had  for  a  long  time  ascites  due  to  venous  stasis,  and  on  whom  repeated  punc- 
tures have  been  practiced.  The  chronic  peritonitis,  however,  is  not  the  direct 
result  of  the  passive  hyperemia  in  such  cases,  but  is,  as  already  hinted,  due  in 
most  instances  to  the  puncturing  of  the  abdomen  during  life  for  the  removal 
of  the  ascitic  fluid.  Exceptionally  a  chronic  peritonitis  occurs  as  a  sequel  to 
some  severe  intestinal  disorder,  such  as  ulceration.  Thus,  chronic  peritonitis 
is  sometimes  observed  to  follow  typhoid  fever. 

Chronic  peritonitis  may  furthermore  be  the  result  of  an  acute  peritonitis. 
The  latter  seldom  terminates  in  this  way,  but  still  it  may,  when  rather  mild 
and  not  quickly  fatal.  The  encapsulated  exudations  of  peritonitis  usually 
persist  a  long  while,  as  was  implied  in  the  preceding  chapter. 

There  is  still  great  uncertainty  about  the  aetiology  of  those  cases  which 
start  in  a  subacute  or  chronic  manner,  without  special  cause.  Sometimes  they 
seem  to  be  due  to  an  injury  of  the  abdomen;  in  other  cases  there  are  special 
constitutional  influences,  such  as  alcoholism,  which  may  occasion  the  disease. 
In  children,  and  less  often  in  adults,  we  sometimes  see  cases  of  "  simple  exu- 
dative peritonitis,"  with  a  serous  exudation.  It  is  possible  that  in  such  in- 
stances pathogenic  organisms  of  various  kinds  occasion  the  inflammation;  but 
in  order  of  frequency  there  is  scarcely  a  doubt  that  tuberculosis  should  be 
named  first.  Just  as  in  pleurisy,  many  cases  of  what  is  apparently  primary 
"  simple  "  peritonitis  turn  out  eventually  to  be  tuberculous. 

The  tuberculous  is  the  most  frequent  form  of  chronic  peritonitis.  It  is 
often  merely  a  part  of  the  tuberculosis  of  serous  membranes  in  general  (vide 
pages  352  and  448),  of  which  mention  has  been  already  repeatedly  made.  In 
these  cases  it  is  usually  due  to  a  conveyance  of  the  process  from  the  pleura 
through  the  diaphragm.  Another  way  in  which  tuberculous  peritonitis  may 
arise  is  by  infection  from  neighboring  tubercular  organs.  Tubercular  intes- 
tinal ulcers  are  among  the  chief  causes  of  this  kind,  the  ulcer  extending  to 
the  peritoneum;  or  the  peritonitis  may  be  excited  by  tuberculous  retroperi- 
toneal or  mesenteric  lymph-glands.  In  women  tuberculous  peritonitis  may  be 
developed  in  consequence  of  tuberculosis  of  the  genital  organs.  Tuberculosis 
of  the  uterus  sometimes  affects  the  Fallopian  tubes  by  direct  extension,  and 
thence  the  virus  enters  the  abdominal  cavity  and  excites  its  specific  inflamma- 
tion. In  conclusion,  we  have  to  mention  that,  in  general  miliary  tuberculosis, 
the  peritoneum  also  may  be  the  seat  of  numerous  tubercles,  although  these 
do  not,  as  a  rule,  give  rise  to  important  symptoms. 

Pathology. — In  severe  cases  of  chronic  peritonitis — and  scarcely  any  others 
have  come  to  autopsy — the  peritoneum  is  usually  found  to  be  considerably 
thickened.  The  intestinal  coils  are  joined  to  one  another  and  to  the  neigh- 
boring organs  by  numerous  and  extensive  adhesions.  The  false  membranes 
are  often  delicate  and  easily  separable,  but  in  some  cases  it  is  a  hard  matter 
to  disentangle  the  confused  mass  into  which  the  intestines  have  been  rolled. 
Sometimes  the  liver  and  spleen  are  covered  by  firm,  tough  capsules.  The 
omentum  and  mesentery  are  much  shrunken,  hence  the  name  peritonitis  de- 
formans. The  omentum  may  indeed  be  transformed  into  a  single  thick  cord. 
As  a  rule,  there  is  little  liquid  effusion,  and  perhaps  none.  In  simple  chronic 
peritonitis,  such  fluid  as  may  be  present  is  usually  a  cloudy  serum,  sero-pus 
being  seldom  seen. 

There  are  sometimes  many  clots  of  fibrin  suspended  in  the  fluid.     If  the 


654  DISEASES  OF  THE  DIGESTIVE  ORGANS 

abdomen  has  been  repeatedly  punctured  during  the  life  of  the  patient,  we 
often  may  recognize  the  separate  punctures,  on  the  inner  surface  of  the  peri^ 
toneum,  from  the  hemorrhages,  adhesions,  or  similar  changes  which  have  oc- 
curred. In  rare  instances  a  peculiar  form  of  chronic  peritonitis  has  been 
observed  as  a  sequel  to  punctures  for  ascites,  called  by  Friedreich  "  chronic 
hemorrhagic  peritonitis  with  hematoma."  In  it  almost  the  entire  peritoneum 
is  covered  by  a  newly  formed  membrane  permeated  with  large  ecchymoses. 

"We  will  also  mention  briefly  a  peculiar  form  of  chronic  peritonitis,  which 
has  not  yet  been  sufficiently  investigated.  This  leads  to  the  formation  of 
numerous  small  nodules  in  the  peritoneum,  which  are  usually  at  first  regarded 
as  tubercles,  but  upon  microscopic  examination  are  found  to  be  nodules  of 
connective  tissue. 

Tuberculous  disease  of  the  peritoneum  may  be  divided  into  two  forms :  tu- 
berculosis of  the  peritoneum,  which  may  be  acute  or  chronic,  and  tuberculous 
peritonitis,  which  is  usually  chronic.  In  tuberculosis  the  peritoneum  is  cov- 
ered with  numerous  tubercular  nodules,  varying  in  size  from  a  millet  seed  up 
to  a  pea;  but  there  is  not  much  coincident  inflammatory  change.  In  genuine 
tuberculous  peritonitis,  on  the  other  hand,  the  inflammatory  changes  above 
described  are  well  marked,  while  sometimes  it  requires  a  microscopic  examina- 
tion to  demonstrate  the  tuberculous  nature  of  the  inflammation,  by  the'  detec- 
tion of  tubercles  and  cheesy  degeneration  in  the  newly  formed  tissue.  Tu- 
berculous peritonitis  is  usually  rather  chronic,  so  that  the  adhesions  are 
numerous  and  strong.  The  amount  of  liquid  effusion  varies,  being  sometimes 
considerable  and  sometimes  scanty.  Just  as  in  tuberculous  pleurisy,  it  is  not 
rare  for  the  exudation  to  be  bloody.  In  long-continued  peritoneal  tuberculosis 
the  omentum  is  found  irregularly  thickened,  and  the  whole  intestinal  cavity 
filled  with  tumor-like  masses  (lymph-glands,  etc.).  Occasionally  localized 
tuberculous  disease  of  the  peritoneum  occurs.  The  ileocascal  tuberculosis,  pre- 
viously referred  to  in  the  chapter  on  intestinal  tuberculosis,  belongs  primarily 
in  this  category.  Among  the  more  important  associated  conditions  we  have 
tuberculosis  of  other  organs,  and  also  the  comparatively  frequent  combination 
of  tuberculous  peritonitis  with  hepatic  cirrhosis  (q.  v.). 

Clinical  History.  Diagnosis. — If  an  acute  peritonitis  becomes  chronic,  the 
violent  symptoms  gradually  abate,  while  another  group  of  symptoms  takes 
their  place.  In  other  cases  the  chronic  disease  develops  gradually  and  in- 
sidiously. 

The  sensitiveness  of  the  abdomen  is  never  so  extreme  as  in  the  acute  in- 
flammation. Sometimes,  to  be  sure,  the  patient  complains  of  dull  pains  and 
a  sense  of  abdominal  oppression,  but  quite  often  the  pain  is  either  constantly 
or  at  times  insignificant.  On  physical  examination  we  usually  find  moderate 
distention  of  the  abdomen.  Frequently  this  is  not  perfectly  uniform,  certain 
coils  of  intestine  being  especially  prominent.  Occasionally  there  is  no  ab- 
dominal distention  whatever,  the  belly  is  flat  or  concave,  and  the  walls  are 
tense  and  unyielding.  The  abdomen  is  more  distended  if  there  is  a  large 
amount  of  liquid  exudation  or  if  there  is  extensive  tuberculous  new  growth. 

In  many  instances  palpation  furnishes  very  characteristic  signs,  for  some- 
times the  thickening  of  the  omentum  and  the  numerous  fibrous  interintestinal 
bands  above  described  can  be  felt  through  the  abdominal  walls  as  peculiarly 
resistant  masses  or  uneven  prominences.     Indeed,  if  the  omentum  is  rolled 


CHRONIC   AND   TUBERCULOUS   PERITONITIS  655 

up  it  may  closely  simulate  a  new  growth.  The  same  is  true  of  enlarged 
lymph-glands.  Not  infrequently,  particularly  in  tuberculous  peritonitis,  the 
liver  is  enlarged  so  that  its  lower  edge  can  be  felt.  But  in  other  cases  of 
chronic  peritonitis  there  are  no  changes  discoverable  by  palpation,  or  they 
may  he  concealed  by  an  effusion  or  by  the  tenseness  of  the  abdominal  walls. 
A  large  exudation  can  be  demonstrated  by  the  great  distention,  or  by  its  caus- 
ing fluctuation,  or  by  the  signs  yielded  on  percussion.  As  a  result  of  the 
adhesions  of  the  intestines  to  one  another,  we  find  that  the  fluid  does  not 
change  its  position  very  readily  upon  change  of  position  of  the  patient.  This 
circumstance  is  indeed  one  means  of  differentiating  between  peritonitic  exu- 
dation and  ordinary  ascites.  Not  infrequently  the  resonance  upon  percussion 
is  very  greatly  impaired,  even  when  there  is  no  large  amount  of  fluid  exuda- 
tion. This  is  probably  due  to  thickening  of  the  peritoneum,  fibrinous  de- 
posits, and  similar  changes.  Peritonitic  friction  sounds  are  sometimes 
audible,  particularly  in  the  hepatic  region.  It  has  been  already  stated  that 
the  distortions  and  flexions  which  the  intestines  may  undergo  in  chronic 
peritonitis  may  result  in  obstruction.  In  the  same  way  the  duodenum 
or  the  ductus  choledochus  may  be  so  occluded  as  to  occasion  persistent 
jaundice. 

The  objective  signs  of  both  the  simple  and  tuberculous  forms  of  chronic 
peritonitis  have  been  embraced  in  one  description,  because  the  abdominal 
signs  of  the  two  are  identical.  To  differentiate  between  them,  other  factors 
must  be  considered.  We  regard  the  patient's  constitution  and  general  ap- 
pearance, and  inquire  into  his  family  history,  or  discover  if  there  are  other 
etiological  factors,  such  as  previous  tuberculous  disease.  A  careful  thoracic 
examination  is  extremely  important.  If  we  find  the  signs  of  coincident  pul- 
monary tuberculosis,  or  of  pleurisy,  then  it  is  almost  indubitable  that  the 
peritonitis  is  tuberculous.  The  course  of  the  fever  and  pulse  is  very  important. 
Persistent  hectic  fever  and  persistent  increasing  frequency  of  the  pulse  with 
moderate  fever  must  always  arouse  strong  suspicions  of  tuberculosis.  The 
character  of  the  exudation  obtained  by  aspiration  may  be  significant,  for  the 
admixture  of  blood  and  a  lymphocytosis  occur  mainly  in  tuberculous  peritoni- 
tis, but  we  may  also  have  serous  exudation  in  tuberculous  peritonitis,  just  as  in 
the  ordinary  tuberculous  pleurisy.  Tubercle  bacilli  are  not  usually  present 
in  the  exudation  of  tuberculous  peritonitis. 

To  diagnosticate  simple  tuberculosis  of  the  peritoneum,  when  not  attended 
by  marked  inflammatory  changes,  is  generally  a  difficult  matter.  Often  it  is 
absolutely  impossible.  Frequently  there  is  no  abdominal  pain  or  tenderness 
whatever.  The  abdomen  is-  usually  but  moderately  distended,  as  a  result  of 
the  effusion  present.  If  we  find  such  a  condition  in  a  patient  who  is  known 
to  have  some  other  tuberculous  affection,  we  are  justified  in  suspecting  that 
there  is  a  simple  tuberculosis  of  the  peritoneum. 

It  is  not  unusual  to  observe  the  combination  of  hepatic  cirrhosis  with 
peritonitis,  which  we  have  already  briefly  mentioned.  We  have  then  splenic 
tumor  and  the  other  signs  of  portal  congestion,  in  addition  to  the  symptoms 
of  chronic  peritonitis,  such  as  pain  and  fever.  The  amount  of  fluid  in  the 
abdomen  is  usually  considerable.  As  a  rule,  the  patients  are  hard  drinkers. 
The  hepatic  cirrhosis  may  be  the  primary  disease,  and  if  so,  it  joins  with  the 
constitutional  results  of  alcoholic  excess  in  promoting  the  liability  to  tuber- 


656  DISEASES   OF   THE   DIGESTIVE   ORGANS 

culous  infection.  We  have  also  observed  a  combination  of  a  syphilitic  atrophic 
liver  and  tuberculous  peritonitis. 

Particular  notice  should  be  given  to  the  chronic  peritonitis  of  children, 
already  mentioned.  The  occurrence  of  ascites  in  children  between  the  ages 
of  two  and  ten  years  has  been  observed  repeatedly,  both  by  other  authors  and 
by  ourselves.  The  ascites,  which  may  be  considerable,  cannot  be  traced  to  any 
cause,  and  after  a  few  months  completely  disappears.  The  child  during  this 
time  is  usually  rather  pale  and  languid,  but  not  much  emaciated,  nor  does 
he  suffer  great  local  discomfort.  There  may  be  no  fever.  Since  the  cases 
often  recover,  their  pathological  anatomy  remains  obscure.  Probably  they 
are  a  mild  form  of  simple  chronic  peritonitis.  Still,  of  course,  there  may  be 
other  causes  for  ascites,  such  as  hereditary  syphilitic  disease  of  the  liver. 

In  children  tuberculous  peritonitis  plays  an  important  part  in  general  tu- 
berculosis of  the  abdominal  organs,  a  condition  formerly  known  as  tabes 
mesenterica.  In  these  cases  the  tuberculosis  probably  originates,  as  we  have 
already  said,  in  the  intestine,  so  that  usually  we  find  the  intestine,  peritoneum, 
liver,  and  abdominal  lymph-glands  all  simultaneously  involved.  The  clinical 
symptoms  are  often  due  mainly  to  the  peritonitis.  The  abdomen  is  distended 
and  painful,  and  there  is  an  effusion.  Often  there  is  also  obstinate  diarrhea, 
as  a  result  of  tubercular  intestinal  ulcers,  with  persistent  fever  of  an  inter- 
mittent character,  emaciation,  and  anaemia.  The  tubercular  process  may 
eventually  involve  the  lungs,  pleura,  meninges,  and  other  organs,  or  it  may 
never  extend  beyond  the  abdomen. 

As  to  the  course  of  chronic  peritonitis  we  have  little  to  say.  The  simple 
chronic  peritonitis  may  terminate  in  recovery,  although  on  account  of  other 
coexisting  lesions  this  event  is  rare,  except  in  the  special  form  which  children 
present.  Many  cases  of  tuberculous  peritonitis  prove  fatal  in  a  few  months 
or  weeks.  The  fatal  termination  of  peritoneal  tuberculosis  may  be  occasioned 
by  a  septic  peritonitis,  due  to  perforation.  We  have  seen  two  cases  of  this 
sort  in  which  the  tuberculous  focus  perforated  the  intestinal  wall  from  its 
outer  side.  In  many  instances,  however,  chronic  tuberculous  peritonitis  has  a 
favorable  issue,  or  at  least  there  is  very  great  abatement  of  all  symptoms. 
This  is  particularly  apt  to  be  the  case  in  what  is  called  primary  tuberculosis 
of  the  serous  membranes  in  general  (vide  supra).  If,  in  this  disease,  there 
is  no  simultaneous  tuberculosis  of  the  lungs,  intestines,  or  other  organs,  then 
the  final  reabsorption  of  the  exudation  is  possible,  just  as  in  tuberculous 
pleurisy.  It  must  be  confessed  that  often  the  recovery  is  not  permanent,  for 
the  tubercles  may  appear  later  in  some  other  part  of  the  body. 

Treatment. — The  means  by  which  we  can  exercise  a  favorable  influence 
upon  the  course  of  chronic  peritonitis  are  scanty.  Nevertheless,  very  satisfac- 
tory results  can  be  obtained  in  some  cases  by  careful  treatment.  Great  weight 
should  be  laid,  above  all,  upon  the  constitutional  treatment  (continuous  fresh 
air  and  rest  cures,  if  necessary,  in  suitable  health  resorts  or  sanatoria,  careful 
nourishment,  etc.).  Besides  this,  certain  local  remedies  act  favorably,  es- 
pecially the  methodical  inunction  of  the  abdomen  with  green  soap  (spiritus 
saponatokalinus,  or  a  salve  containing  equal  parts  of  green  soap  and  simple 
ointment).  Alcohol  compresses  (thirty  per  cent),  hot  applications,  Priessnitz 
applications,  are  also  often  of  use.  Inunctions  of  blue  ointment,  iothion  salve, 
etc.,  may  also  be  tried.    Internal  remedies  are  usually  only  indicated  as  symp- 


ASCITES  657 

tomatic  therapy  (opium,  cathartics,  etc.).  If  there  is  considerable  exudation, 
diurctin,  acetate  of  potassium,  and  similar  diuretic  remedies  are  indicated. 
Whether  curative  results  are  to  be  expected  from  tuberculin  further  experience 
must  determine. 

Of  late  the  surgical  treatment  of  peritoneal  tuberculosis  has  had  very 
favorable  results.  It  has  been  observed  that  in  many  cases  of  tuberculous  peri- 
tonitis, laparotomy,  with  as  complete  an  evacuation  of  the  exudation  as  pos- 
sible (better  than  can  be  accomplished  by  mere  puncture  of  the  abdomen), 
exercises  a  wonderfully  beneficial  influence  upon  the  course  of  the  disease, 
and  even  seems  in  many  cases  to  occasion  complete  recovery.  This  fact  is 
interesting,  although  not  yet  wholly  explained.  Further  observations  must  be 
collected  with  regard  to  this  procedure,  but  our  own  experience  justifies  us 
in  recommending  it  in  suitable  cases.  Particulars  with  regard  to  its  em- 
ployment are  taught  in  works  on  surgery. 


CHAPTEE    III 

ASCITES 
(Hydroperitoneum) 

The  name  ascites  is  given  to  a  collection  of  transuded  serum  in  the  ab- 
dominal cavity  due  to  venous  stasis.  The  peritoneal  veins  belong  to  the  portal 
system,  so  that  among  the  diseases  which  lead  to  ascites  those  which  impede 
the  portal  circulation  are  chief.  As  we  shall  see  in  the  next  section,  ascites  is, 
therefore,  of  frequent  occurrence  in  cirrhosis  of  the  liver,  syphilitic  disease  of 
the  liver,  compression  of  the  portal  vein  by  tumors,  thrombosis  of  the  portal 
vein,  and  similar  disorders.  Ascites  is  also  frequently  present  as  one  of  the 
dropsical  symptoms  in  the  general  circulatory  disturbances,  of  cardiac  disease, 
and  in  the  course  of  various  acute  and  chronic  renal  affections. 

The  clinical  significance  of  ascites  is  due  partly  to  the  local  discomfort  oc- 
casioned by  the  presence  of  any  considerable  amount  of  fluid  within  the  ab- 
dominal cavity.  Small  quantities  of  serum  are  often  unnoticed  by  the  patient ; 
but,  where  many  quarts  (15  to  20,  or  even  more)  of  transudation  exist,  the 
abdominal  walls  become  greatly  distended,  and  the  patient  has  a  very  trouble- 
some feeling  of  pressure,  weight,  and  tension.  What  is  of  still  greater  im- 
portance is  the  crowding  upward  of  the  diaphragm.  Bespiration  is  thereby 
not  a  little  impeded.  If  the  ascites  is  great,  the  lower  lobes  of  the  lungs  are 
so  compressed  that  a  considerable  degree  of  atelectasis  is  produced. 

To  demonstrate  ascites  by  physical  examination  is  possible  only  when  a 
considerable  accumulation  exists.  Then  the  belly  is  prominent,  its  walls  are 
tense  and  shining,  and,  the  base  of  the  thorax  being  gradually  distended  by 
the  pressure  of  the  liquid,  the  lower  part  of  the  thorax  seems  much  broader 
than  the  upper.  Distended  veins  are  usually  visible  through  the  skin  of  the 
abdomen,  like  blue  lines,  here  and  there.  These  represent  collaterals  used  for 
the  obstructed  venous  circulation.  As  soon  as  the  abdominal  tension  has  at- 
tained a  certain  degree,  fluctuation  can  be  perceived  by  laying  both  hands  upon 
the  abdomen  and  imparting  gentle  but  quick  impulses  to  the  fluid  through  the 


658  DISEASES   OF  THE   DIGESTIVE   ORGANS 

walls.  Percussion  gives  a  dull  sound  everywhere  that  the  fluid  is  in  contact 
with  the  abdominal  walls.  Gravity,  of  course,  leads  the  liquid  to  occupy  the 
dependent  parts.  In  the  dorsal  decubitus,  and  when  the  transudation  is  of 
medium  amount,  the  dullness  is  bounded  in  the  central  and  upper  parts  of  the 
abdomen  from  a  region  of  tympanitic  resonance  by  a  line  concave  toward  the 
head  of  the  patient.  The  surface  of  the  liquid  being  horizontal,  of  course  the 
dullness  extends  higher  along  the  sides  of  the  abdomen,  while  the  tympanitic 
resonance  is  present  in  the  central  part.  We  would  add  that,  where  the  layer 
of  ascitic  fluid  is  thin,  we  can  obtain  dullness  only  by  light,  superficial  percus- 
sion. If  the  pleximeter  or  finger  is  pressed  deeply  in,  the  fluid  is  crowded  to 
one  side,  and  we  get  a  tympanitic  sound  from  the  underlying  coils  of  intestine. 
A  factor  of  great  diagnostic  value  is  the  change  of  dullness  on  change  of  posi- 
tion of  the  patient.  If  he  lies  upon  one  side,  the  fluid  seeks  the  dependent 
portions  of  the  cavity,  and  gives  rise  to  extensive  dullness  there,  while  the 
opposite  side  now  yields  a  tympanitic  resonance.  Or,  if  he  changes  to  the 
other  side,  it  in  turn  becomes  dull,  and  the  side. previously  dull  becomes  tym- 
panitic. Similar  differences  are  found  between  the  results  of  percussion  in  a 
horizontal  and  in  a  sitting  posture.  It  is  only  when  the  accumulation  is  very 
abundant  that  there  is  dullness  over  the  entire  abdomen. 

The  signs  mentioned  enable  us  in  most  cases  to  make  a  diagnosis  of  ascites 
with  ease  and  certainty.  It  is,  indeed,  not  always  easy  to  distinguish  a  transu- 
dation of  serum  from  the  exudation  of  chronic  peritonitis,  for,  of  course,  either 
sort  of  fluid  would  yield  the  same  physical  signs.  Only,  the  change  in  the 
area  of  dullness  consequent  upon  a  change  of  position  is  less  pronounced  in 
case  of  an  exudation,  because  the  peritonitic  adhesions  impede  the  movements 
of  the  fluid ;  and  we  have,  besides,  all  the  other  symptoms  to  guide  us :  there 
may  be  pain,  fever,  or  thickening  of  the  peritoneum  discoverable  on  palpation, 
or  signs  of  tuberculosis;  or,  on  the  other  hand,  there  may  be  some  cardiac  or 
hepatic  disease  which  would  render  ascites  probable.  If  the  fluid  is  drawn 
off,  its  character  will  sometimes  aid  us  in  diagnosis.  Ascites  yields  pure  serum, 
containing  almost  no  morphological  constituents.  Its  specific  gravity  is  usu- 
ally less  than  that  of  a  peritonitic  exudation,  because  it  contains  less  albumen. 
We  may  say  that  the  specific  gravity  of  the  fluid  found  in  peritonitis  is  gener- 
ally above  1.018,  and  that  of  ascites  about  1.012,  or  even  lower.  The  albumen 
content  of  ascitic  fluid  is  about  one  to  three  per  cent,  while  that  of  peritonitic 
exudate  is  as  high  as  four  to  six  per  cent.  Hemorrhagic  ascites  sometimes 
occurs  in  ansemic  patients  who  are  suffering  from  marked  portal  obstruction, 
as  we  have  ourselves  seen,  for  example,  in  hepatic  syphilis. 

Chylous  ascites  due  to  an  abundance  of  fat  in  the  fluid  may  appear  as  a 
result  of  occlusion  of  the  thoracic  duct,  but  it  should  be  pointed  out  that  ascitic 
fluid  has  sometimes  a  chylous  opacity,  even  when  it  contains  no  fat  (emulsion 
of  albuminous  substances?). 

There  may  be  equal  difficulty  in  the  exclusion  of  ovarian  cysts,  particularly 
since  the  cysts  are  sometimes  so  large  as  to  fill  the  whole  abdominal  cavity. 
We  must  first  map  out  accurately  the  dullness  on  percussion,  and  also  see  if  it 
varies  with  changes  of  position.  In  cases  of  ovarian  tumor,  change  of  position 
does  not  make  much  difference.  The  resonance  on  percussion  of  the  deepest 
and  most  dependent  portions  of  the  abdomen  may  be  misleading,  in  this  way, 
that  even  in  ascites  a  narrow  zone  here  may  be  tympanitic.    This  should  be 


ASCITES  659 

remembered.  Thus,  just  above  the  symphysis,  there  is  sometimes  a  tympanitic 
resonance  in  ascites  which  might  readily  be  mistaken  for  a  proof  of  the  exist- 
ence of  an  ovarian  tumor.  The  explanation  is  thai  in  the  places  indicated  a 
coil  of  intestine  with  a  short  mesenteric  attachment  may  remain  in  contact 
with  the  abdominal  wall  in  spite  of  ascitic  accumulations.  Further  aid  in  the 
differential  diagnosis  is  to  he  obtained  from  the  history  of  the  case  (place 
where  the  swelling  began),  from  a  consideration  of  possible  causative  diseases, 
and  from  a  vaginal  examination,  including  direct  palpation  of  the  ovaries.  In 
ascites  the  uterus  is  freely  movable,  while  in  case  of  ovarian  tumors  it  is  often 
bound  down  by  adhesions.  Further  particulars  may  be  sought  in  books  on 
gynecology. 

Treatment. — The  treatment  of  ascites  depends  largely  upon  the  disease  of 
which  it  is  a  symptom.  As  to  the  symptomatic  treatment  of  ascites  itself,  we 
will  confine  ourselves  to  a  few  words  about  tapping.  This  operation  is  indi- 
cated when  the  local  disturbances  caused  by  the  ascites  are  great;  that  is,  if 
there  is  an  unbearable  sensation  of  pressure  and  tension,  and,  above  all,  if  the 
crowding  up  of  the  diaphragm  causes  much  dyspnoea.  The  instrument  to  be 
used  is  a  common  trocar  of  medium  size.  If  strength  permits,  the  puncture 
can  be  most  conveniently  done  with  the  patient  sitting  in  a  chair,  or  crosswise 
on  the  edge  of  the  bed.  We  usually  choose  as  the  best  place  for  the  puncture 
a  point  in  the  left  lower  part  of  the  abdomen,  or,  if  the  patient  is  seated, 
one  in  the  linea  alba,  about  halfway  between  the  navel  and  the  symphysis.  Of 
course  we  should  first  see  that  the  bladder  has  been  emptied.  In  the  majority 
of  cases  we  are  obliged  to  make  the  puncture  with  the  patient  in  the  lateral 
position;  we  then  insert  the  instrument  in  the  lower  and  left  side  of  the 
abdomen,  about  halfway  between  the  navel  and  the  anterior  superior  spine. 
The  exudation  should  never  be  allowed  to  escape  too  rapidly.  We  may  permit 
large  amounts  of  liquid  (5  or  10  quarts,  or  more)  to  flow  slowly  away  at  one 
tapping.  We  close  the  puncture  with  sterile  cotton  and  adhesive  plaster,  or 
with  iodoform  collodion.  Often  the  fluid  trickles  out  through  the  opening, 
because  the  abdominal  walls  have  lost  their  elasticity  on  account  of  the 
persistent  distention.  We  may  then  employ  a  suture  to  close  it.  After 
tapping,  the  laxness  of  the  walls  is  favorable  to  palpation  of  the  abdominal 
organs. 

Inasmuch  as  tapping  does  not  remove  the  cause,  there  is  in  most  cases  a 
very  rapid  reaccumulation  of  fluid.  Thus  the  system  is  deprived  of  much 
albumen,  and  nutrition  is  impaired,  so  that  not  infrequently  the  operation  is 
followed  by  decided  loss  of  strength.  Therefore,  we  should  not  tap  in  ascites, 
as  a  rule,  unless  the  indications  for  the  operation  are  urgent. 

[If,  as  is  very  frequently  the  case,  the  fluid  continues  to  drain  away  through 
the  puncture  after  the  trocar  is  withdrawn,  good  rather  than  harm  results,  pro- 
vided the  danger  of  irritation  of  the  skin  and  of  bedsores  is  kept  in  mind  and 
guarded  against,  and  an  instrument  of  moderate  size  is  used. 

Flint  advocates  early  and  repeated  tappings  if  the  fluid  causes  discomfort 
and  does  not  yield  to  diuretics  or  cathartics.  The  pressure  is  removed  in  a 
measure  from  the  abdominal  and  thoracic  organs,  and  nutrition  is  thus  pro- 
moted. The  fluid  is  likely  to  return,  but  it  does  not  always  do  so,  or  it  may 
do  so  only  slowly.  He  reports  cases  in  which,  after  repeated  removal,  the  fluid 
ceased  to  return  and  the  patient  remained  apparently  well.     The  result  must 


660  DISEASES   OF   THE   DIGESTIVE   ORGANS 

depend,  of  course,  chiefly  on  the  underlying  cause,  which  is  sometimes  very 
obscure. 

In  cases  of  cirrhosis  the  same  principles  govern  Flint's  treatment.] 


CHAPTER   IV 
CANCER    OF    THE    PERITONEUM 

Cakcinoma  is  the  only  new  growth  of  any  practical  importance  to  which 
the  peritoneum  is  liable.  Primary  endothelial  cancer,  analogous  to  the  growth 
which  attacks  the  pleura,  is  very  rare.  Cancerous  growths  here  are  usually 
secondary  to  cancer  of  the  stomach,  intestine,  pancreas,  liver,  or  some  other 
organ.  Often  the  secondary  nodules  are  numerous,  and  almost  as  small  as 
peas,  presenting  what  is  called  miliary  carcinosis  of  the  peritoneum.  They 
cover  the  omentum,  mesentery,  and  parietal  peritoneum.  Separate  nodules  of 
larger  size  are  less  frequent.  These  may  be  found  in  the  omentum,  in  Douglas's 
pouch,  around  the  navel,  or  in  other  situations.  Colloid  cancer  attains  the 
most  diffuse  and  extensive  development  of  any  variety.  The  retroperitoneal 
lymph-glands  may  also  present  at  the  same  time  large  cancerous  growths. 
Often  the  development  of  cancer  in  the  peritoneum  is  attended  with  pro- 
nounced inflammatory  disturbances — that  is,  we  have  a  cancerous  peritonitis. 

Symptoms. — The  symptoms  of  peritoneal  cancer  resemble  in  many  points 
those  of  chronic  tuberculous  peritonitis.  Simple  miliary  carcinosis  may  be  very 
insidious  and  give  rise  to  no  special  symptoms,  so  that  it  often  is  unsuspected. 
In  many  cases  a  moderate  amount  of  fluid  collects  in  the  abdomen,  and  this, 
if  we  are  aware  of  the  existence  of  a  primary  cancerous  growth,  may  lead  us 
to  surmise  a  secondary  peritoneal  carcinosis.  The  symptoms  are  much  more 
pronounced  if  there  is  cancerous  peritonitis.  In  that  case  there  is  usually  very 
severe  pain,  marked  abdominal  distention,  and  constipation.  We  may  some- 
times feel  the  larger  nodules  in  the  omentum  or  upon  the  inner  surface  of  the 
anterior  wall  of  the  abdomen,  or  even  those  in  the  lowest  part  of  the  abdomen, 
by  palpation  through  the  vagina  or  the  rectum.  "We  have  repeatedly  observed 
the  development  of  nodules  in  the  navel  in  carcinosis  of  the  peritoneum,  which 
could  be  distinctly  felt  externally  as  an, infiltrated  edge  of  the  umbilicus.  We 
have  repeatedly  felt  a  hard  round  strand  running  down  the  linea  alba  from  the 
navel — probably  a  carcinomatous  infiltrated  lymph-vessel.  The  exuded  fluid 
in  the  abdominal  cavity  is  sometimes  merely  serous,  but  it  may  be  hemorrhagic. 
When  the  new  growth  has  been  diffuse,  and  particularly  in  case  of  colloid 
cancer,  the  exudation  has  repeatedly  been  found  to  present  a  milky  opacity. 
Sometimes  this  fluid  also  has  been  tinged  with  blood.  The  opacity  is  due  to 
fat,  from  fatty-degenerated  and  disintegrated  cancer  cells.  Occasionally  the 
microscope  reveals  characteristic  cancerous  elements  in  the  fluid.  [Diagnosis 
based  upon  the  microscope  alone  has  repeatedly  proved  to  be  erroneous. — V.] 

Diagnosis. — The  diagnosis  cannot  be  made  with  any  positiveness  unless, 
as  a  sequel  to  a  primary  cancerous  growth  already  demonstrated,  we  observe 
the  evident  tokens  of  peritoneal  disturbance,  such  as  free  fluid,  pain,  points  of 
resistance  on  palpation,  and  distention  of  the  abdomen.     Other  factors  are 


CATARRHAL   JAUNDICE  661 

the  patient's  age,  cancerous  cachexia,  and  secondary  glandular  enlargements, 
particularly  in  the  groins  and  supraclavicular  spaces. 

Treatment. — Treatmenj  must  be  confined  to  efforts  at  mitigation  of  the 
suffering.  Warm  applications  and  morphin  are  chiefly  employed.  A  puncture 
may  be  indicated  in  marked  distention  of  the  abdominal  walls. 


SECTION   VII 
Diseases  of  the  Liver,  Bile  Ducts,  and  Portal  Vein 

CHAPTEE    I 

CATARRHAL    JAUNDICE 

(Icterus  catarrhalis.     Gastroduodenal  Catarrh  with  Jaundice) 

iEtiology  and  Pathological  Anatomy. — Catarrhal  jaundice  is  still  the  al- 
most universal  term  applied  to  the  most  common  form  of  jaundice.  It  de- 
velops in  previously  healthy  individuals,  usually  in  a  rather  acute  manner,  and 
sooner  or  later  (as  a  rule,  after  some  weeks)  terminates  in  complete  recovery. 
There  can  be  scarcely  any  doubt  that  a  simple  catarrhal  inflammatory  process 
in  the  bile  ducts  is  the  cause  of  this  not  infrequent  clinical  picture.  We  do 
not  know  exactly  by  which  infectious  agent  the  catarrh  is  produced,  nor  where 
it  begins  and  how  far  it  extends,  inasmuch  as  the  benignancy  of  the  disease 
hardly  ever  affords  an  opportunity  for  anatomical  investigations.  It  is  not 
improbable  that  the  infectious  material  enters  the  larger  bile  ducts  from  the 
duodenum.  It  has  not  been  proved,  however  (at  least  not  for  all  cases),  that 
the  development  of  the  jaundice  is  always  preceded  by  an  actual  catarrh  of 
the  stomach  and  the  duodenal  mucous  membrane.  This  was  formerly  assumed, 
and  the  term  "  gastroduodenal  jaundice  "  applied.  This  can  be  decided  only 
by  a  study  of  the  clinical  course.  It  is  certain  at  least  that  a  more  or  less 
complete  occlusion  of  the  common  bile  duct  or  even  the  other  bile  ducts  does 
occur.  This  is  due  to  a  swelling  of  the  mucous  membrane,  and  perhaps  also 
to  the  mucus  itself  and  the  desquamated  epithelial  cells.  The  occlusion  of 
the  bile  ducts  leads  to  biliary  obstruction  in  the  liver,  and  this  to  jaundice 
{vide  infra). 

Opposed  to  this  explanation  of  "  catarrhal  jaundice,"  which  in  my  opinion 
is  the  most  natural  and  probable,  a  number  of  authors  have  lately  proposed 
another  theory.  According  to  this,  the  jaundice  should  not  be  regarded  as  an 
"  obstructive  jaundice,"  but  as  a  result  of  a  disturbed  function  of  the  liver 
cells  ("paracholia"),  so  that  the  bile  is  no  longer  secreted  into  the  smallest 
bile  ducts,  but  directly  into  the  blood  and  lymph  capillaries.  In  our  opinion, 
this  assumption  is  worthy  perhaps  of  further  investigation  in  certain  other 
forms  of  jaundice  that  occur  after  acute  intoxications.  For  ordinary  catarrhal 
jaundice,  however,  it  appears  to  us  much  too  artificial,  and  by  no  means  sat- 
isfactory. We  believe  that  the  assumption  of  an  infectious  toxic  disease  of  the 
mucous  membrane  is  much  more  plausible.  Naturally,  it  is  not  certain  whether 
42 


662  DISEASES  OP  THE  DIGESTIVE  ORGANS 

the  same  infectious  agent,  such  as  the  colon  bacillus,  is  always  the  exciting 
cause,  or  whether  there  are  a  variety  of  organisms.  The  rather  frequent  epi- 
demic and  endemic  occurrence  of  catarrhal  jaundice  that  has  been  observed  is 
most  instructive.  This  undoubtedly  points  to  a  definite  infectious  cause. 
Bather  extensive  epidemics  of  jaundice  have  been  repeatedly  observed  in  bar- 
racks, prisons,  and  communities  in  a  manner  to  be  explained  only  by  the  sup- 
position of  some  local  source  of  infection.  We  once  observed  a  small,  benign 
epidemic  of  jaundice  among  many  members  of  a  student  fraternity.  In  this 
instance  the  beer  that  had  been  drunk  was  held  responsible.  In  some  in- 
stances the  epidemics  of  jaundice  have  followed  revaccination,  obliging  one  to 
think  of  the  transfer  of  the  pathogenic  organisms  by  means  of  inoculation. 
As  a  rule,  to  be  sure,  jaundice  occurs  sporadically,  and  it  is  not  usually  pos- 
sible to  demonstrate  any  special  cause  for  the  disease,  except  that  there  is 
often  a  connection  with  some  marked  error  in  diet,  with  catching  cold,  or 
some  mental  excitement,  such  as  anger.  Catarrhal  jaundice  is  observed  chiefly 
in  youthful  individuals;  sex  has  no  marked  influence. 

Symptoms  and  Clinical  Course. — Very  frequently,  though  not  invariably, 
there  are,  for  some  days  before  the  appearance  of  the  jaundice,  definite  signs 
of  gastrointestinal  disturbance,  as  well  as  certain  constitutional  symptoms. 
Obstinate  vomiting,  marked  pain  in  the  stomach,  and  similar  symptoms  are 
not  infrequent.  Very  often  the  trouble  begins  with  loss  of  appetite,  a  bad 
taste  in  the  mouth,  nausea,  a  sense  of  pressure  in  the  epigastrium,  eructations, 
and  constipation,  accompanied  by  languor.  Soon  after,  the  patient  himself 
notices  the  yellow  color  of  the  skin,  or  his  attention  is  called  to  it  by  those 
about  him. 

"We  still  hold  provisionally  to  the  view  that  the  cause  of  catarrhal  jaundice 
is  mechanical ;  and  we  desire,  with  a  view  to  preventing  repetition,  to  describe 
here  with  some  minuteness  those  symptoms  which  occur  in  varying  severity  in 
all  cases  of  obstructive  jaundice. 

The  bile  is  secreted  in  the  liver  under  an  extremely  low  pressure,  and  con- 
sequently a  comparatively  slight  obstruction  in  the  bile  ducts  suffices  to  pre- 
vent the  discharge  of  bile  into  the  intestine.  In  ordinary  catarrhal  jaundice, 
and  also  in  other  varieties  of  jaundice,  the  obstruction  to  the  flow  of  bile  is 
seldom  complete,  and  if  so,  only  for  a  time.  Still,  a  considerable  amount  of  bile 
collects,  and  distends  even  the  intrahepatic  duct.s.  As  soon  as  this  stasis  has 
reached  a  certain  point,  the  stagnant  bile  is  absorbed  mainly  by  the  hepatic 
lymph-vessels,  and  perhaps  also  directly  by  the  blood  vessels  of  the  liver.  Thus 
the  bile  and  all  its  constituents  are  poured  into  the  blood  and  carried  to  all 
parts  of  the  body.  No  more  than  a  few  days  need  elapse  before  the  bile  pig- 
ments are  absorbed  into  the  tissues,  and  give  rise  to  the  evident  yellow  color 
of  the  skin  and  visible  mucous  membranes  which  we  call  jaundice.  Usually 
the  yellowness  of  the  conjunctiva  is  the  first  thing  to  attract  attention.  Later 
the  entire  skin  becomes  yellow,  and  the  same  color  is  plainly  visible  in  the 
mucous  membrane  of  the  mouth  and  throat,  especially  after  we  have  produced 
temporary  aneemia  by  pressure,  as  in  the  lips.  The  intensity  of  the  yellow 
discoloration  presents  the  most  varying  degrees.  With  artificial  illumination 
(with  the  exception  of  the  white  electric  light)  the  icteric  coloring  of  the  skin 
is  scarcely  noticeable.  The  internal  organs,  which  we  cannot  see,  are  likewise 
stained  to  a  greater  or  lesser  extent.    Any  abnormal  collection  of  liquid  will 


CATARRHAL   JAUNDICE  663 

also  have  a  marked  yellow  color.  The  cornea,  the  peripheral  aerves,  and  the 
cartilages  alone  escape  unstained.  In  other  parts  we  may  not  only  find  this 
diffuse  impregnation  with  the  biliary  pigments,  hut  even  solid  granules  of 
the  latter. 

A  jaundiced  patient  often  presents  other  indications  of  the  presence  of 
biliary  coloring  matter  than  the  color  of  his  skin.  There  is  often  an  itching 
of  the  skin,  which  may  be  very  troublesome.  It  may  he  so  bad  at  night  as  to 
disturb  sleep.  The  scratching  thus  induced  often  causes  numerous  excoria- 
tions and  fissures,  which  may  even  occasion  quite  large  furuncles.  Urticaria 
is  also  sometimes  observed.  The  cause  of  the  marked  irritation  of  the  sensory 
nerves  of  the  skin  is  not  quite  clear.  Sometimes,  in  spite  of  the  most  extreme 
jaundice,  the  itching  of  the  skin  is  entirely  absent;  in  other  cases,  even  with 
slight  icterus,  it  is  very  marked  and  distressing.  A  peculiar  disease  of  the 
skin,  which  has  been  described  in  connection  with  chronic  jaundice,  is  called 
xanthelasma  or  xanthoma.  It  presents  bright-yellow  spots,  usually  somewhat 
elevated,  which  look  like  yellow  fat  droplets  and  are  found  mainly  on  the 
eyelids,  though  present  also  on  other  parts  of  the  body. 

The  remaining  symptoms  of  hepatogenous  jaundice  may  be  divided  into 
two  groups.  The  first  group  comprises  the  symptoms  excited  by  the  presence 
of  the  biliary  constituents,  and  particularly  of  the  biliary  acids,  in  the  blood, 
while  the  second  group  is  due  to  the  lack  of  bile  in  the  intestinal  canal. 

We  have  seen  that,  when  the  biliary  outlets  are  occluded  or  narrowed,  the 
constituents  of  the  bile  are  absorbed.  We  have  already  learned  in  part  what 
becomes  of  the  bile  pigment  thus  conveyed  into  the  blood  vessels.  That  it  also 
displays  poisonous  properties  has  not  yet  been  absolutely  proved.  The  pres- 
ence of  the  bile  acids  in  the  blood  at  any  rate  is  of  considerable  clinical  impor- 
tance. Physiology  has  shown  that  these  acids  possess  certain  injurious  quali- 
ties, and,  among  others,  the  power  to  destroy  red  blood  corpuscles.  But  in 
reality  few  if  any  blood  corpuscles  are  destroyed  by  the  bile  acids  in  the  blood, 
because  they  are  too  much  diluted,  and  besides,  seem  in  large  part  to  be 
quickly  decomposed  after  absorption.  These  acids  do  really,  however,  excite  cer- 
tain nervous  centers  in  a  way  to  give  rise  to  decided  clinical  symptoms.  The 
most  frequent  effect  is  that  produced  by  the  cholate  of  sodium  upon  the  cardiac 
ganglia,  or  possibly  also  upon  the  center  for  the  vagus,  and  it  is  evinced  by  a 
slowing  of  the  pulse.  This  is  an  almost  invariable  phenomenon,  provided 
there  be  no  fever  or  other  complication,  and  is  seen  not  only  in  simple  catarrhal 
jaundice  but  in  all  cases  of  hepatogenous  icterus.  The  pulse  rate  is  from  64 
to  50,  or  even  less.  Slight  irregularity  in  the  heart's  action  is  not  infrequent. 
There  are  certain  other  nervous  disturbances  often  seen  in  jaundice,  referable 
to  the  presence  in  the  blood  of  biliary  constituents,  and  in  particular  of  biliary 
acids.  Sometimes  there  is  a  striking  languor  and  muscular  weakness,  or  head- 
ache, insomnia,  or  the  patient  is  "  out  of  sorts."  Grave  nervous  symptoms, 
sometimes  seen  in  jaundice  and  grouped  under  the  name  of  cholamiia,  will 
be  separately  discussed  later.  It  also  deserves  a  brief  mention  here  that  many 
cases  with  marked  jaundice  have  a  noticeable  tendency  to  bleeding — that  is,  a 
sort  of  "  hemorrhagic  diathesis  "  with  hemorrhages  into  the  skin  and  in  the 
viscera,  epistaxis  and  analogous  occurrences. 

We  come  now  to  a  consideration  of  those  symptoms  which  arise  because  the 
bile  does  not  reach  the  intestine.    In  this  regard  the  standpoint  of  modern  physi- 


664  DISEASES  OF  THE  DIGESTIVE  ORGANS 

ology  is  essentially  different  from  the  old  views.  Formerly  the  bile  was  valued 
as  an  important  digestive  secretion;  now  it  is  regarded  by  many  merely  as  an 
excretion,  containing  certain  end  products  of  metabolism;  but  perhaps  this 
view  is  extreme,  for  the  very  fact  that  the  bile  is  discharged  into  the  upper  part 
of  the  intestine  suggests  that  it  has  a  certain  significance  in  the  processes  to 
which  the  intestinal  contents  are  subjected,  and  there  is  certainly  one  function 
of  the  bile  which  is  indisputable— viz.,  that  it  promotes  the  absorption  of  fat. 
The  bile  both  contributes  to  the  emulsifying  of  fat,  and  also  promotes  the  pas- 
sage of  the  fat  drops  through  the  intestinal  walls  into  the  lacteals.  Now,  in 
hepatogenous  icterus  this  work  remains  undone,  as  is  shown  by  the  fatty  stools. 
From  time  immemorial  the  white  clay-colored  stools  of  jaundice  have  been  well 
known,  and  are  employed  as  the  best  measure  of  the  completeness  of  biliary 
retention.  The  light  color  of  the  stools  is  due  partly  to  the  lack  of  biliary  pig- 
ment, for  it  is  that  chiefly  which  imparts  to  normal  feces  their  dark -brown 
color;  but  the  characteristic  white  clay  color  is  due  exclusively  to  the  presence 
of  undigested  fat  in  large  amounts.  If  an  icteric  patient  is  put  upon  a  diet, 
as  free  of  fat  as  possible,  the  stools  are  by  no  means  clay-colored,  but  light 
brown.  Upon  microscopic  examination  of  the  feces  in  jaundice,  sheaf -like 
aggregations  of  crystals'  are  almost  invariably  observed.  These  were  formerly 
supposed  to  be  tyrosin,  but  Oesterlein  has  shown  them  to  be  in  reality  lime  or 
magnesia  soap. 

Besides  this  influence  upon  the  absorption  of  fat,  there  have  been  two  other 
properties  ascribed  to  the  bile,  having  apparent  significance  for  the  pathology  of 
jaundice.  In  the  first  place,  there  is  the  antiseptic  power  of  the  bile ;  this  was 
said  to  explain  the  fact  that  in  patients  with  biliary  obstruction  the  feces  usually 
have  a  particularly  bad  odor,  and  also  that  there  are  often  excessive  tympanites 
and  flatulence.  Secondly,  the  bile  was  reputed  to  exert  an  influence  upon  intes- 
tinal peristalsis — hence,  the  constipation  frequently  seen  in  jaundice.  Of  late, 
however,  authorities  have  had  doubts  about  ascribing  either  of  these  properties 
to  the  bile.  The  foul  odor  of  the  feces  may  be  associated  with  the  imperfect 
digestion  of  fat,  and  the  constipation  with  the  change  in  the  diet  and  with  other 
circumstances. 

We  must  mention  one  other  point :  If  the  obstruction  to  the  discharge  of  bile 
is  actually  situated  at  the  papilla  duodenalis — and  this  was  formerly  regarded 
as  certain  in  catarrhal  jaundice — then  the  discharge  of  pancreatic  juice  must 
also  be  affected,  and  we  must  also  consider  the  results  of  the  exclusion  of  this 
secretion  from  the  intestinal  contents.  The  presence  of  fatty  stools  may  very 
well  be  partly  dependent  upon  this  point.  We  will  discuss  later  the  various 
other  consequences  of  a  disordered  pancreatic  function. 

We  must  now  inquire  what  becomes  of  the  absorbed  bile.  As  to  the  biliary 
acids,  we  have  already  said  that  they  probably  undergo  decomposition.  Of  the 
other  constituents,  including  the  taurin  and  cholesterin  and  the  pigmentary 
matter,  we  know  the  fate  of  the  last-named  only — that  is,  we  have  learned  how 
Nature  seeks  to  rid  herself  of  this  foreign  substance.  As  soon  as  the  amount 
of  bile  pigment  in  the  blood  and  tissues  becomes  considerable,  excretory  efforts 
are  made,  in  which  the  kidneys  take  the  chief  share.  Certain  changes  take 
place  in  the  urine  almost  simultaneously  with,  or  even  frequently  somewhat  be- 
fore, the  first  appearance  of  a  jaundiced  hue  in  the  skin ;  and  these  changes  are 
due  to  the  urine  containing  excreted  biliary  coloring  matter. 


CATARRHAL   JAUNDICE  665 

The  urine  of  jaundice  is  generally  recognizable  from  its  color,  which  is  dark 
brown,  like  beer.  The  foam  caused  by  shaking  it  is  not  white,  hut  decidedly 
yellow.    A  bit  of  white  filter  paper  dipped  in  the  urine  is  stained  yellow.    If  the 

urine  is  shaken  with  chloroform  in  a  test-tube,  the  chloroform  dissolves  the  pig- 
ment, and,  on  being  allowed  to  collect  at  the  bottom  of  the  tube,  displays  a  de- 
cided yellow  color.  This  is  known  as  the  "  chloroform  test."  Another  reaction 
which  usually  gives  a  satisfactory  result,  but  not  always,  is  Gmelin's.  If  urine 
containing  bile  pigment  is  slowly  poured  down  the  sides  of  a  test-tube  contain- 
ing a  few  cubic  centimeters  of  nitric  acid,  the  zone  between  these  two  liquids 
exhibits  a  fine  play  of  colors.  The  oxidizing  effect  of  the  acid  upon  the  biliary 
pigment  produces  a  number  of  colored  rings,  the  highest  and  most  character- 
istic of  which  is  green ;  next  comes  blue,  then  violet  and  red.  Gmelin's  test 
often  shows  very  prettily  if  one  filters  the  urine  and  then  adds  a  drop  of  nitric 
acid  to  what  remains  upon  the  moist  filter  paper.  The  characteristic  colored 
rings  form  around  this  drop.  Instead  of  nitric  acid,  we  may  use  tincture  of 
iodin,  diluted  with  nine  parts  of  water.  If  a  small  amount  of  this  solution  is 
poured  upon  urine  containing  bile,  in  a  test-tube,  there  is  usually  developed  a 
ring  of  a  beautiful  green  color  between  the  two  fluids. 

The  biliary  acids  also  may  be  detected  in  the  urine  of  jaundice;  but  the 
process  is  somewhat  tedious,  and  the  knowledge  gained  is  of  no  great  practical 
importance. 

The  urine  very  often  contains  pathological  elements  which  are  the 
result  of  kidney  involvement  subsequent  to  the  irritative  effect  of  the  ex- 
cretion of  the  abnormal  products  in  the  system.  JSTothnagel  was  the  first  to 
describe  minutely  the  icteric  casts — that  is,  hyaline  casts  which  usually  have  a 
yellow  tinge  and  quite  often  are  completely  covered  with  dark-yellow  granules 
or  with  epithelium.  The  urine  may  contain  a  little  albumen  also,  but  this  is 
not  constant.  If  we  add  acetic  acid,  there  may  be  an  opacity  developed  which 
is  said  to  be  due  to  nuclein. 

[The  presence  or  absence  of  albumen  depends  largely  on  the  amount  of  the 
biliary  constituents  and  on  the  length  of  time  they  continue  in  action  on  the 
kidneys ;  their  effect  on  these  organs  is  more  or  less  that  of  an  irritant.  ] 

The  sweat  glands  also  take  part  in  the  excretion  of  bile  pigment.  The  lat- 
ter can  be  demonstrated  in  the  perspiration  of  jaundiced  persons,  as  well  as  in 
their  urine.  Not  infrequently  the  patient's  linen  is  colored  yellow  by  the  sweat. 
On  the  other  hand,  no  bile  pigment  is  found  in  the  tears,  saliva,  gastric  juice, 
milk,  or  the  cerebro-spinal  fluid. 

Having  now  considered  the  phenomena  common  to  all  cases  of  hepatogenous 
icterus,  we  revert  to  the  subject  of  simple  catarrhal  jaundice.  The  prodromal 
gastric  symptoms  usually  last  a  few  days,  more  rarely  a  week  or  two,  when  the 
skin  becomes  evidently  jaundiced  and  the  other  residts  of  the  icterus  are  also 
seen.  The  urine  grows  dark  with  biliary  pigment,  the  stools  become  light-col- 
ored and  more  or  less  clay-colored.  The  nervous  system  is  not  usually  seriously 
deranged,  but  still  most  patients  feel  very  languid,  and  have  anorexia  and  a 
tendency  to  constipation.  The  pulse  often  becomes  somewhat  slower  than 
normal,  and  sometimes  the  temperature  also  is  subnormal,  97°  or  98°  F.  (36° 
to  3G.5°  C),  but  there  may  be  slight  fever. 

In  most  cases  the  physical  examination  of  the  liver  is  of  interest,  the  organ 
being  enlarged  from  the  retained  bile.     Accordingly,  the  lower  boundary  of 


666  DISEASES  OF  THE  DIGESTIVE  ORGANS 

hepatic  dullness  usually  extends  the  breadth  of  two  or  three  fingers  below  the 
edge  of  the  ribs,  and  not  infrequently  the  lower  margin  of  the  organ  can  be 
plainly  felt.  Often  the  gall  bladder  is  so  distended,  both  by  bile  and  possibly 
by  the  mucus  which  the  bladder  itself  secretes,  that  it  projects  from  under  the 
edge  of  the  liver.  In  such  cases,  as  Gerhardt  tells  us,  we  may  sometimes  make 
out  by  percussion  a  convexity  in  the  lower  line  of  hepatic  dullness,  which  corre- 
sponds to  the  gall  bladder.  If  the  abdominal  walls  are  lax,  we  may  feel  the 
distended  viscus.  As  a  rule,  there  is  not  much  distress  in  the  hepatic  region, 
although  now  and  then  there  is  a  certain  sensation  of  pressure  or  tension. 
I  have  occasionally  found  the  spleen  distinctly  swollen  in  severe  cases  of  catar- 
rhal jaundice. 

The  symptoms  depicted  seldom  last  longer  than  a  few  weeks.  Usually  a 
patient  who  takes  proper  care  of  himself  begins  to  feel  better  in  even  less  time. 
The  urine  grows  lighter-colored,  the  stools  darker,  and  the  pulse  more  rapid. 
The  yellow  color  of  the  skin  often  remains  visible  for  quite  a  while,  although 
gradually  diminishing,  even  after  the  patient  feels  perfectly  well ;  but  at  last 
the  jaundice  disappears  also  and  recovery  is  complete.  Eelapses  are  indeed 
possible,  particularly  after  errors  in  diet,  but  they  are  rare. 

The  termination  of  catarrhal  jaundice  is,  therefore,  almost  invariably  favor- 
able. The  entire  course  of  the  disease  occupies  about  three  to  six  weeks,  rarely 
a  longer  period.  I  have  seen  cases  of  icterus,  to  be  sure,  especially  in  children, 
which,  on  account  of  their  benignancy  and  final  satisfactory  outcome,  could 
only  be  classified  as  catarrhal  icterus,  but  which  lasted  half  a  year  and  even 
longer.  The  general  condition  was  little  disturbed,  but  the  liver  was  mark- 
edly swollen  and  the  spleen  was  rather  decidedly  enlarged.  It  is  a  very  excep- 
tional occurrence,  but  one  which  we  must  always  think  of  as  possible,  for  this 
apparently  mild  and  secure  condition  to  be  suddenly  merged  into  the  grave, 
pernicious  variety  of  jaundice.  (See  the  chapter  on  Acute  Yellow  Atrophy  of 
the  Liver  and  Pernicious  Jaundice.) 

Diagnosis. — Catarrhal  jaundice  is  usually  easily  diagnosticated.  The  diag- 
nosis is  made  chiefly  from  the  course  of  the  disease — the  development  of  jaun- 
dice, preceded  by  gastrointestinal  symptoms,  in  a  previously  healthy  person, 
and  generally  in  a  youthful  individual.  It  is  very  important  to  exclude  other 
conditions  which  might  occasion  jaundice.  We  must  consider,  therefore, 
whether  the  history  of  the  case  suggests  the  presence  of  gallstones  (pain,  hepatic 
colic),  and  be  vigilant  in  our  physical  examination  to  detect  a  possible  cirrhosis 
or  new  growth.  In  the  case  of  elderly  patients,  particularly,  it  is  not  rare  for 
what  was  at  first  regarded  as  an  attack  of  ordinary  catarrhal  jaundice  eventually 
to  disclose  itself  as  a  grave  chronic  disease,  such  as  cancer  of  the  gall  bladder. 
We  should  not  make  a  diagnosis  of  catarrhal  jaundice  until  we  have  carefully 
weighed  all  the  rational  and  objective  signs. 

Treatment. — Most  cases  of.  catarrhal  jaundice  terminate  favorably  and  re- 
quire no  active  treatment.  Eest  and  prudence  are  indicated,  and  the  diet 
should  be  carefully  regulated.  Fat  must  not  be  eaten,  for,  as  we  have  seen,  it 
is  poorly  assimilated,  and  only  excites  abnormal  processes  of  decomposition  in 
the  intestinal  canal.  Lean  meat,  bread,  soups,  if  not  too  rich,  vegetables,  cooked 
fruit,  and  lemonade  or  tamarind  water  are  allowable.  Milk  [unless  skimmed] 
is  to  be  avoided,  as  a  rule,  because  of  the  fat  it  contains,  but  yet  it  is  often  well 
borne.    Alcohol  is  to  be  allowed  very  sparingly  if  at  all. 


CATARRHAL  JAUNDICE  007 

We  should  also  employ  internal  remedies  to  mitigate  the  assumed  gastric 
catarrh.  The  various  stomachic  tonics  are  frequently  prescribed.  Rhubarb  i- 
a  favorite  drug.     A  very  good  medicine  is  Carlsbad  water,  or  the  artificial 

Carlsbad  salts,  of  which  latter  the  dose  is  half  a  tablespoonful  to  a  tabiespoon- 
ful,  in  a  tumbler  of  warm  water,  before  breakfast,  or  twice  a  day.  The  alkalies 
are  said  to  have  a  favorable  influence  upon  the  gastrointestinal  mucous  mem- 
brane, and  they  are  also  laxative ;  that  they  furthermore  promote  the  secretion 
of  bile,  as  many  assume,  is  doubtful ;  but  there  is  no  doubt  that  the  flushing  of 
the  kidneys  by  an  abundance  of  liquid  is  beneficial.  If  there  is  obstinate  con- 
stipation we  are  obliged  sometimes  to  resort  to  more  powerful  remedies,  such 
as  castor  oil,  calomel,  or  rhubarb. 

Lately  much  enthusiasm  has  been  displayed  about  the  treatment  of  catarrhal 
jaundice  by  large  enemata  of  cold  water.  The  injections  are  said  to  overcome 
the  biliary  retention  by  exciting  peristalsis,  and  possibly  by  also  promoting  the 
secretion  of  bile.  Once  a  day  a  quart  or  two  of  water,  at  60°  to  70°  F.  (12°  to 
18°  R.),  is  injected,  and  is  retained  as  long  as  possible.  The  good  effect  is  said 
to  be  observable  in  a  few  days,  both  in  the  general  condition  of  the  patient  and 
in  the  diminished  amount  of  bile  pigment  in  the  urine,  as  well  as  the  darker 
color  of  the  stools.  Other  physicians  recommend  injections  of  a  pint  to  a  quart 
(0.5  to  1  liter)  of  lukewarm  water  several  times  a  day.  We  have  tried  both 
methods  repeatedly  without  being  able  to  convince  ourselves  that  the  course 
of  the  disease  is  thus  rendered  very  different  from  that  under  simple  dietetic 
management;  still,  one  may  try  irrigations,  especially  if  the  case  is  obstinate. 
Whether  there  are  any  internal  remedies  which  promote  the  secretion  of  bile 
is  very  doubtful.  The  drug  which  is  most  recommended  for  this  purpose,  and  is 
much  employed  in  catarrhal  jaundice,  is  salicylate  of  sodium,  in  the  dose  of 
8  to  15  gr.  (gm.  0.5  to  1),  several  times  a  day.  The  biliary  acids  have  also 
been  tried,  in  the  form  of  purified  ox  gall,  and  also  salol,  podophyllin,  calomel, 
and  many  others.  We  believe  that  all  these  remedies  may  generally  be  dis- 
pensed with. 

The  effort  has  also  been  made  to  empty  the  gall  bladder  by  manipulation. 
Gerhardt  states  that  sometimes  the  distended  viscus  can  not  only  be  felt  through 
the  abdominal  walls  (vide  supra),  but  it  can  be  so  firmly  compressed  as  to 
squeeze  its  contents  into  the  duodenum.  Sometimes  the  obstruction  is  said  to 
yield  suddenly,  as  if  a  plug  were  driven  out.  This  method  has  not  been 
extensively  adopted.  It  seems  applicable  only  in  a  limited  number  of  cases, 
and  is  probably  not  free  from  danger.  The  suggestion  of  external  faradization 
as  a  means  to  stimulate  the  gall  bladder  to  contract  and  discharge  its  contents 
appears  to  me  to  be  entirely  illusory. 

Among  symptoms,  the  troublesome  itching  deserves  particular  attention. 
The  remedies  which  may  be  recommended  for  this  are  bathing  with  cold  water, 
rubbing  the  skin  with  slices  of  lemon,  or  the  application  of  a  two-per-cent  solu- 
tion of  carbolic  acid,  or  of  salicylic  acid  or  thymol  dissolved  in  alcohol  (one 
to  three  per  cent) ;  also  menthol  (headache  pencil)  and  choloroform  mixed 
with  olive  oil.  Sometimes  temporary  relief  is  afforded  by  a  dose  of  antipyrin 
or  salicylate  of  soda  internally.  We  have  sometimes  found  baths,  to  which  were 
added  10  to  15  drops  of  a  mixture  containing  menthol,  oij  (gm.  7.5),  and 
spiritus  mentholi  crispati,  §ij   (50  c.c),  very  useful. 


668  DISEASES   OF   THE   DIGESTIVE   ORGANS 

APPENDIX 

CERTAIN  SPECIAL  FORMS  OF  JAUNDICE 

1.  Acute  Febrile  Jaundices.  Infectious  Jaundice.  Weil's  Disease. — There 
is  a  peculiar  acute  infectious  disease  which  was  first  described  by  Weil,  and 
then  more  fully  by  Fiedler  and  others,  which  seems  to  be  always  associated 
with  an  acute  infectious  inflammation  of  the  gall  ducts,  and,  having  jaundice 
for  a  symptom,  it  may  properly  be  described  in  this  connection. 

The  disease  is  most  frequent  in  the  months  of  summer.  It  attacks  by  pref- 
erence young  and  middle-aged  men.  Fiedler  was  struck  by  the  frequency  with 
which  butchers  suffered  from  it.  The  symptoms  usually  begin  suddenly.  Ex- 
treme chilliness,  fever,  headache,  and  malaise  are  almost  always  present  at  the 
onset.  Jaundice  usually  appears  on  the  second  day,  or  soon  after,  and  it  may 
become  severe.  Its  immediate  cause  is  doubtless  obstruction  of  bile,  for  the 
stools  are  colorless  and  the  urine  contains  an  abundance  of  bile  pigment.  The 
constitutional  symptoms  remain  for  several  days  quite  severe.  The  patient 
complains  of  violent  headache,  wakefulness,  and  vertigo.  Sometimes  there  is 
evident  stupor  or  mild  delirium.  Upon  physical  examination  we  not  infre- 
quently notice  herpes  on  the  lips,  besides  the  icterus.  The  tongue  is  coated. 
There  is  nothing  unusual  about  the  lungs  or  heart,  except  that  the  pulse  is  apt 
to  be  quite  rapid.  The  abdomen  is  not  particularly  distended.  The  liver  is 
often  enlarged,  but  not  always.  An  acute  splenic  tumor  is  very  often,  but  not 
invariably,  present.  There  is  usually  diarrhea.  Vomiting  may  occur.  The 
urine  almost  invariably  contains  albumen,  and,  as  a  rule,  we  find  blood,  epi- 
thelium, and  casts,  indicating  a  considerable  amount  of  nephritis.  In  a  few 
cases  there  are  anuria  and  uraemia.  Finally,  a  very  characteristic  symptom  is 
the  violent  pain  in  the  muscles,  particularly  in  the  calves  of  the  legs,  of  which 
most  patients  complain.  Epistaxis  and  hemorrhages  into  the  skin  have  also 
been  repeatedly  observed. 

With  these  symptoms  the  disease  persists  for  from  five  to  eight  days,  dur- 
ing which  period  the  fever  is  often  very  considerable.  Temperatures  of  105° 
to  107°  F.  (40°  to  41°  C.)  are  not  rare.  Then  the  fever  falls  by  crisis  or  rapid 
lysis,  although  seldom  with  perfect  regularity.  At  the  same  time  the  other 
symptoms  abate  also,  and  convalescence  ensues  after  an  illness  of  ten  to 
fourteen  days  in  all.  Many  of  the  milder  cases  recover  promptly,  while  others 
are  prolonged  by  various  sequelae  and  fresh  exacerbations.  An  unfavorable 
termination  seems  to  be  exceptional :  it  may  result  from  uraemia. 

It  is  highly  probable  that  this  perfectly  specific  disease,  the  most  important 
symptoms  of  which  are,  as  we  have  seen,  jaundice,  fever,  swelling  of  the  spleen, 
albuminuria,  and  pain  in  the  muscles,  is  an  acute  infectious  process,  with  a 
special  involvement  of  the  biliary  ducts ;  but  we  do  not  yet  possess  any  precise 
information  as  to  its  aetiology.  It  seems,  however,  that  bacteria  belonging  to 
the  colon-bacillus  group  are  most  probably  connected  with  its  development, 
inasmuch  as  the  serum  of  patients  suffering  from  Weil's  disease  has  been  re- 
peatedly found  to  have  an  agglutinating  effect  upon  typhoid  bacilli  (Widal's 
reaction).  Possibly  we  do  not  always  have  to  deal  with  absolutely  the  same 
morbific  process,  but  with  several  allied  conditions.     A  sharp  differentiation 


BILIARY   CALCULI  669 

of  Weil's  disease  from  simple  catarrhal  jaundice  is  Likewise  not  possible,  ae  the 
latter,  as  already  mentioned,  often  presents  individual   features  which   point 

to  an  infectious  origin  (splenic  tumor,  slight  elevations  of  temperature,  etc.). 
We  have  also  repeatedly  ohserved  cases  of  benign,  but  still  quite  severe,  febrile 
jaundice,  without  albuminuria  or  muscle  pains,  hut  with  continuous  high 
temperatures.  These  could  only  he  interpreted  as  cases  of  primary  infectious 
cholangitis.  One  of  these  cases  was  complicated  by  a  unilateral  pyelitis 
which  also  pointed  to  a  colon-bacillus  infection. 

The  treatment  must  be  purely  symptomatic.  In  the  beginning  calomel  is 
useful.  Later  we  prescribe  Carlsbad  salts,  salicylate  of  sodium,  stomachics,  or 
the  like.  The  headache  is  often  relieved  by  an  ice  bag  or  antipyrin ;  the  mus- 
cular pain  by  the  inunction  of  chloroform  oil.  From  the  first,  the  diet  must 
be  such  as  not  to  aggravate  the  nephritis  (milk,  simple  soups). 

2.  Chronic  Hereditary  or  Family  Jaundice. — The  occurrence  of  a  chronic 
jaundice  in  several  members  of  the  same  family  has  been  described  by  various 
authors  (Murchison,  Minkowski,  etc.).  The  anatomical  basis  of  this  condition 
is  still  not  clear.  It  is  usually  explained  by  a  congenital  anomaly  of  the  bile 
ducts  or  liver  cells.  In  some  of  these  cases  a  decided  splenic  enlargement  is 
found.  Minkowski  found  a  pronounced  deposit  of  iron  in  the  kidney,  which 
points  to  an  abnormal  destruction  of  red  blood  cells. 

3.  Icterus  Gravidarum.  Menstrual  Jaundice. — Certain  isolated  observa- 
tions point  to  a  peculiar,  perhaps  toxicogenic,  relation  between  jaundice  and 
the  female  sexual  functions.  The  repeated  occurrence  of  jaundice  with  each 
pregnancy  has  been  observed  by  Brauer,  and  the  occurrence  of  jaundice  during 
menstruation — so-called  menstrual  jaundice — has  also  been  described. 

4.  Congenital  Chronic  Jaundice. — This  is  a  remarkable  condition  and  only 
very  rarely  observed.  It  persists  without  much  other  disturbance  throughout 
life,  and  depends  probably  upon  a  congenital  anomaly  of  the  bile  ducts. 


CHAPTEE   II 

BILIARY    CALCULI 

(Hepatic  Colic.     Cholelithiasis) 

etiology. — Gallstones  are  of  very  frequent  occurrence ;  Riedel  asserts  that 
some  two  millions  of  the  inhabitants  of  Germany  have  gallstones,  although 
this  estimate  seems  to  be  very  high.  Despite  their  frequency,  we  have  little 
positive  knowledge  of  their  causation.  We  can  merely  state  certain  circum- 
stances which  in  all  probability  favor  the  formation  of  these  concretions. 

Biliary  retention  certainly  acts  in  this  way,  both  directly  and  by  leading 
to  an  increased  consistence  and  increased  concentration  of  the  bile.  As  a 
result,  certain  constituents  which  were  before  held  in  solution  are  thrown 
down.  And  yet  this  cause,  however  potent  (vide  supra),  cannot  be  regarded 
as  the  only  one.  The  chemical  composition  of  gallstones  suggests  that  their 
formation  must  he  preceded  by  certain  abnormal  chemical  processes  of  decom- 
position and  of  transformation.  We  cannot  otherwise  explain  why  the  con- 
stituents of  gallstones  should  differ,  as  they  do  in  many  ways,  from  the  mat- 


670  DISEASES   OF  THE   DIGESTIVE   ORGANS 

ters  which  normal  bile  holds  in  solution.  For  example,  the  pigment  in 
gallstones  is  never  found  unchanged,  but  invariably  exists  in  composition 
with  lime.  Now,  normal  bile  contains  only  a  trace  of  lime,  so  that  long  ago 
Frerichs  expressed  the  opinion  that  the  lime  comes  from  the  mucous  mem- 
brane of  the  gall  bladder.  It  is  an  important  fact  that  the  cholesterin  and 
probably  also  a  portion  of  the  pigmentary  matters  are  held  in  solution  in 
normal  bile  by  the  combination  of  sodium  with  the  biliary  acids  which  it 
contains.  If  this  sodium  salt  were  decomposed  from  any  cause,  the  matters 
named  would  naturally  be  precipitated.  The  decomposition  of  the  salts 
formed  by  the  bile  acids  is  greatly  promoted  if  the  bile  acquires  an  acid 
reaction;  but  of  the  circumstances  in  which  this  last-mentioned  change  occurs 
we  do  not  yet  have  any  accurate  knowledge.  Lately  Naunyn,  after  extensive 
investigations,  has  propounded  a  theory  that  the  formation  of  calculi  is  due 
in  most  cases  to  a  primary  disease  of  the  mucous  membrane  of  the  gall  bladder 
and  the  bile  ducts.  The  disease  causes  the  destruction  of  great  numbers  of 
the  epithelial  cells  of  the  mucous  membrane,  with  a  resultant  production  of 
cholesterin,  and  of  a  compound  of  lime  with  bilirubin.  Thus  are  formed 
friable  masses  of  detritus,  which  are  gradually  changed  into  gallstones,  in 
the  interior  of  which  it  is  still  possible  at  an  early  stage  to  demonstrate  the 
original  pultaceous  mass.  As  the  cholesterin  and  the  compound  of  lime  with 
bilirubin  continue  to  form  by  crystallization,  and  fresh  deposits  of  firm  mate- 
rial takes  place,  the  stone  gradually  grows  harder  and  larger.  Very  often, 
also,  there  is  added  at  this  stage  a  deposit  of  carbonate  of  lime.  The  cause 
of  the  original  lithogenous  catarrh  is  not  known.  Perhaps  the  mere  mechan- 
ical obstruction  of  bile  is  causative,  perhaps  infection.  In  particular,  the 
Bacterium  coli  commune,  which  originates  in  the  intestines,  seems  to  be 
important — or  at  least,  if  not  this,  a  very  similar  kind  of  bacillus.  If  the 
supposition  were  confirmed  that  infection  of  this  sort  is  a  factor,  it  would 
also  be  natural,  as  shown  by  what  has  been  previously  stated,  to  consider  that 
such  an  infection  would  have  an  influence  upon  the  bile  itself. 

We  have  rather  more  knowledge  as  to  predisposing  causes  than  about  the 
chemical  processes  involved  in  the  formation  of  gallstones.  Age  seems  to  be 
an  important  factor.  The  great  majority  of  patients  are  over  forty.  Gall- 
stones are  much  less  frequent  between  twenty  and  forty  years  of  age,  although 
we  have  not  very  infrequently  observed  typical  cholelithiasis  in  younger  indi- 
viduals, and  even  occasionally  in  children.  One  reason  why  elderly  people  are 
so  liable  to  this  trouble  is  said  to  be  the  senile  weakness  of  the  muscular 
fibers  of  the  gall  bladder.    Thus  stagnation  and  retention  of  bile  are  promoted. 

Sex  also  has  a  decided  influence.  All  authors  agree  that  gallstones  are 
more  frequent  in  females  than  in  males,  the  proportion  being  about  three  to 
two.  An  explanation  of  this  fact  has  been  sought  in  the  sedentary  life  of 
women,  and  particularly  in  the  mechanical  effect  of  women's  clothes  and  tight 
lacing  impeding  the  outflow  of  bile.  It  is  a  fact  which  certainly  deserves 
consideration  that  we  are  very  apt  to  find  gallstones  and  a  corset  liver  in  the 
same  individual.  Far  more  important,  still,  appears  to  us  the  influence  of 
pregnancy.  With  comparative  frequency  the  first  attacks  of  colic  appear 
during  pregnancy  or  the  puerperium.  At  any  rate,  gallstones  are  found  in 
women  who  have  borne  children  much  oftener  than  in  childless  women. 

Much  has  been  said  about  certain  peculiarities  of  constitution,  in  their 


BILIARY   CALCULI  071 

relation  to  the  formation  of  gallstones;  and  it  is  asserted  that  the  mode  of 
life  may  favor  their  development — as  when  too  much  food  ia  taken,  particu- 
larly an  excess  of  fat  and  meat,  and  when  there  is  insufficient  bodily  exercise. 
In  general,  statements  of  this  sort  musl  be  viewed  with  much  suspicion;  still, 
we  cannot  deny  that  cholelithiasis  is  seen  with  striking  frequency  in  ohese 
women,  and  that  the  trouble  seems  to  be  somewhat  more  common  among  the 
favored  classes  than  among  the  poor.  There  often  seems  to  be  an  hereditary 
predisposition  to  gallstones,  which  fact  also  points  to  constitutional  cai 

It  has  heen  said  that  there  is  a  relation  between  cholelithiasis  and  gout, 
arteriosclerosis,  and  other  diseases.  This  is  not  at  all  certain,  though  worthy 
of  note.  It  is  an  interesting  fact  that  sometimes  the  same  individual  has 
gallstones  and  renal  calculi. 

In  rare  cases  there  may  be  disease  of  the  liver  and  of-  the  bile  ducts  them- 
selves, leading  to  persistent  obstruction,  and  thus  causing  gallstones. 

The  reversed  relation  is  very  much  more  important,  namely,  that  gall- 
stones may  lead  to  secondary  diseases  of  the  liver,  such  as  carcinoma,  biliary 
cirrhosis,  and  suppurative  hepatitis. 

Occurrence  and  Chemical  and  Physical  Properties  of  Gallstones. — The 
place  where  gallstones  are  most  frequently  formed  and  found  is  the  gall  blad- 
der. We  may  find  in  it  any  number,  from  one  or  two  up  to  a  hundred  and 
more.  The  size  varies  from  that  of  a  grain  of  sand  to  that  of  a  hen's  egg. 
The  large  stones  may  completely  fill  the  gall  bladder;  and  sometimes  the 
smaller  stones  are  numerous  enough  to  fill  it  also.  The  stones  usually  lie 
free  in  the  bladder,  although  exceptionally  they  may  be  found  adherent  to 
its  walls.  Barely  the  bladder  presents  a  diverticulum,  in  which  a  stone  has 
been  formed.  The  lining  membrane  of  the  viscus  often  presents  quite  a  severe 
catarrhal  inflammation.  This  may  have  preceded  the  formation  of  the  stone 
(vide  supra),  but,  on  the  other  hand,  it  may  have  developed  as  a  result  of 
the  mechanical  irritation  of  the  mucous  membrane  occasioned  by  the  concre- 
tions or  by  secondary  infectious  influences.  Very  often  the  wall  of  the  gall 
bladder  and  the  neighboring  tissues  are  affected  by  mild  or  even  severe  inflam- 
matory processes,  suppuration,  adhesive  peritonitis,  necrosis,  perforation,  and 
similar  lesions  (vide  infra). 

Stones  which  are  found  in  the  larger  bile  ducts  are  not  formed  in  them, 
but  they  have  become  wedged  in  them  while  on  their  way  to  the  intestine. 
Sometimes,  however,  stones  are  formed  in  the  liver  itself  ("  hepatic  calculi  "). 
These  are  seldom  primary,  but  are  usually  the  result  of  biliary  obstruction 
because  of  persistent  stenosis  of  the  common  duct.  Hepatic  gallstones  of  this 
sort  may  reach  a  diameter  of  a  half  to  one  centimeter.  In  such  cases  the 
small  intrahepatic  bile  ducts  are  usually  a  good  deal  widened;  or  occasionally 
they  present  niches  in  which  the  stones  lie.  As  a  rule,  the  hepatic  parenchyma 
surrounding  the  stone  is  in  a  state  of  chronic  or  acute  purulent  inflammation 
(vide  infra). 

In  form,  gallstones  vary  infinitely.  The  smallest  are  irregular  masses,  well 
described  by  the  name  of  "gall  sand."  The  larger  stones  are  more  or  less 
round,  oval,  or  polyhedral.  The  polyhedra  are  usually  due  to  the  mutual 
rubbing  and  pressure  of  a  number  of  stones  upon  one  another.  In  color,  the 
stones  vary  according  to  the  amount  of  pigment  they  contain,  from  almost 
black  or  dark  brown  to  a  lighter  greenish  or  bright-yellow  shade.     A  fresh 


672  DISEASES   OF   THE   DIGESTIVE   ORGANS 

gallstone  always  sinks  in  water ;  but  when  dry,  gallstones  contain  air  and  gen- 
erally float.  On  cross-section,  the  hard  stones  are  found  to  be  either  homo- 
geneous or  composed  of  layers.  As  a  rule,  there  is  a  nucleus,  darkly  pig- 
mented, which  is  surrounded  by  a  lighter-colored  envelope,  itself  either  made 
up  of  concentric  layers  or  evidently  crystalline.  Often  the  outermost  layers 
are  still  distinguishable  as  peculiar  darker  and  harder  strata.  If  we  ex- 
amine thin  scales  of  gallstones  microscopically  we  shall  find  in  them  (as  in 
renal  calculi)  an  organic  cement  which  holds  the  minute  crystals  together 
(Posner). 

As  to  chemical  composition,  gallstones  are  usually  divided  into  several 
groups.  By  far  the  most  frequent  variety  is  made  up  of  cholesterin  and  pig- 
ment (bilirubin)  mixed  together  in  greatly  varying  proportions.  The  pigment 
is  in  great  part  combined  with  lime.  On  the  average,  stones  contain  about 
seventy  to  eighty  per  cent  of  cholesterin.  Besides  these  two  chief  ingredients, 
most  stones  also  contain  lime  and  magnesium.  In  color  they  are  light  or  dark, 
according  to  the  smaller  or  greater  proportion  of  coloring  matter  they  contain. 
Stones  of  pure  cholesterin  are  less  common.  These  are  usually  found  singly, 
are  soft,  and  often  are  almost  transparent.  Most  cholesterin  stones  have  a 
nucleus  of  pigment  and  lime  in  combination.  Pure  pigmentary  concretions 
are  rare,  and  are  generally  small,  like  coarse  sand.  A  still  greater  rarity  is 
a  stone  made  up  entirely  of  lime.     Such  a  stone  is  small  and  very  hard. 

Anatomical  and  Clinical  Kesults  of  Gallstones. — It  is  by  no  means  rare 
for  gallstones  to  be  present  even  in  considerable  number  and  size  without 
causing  the  slightest  discomfort.  This  is  proved  by  the  fact  that  often  at 
autopsy  gallstones  are  found  by  chance,  although  there  had  never  been  a 
symptom  suggesting  their  presence.  In  such  cases  it  is  evident  that  the  con- 
cretions have  formed  very  gradually  in  the  gall  bladder,  and  never  have  led 
to  mechanical  or  inflammatory  disturbance. 

In  other  cases,  probably  very  numerous,  the  gallstones  occasion  certain 
disturbances,  but  these  are  comparatively  insignificant  and  not  of  such  a 
character  as  to  enable  the  physician  to  make  an  absolute  diagnosis.  Patients 
of  this  sort  complain  at  times  of  slightly  painful  or  disagreeable  sensations  in 
the  stomach  and  liver,  particularly  after  bodily  exertion,  and  they  may  also 
have  other  symptoms,  such  as  slight  dyspepsia.  The  objective  examination 
yields  nothing  positive.  The  physician  suspects  a  gastric  disorder,  a  floating 
kidney,  or  a  neurosis.  It  is  important  that  he  should  always  in  such  cases, 
particularly  in  women,  consider  the  possibility  of  gallstones ;  for  it  is  possible, 
if  there  is  an  actual  cholelithiasis,  that  at  any  time  there  may  be  severe 
symptoms,  the  correct  interpretation  of  which  will  be  rendered  much  easier 
if  these  mild  prodromata  have  been  duly  appreciated. 

In  a  third  class  of  cases  the  gallstones  cause  severe,  and  sometimes  actually 
fatal,  illness.  The  symptoms  may  be  very  characteristic,  so  that  they  can  be 
recognized  easily  and  absolutely ;  but  not  infrequently  the  condition  is  difficult 
to  interpret,  and  misleading. 

The  form  of  the  disease  which  can  be  recognized  most  certainly  and  which 
has  been  longest  known  to  clinicians  is  characterized  by  the  occurrence  of 
distinct  and  peculiar  paroxysms.  These  are  usually  termed  biliary  colic.  An 
attack  of  this  sort  may  occur  suddenly,  while  the  patient  is  apparently  in 
perfect  health.    More  often,  however,  the  first  distinct  attack  is  preceded  for 


BILIARY   CALCULI  673 

a  long  time  by  mild  disturbances  (vide  supra),  although  these  latter  often 
receive  little  attention,  and  are  apt  to  be  misinterpreted. 

The  typical  attack  of  biliary  colic  begins  either  with  absolute  suddenness 
or  after  some  slight  prodromata,  such  as  chilliness,  nausea,  and  malaise.  It 
may  occur  at  an}'  time,  day  or  night.  The  comparatively  frequent  sudden 
appearance  of  the  pains  in  the  evening  hours,  or  even  during  the  night  in 
sleep,  is  particularly  characteristic.  Usually  there  is  no  exciting  cause  to  be 
discovered.  Sometimes  the  paroxysm  is  preceded  by  a  slight  injury  or  some 
other  harmful  influence,  such  as  errors  in  diet,  mental  excitement,  and  the 
like.  The  chief  symptom  of  the  attack  is  the  pain.  This  may  be  extreme 
from  the  start,  or  it  may  begin  mildly  and  then  rapidly  or  slowly  become 
extreme.  Usually  the  patient  refers  the  pain  chiefly  to  the  epigastrium  and 
to  the  right  hypochondrium,  but  from  here  it  radiates  into  the  left  side,  the 
back,  the  shoulders,  and  even  the  right  arm,  and  much  more  rarely  down 
into  the  hypogastrium  and  the  thighs.  In  some  paroxysms  the  pain  increases 
to  extreme  severity;  and  convulsive  movements  have  been  repeatedly  ob- 
served, particularly  in  nervous  persons,  as  a  result  of  the  pain.  Some  patients 
assume  the  most  peculiar  positions,  such  as  doubling  themselves  up  to  dull 
the  pain.  The  pain  may  be  accompanied  by  nausea,  eructations,  and  repeated 
vomiting.  The  vomitus  usually  consists  of  strongly  bile-colored  fluid  and 
food  remnants.  The  bowels  are  usually  constipated,  but  sometimes  there  is 
diarrhea.  The  constitutional  disturbance  is  marked;  the  patient  feels  ex- 
tremely feeble  and  exhausted,  and  gives  the  impression  of  anguish  and  col- 
lapse. The  pulse  is  small,  usually  accelerated,  but  sometimes  infrequent. 
The  bodily  temperature  is  normal  in  a  part  of  the  cases;  often  there  is  slight 
fever,  and  sometimes  a  considerable  rise  of  temperature,  to  104°  F.  (40°  C.) 
and  more.  At  the  beginning  of  the  attack,  and  also  later,  there  is  apt  to  be 
chilliness,  or  a  well-marked  rigor;  and  this  is  often,  but  not  invariably,  asso- 
ciated with  high  fever. 

Upon  objective  examination  of  the  abdomen  we  find  its  upper  portion, 
particularly  the  region  of  the  liver  and  gall  bladder,  slightly  prominent  or 
even  markedly  so.  The  same  region  is  sensitive  to  pressure,  and  this  tender- 
ness may  be  diffuse  or  localized.  Sometimes  the  point  of  greatest  sensitive- 
ness is  in  the  back  to  the  right  of  the  lower  dorsal  vertebras  (Boas).  Some- 
times an  enlargement  of  the  liver  can  be  distinctly  made  out  (vide  infra), 
and  sometimes  when  the  abdominal  walls  are  yielding  we  can,  upon  careful 
palpation,  feel  the  enlarged,  tense,  and  tender  gall  bladder  (vide  infra).  In 
exceptional  cases,  it  is  claimed  that  we  can  even  feel  the  grating  of  the  stones 
upon  one  another,  and  with  a  stethoscope  hear  the  crepitation  thus  produced; 
but  in  other  cases  it  is  impossible  to  make  out  with  certainty  any  change, 
either  in  the  liver  or  the  gall  bladder ;  or  the  abdominal  walls  may  be  so  thick 
and  rigid  that  a  good  examination  is  impossible.  In  any  case  of  this  sort  the 
physician  looks  with  special  attention  for  the  appearance  of  jaundice.  Even 
a  slight  icteric  hue  of  the  eyes  and  the  skin  is  important,  for  the  appearance 
of  jaundice  is  often  decisive  in  leading  to  an  absolute  diagnosis.  Sometimes 
the  jaundice  is  very  marked;  in  such  cases  the  urine  contains  an  abundance 
of  bile  pigment.  It  cannot,  however,  be  too  much  insisted  upon  that  it  is  by 
no  means  exceptional  to  have  no  jaundice  at  all  in  an  attack  of  biliary  colic 
(vide  infra).    Not  very  rarely,  the  icteric  discoloration  of  the  skin  is  absent, 


674  DISEASES   OF   THE   DIGESTIVE   ORGANS 

while  the  examination  of  the  urine  distinctly  shows  some  bile  pigment.  Itch- 
ing of  the  skin  is  quite  frequent  with  or  without  marked  jaundice.  The 
stools  in  continuous  biliary  obstruction  become  light,  acholic,  and  fatty.  With 
regard  to  finding  gallstones  in  the  feces,  vide  infra. 

The  duration  of  an  attack  of  biliary  colic  varies  greatly.  Many  attacks 
last  merely  a  few  hours  or  a  day;  more  severe  attacks  continue  two  to  four 
days,  and  even  much  longer.  It  is  equally  impossible  to  establish  any  uni- 
versal rule  as  to  the  frequency  with  which  the  attacks  recur.  Sometimes  a 
second  attack  will  come  after  a  short  interval;  sometimes  not  until  months  or 
years  have  elapsed.  Not  infrequently  there  will  be  several  attacks  in  close 
succession,  and  then  none  for  a  long  time;  or  there  may  never  be  any  more. 
Again,  the  early  attacks  of  simple  colic  may  be  followed  later  by  a  complicated 
disorder,  due  to  one  of  the  numerous  sequela?  to  which  gallstones  may  lead. 

We  intend  to  discuss  the  remote  results  of  gallstones,  but  we  must  first 
answer  the  question :  What  abdominal  processes  occasion  the  attacks  of  biliary 
colic,  of  which  we  have  just  presented  the  clinical  picture?  Until  within  a 
few  years  the  answer  to  this  question  seemed  very  simple.  Almost  all  authori- 
ties conceived  that  the  attack  was  due  mainly  to  the  moving  about  of  the  cal- 
culi and  their  expulsion.  It  was  said  that  the  stones  moved  into  the  cystic 
duct  because  of  their  own  weight,  the  pressure  of  the  diaphragm,  and,  above 
all,  the  contractions  of  the  gall  bladder ;  and  being  once  in  the  duct,  they  were 
forced  along  through  the  cystic  and  the  hepatic  ducts.  The  attack  was  suc- 
cessfully ended  when  at  last  the  concretion  escaped  from  the  common  duct 
into  the  duodenum.  The  incarceration  of  the  stone  in  the  common  duct  neces- 
sitated jaundice.  If  the  stone  stopped  in  the  cystic  duct,  or,  as  was  often  sup- 
posed to  be  the  case,  went  back  into  the  gall  bladder  again,  there  would  be  no 
jaundice. 

This  old  doctrine  of  the  causes  of  biliary  colic  has  lately  been  modified 
and  extended  in  many  important  points.  This  has  been  particularly  the  result 
of  the  experiences  of  various  surgeons  (Eiedel,  Kehr,  Korte,  and  others)  in 
the  operative  opening  of  the  stone-filled  gall  bladder  and  the  biliary  passages. 
Even  now  it  must  be  confessed  that  small  stones  can  be  driven  from  the  gall 
bladder  through  the  cystic  and  common  ducts  into  the  intestine  in  the  way 
above  mentioned.  If  the  stone  is  very  small,  its  passage  may  take  place  almost 
without  symptoms,  and  produce  only  slight  signs  which  can  scarcely  be  defi- 
nitely interpreted.  The  passage  of  somewhat  larger  stones,  however,  produces 
typical  attacks  of  biliary  colic  in  the  older  sense.  In  our  opinion  many  com- 
paratively brief  attacks,  often  repeated,  very  painful,  and  accompanied  by 
vomiting  and  slight  jaundice,  can  scarcely  be  otherwise  interpreted.  We  be- 
lieve that  the  chief  cause  of  the  pain  are  the  cramp-like  contractions  of  the 
smooth  muscle  fibers.  In  other  cases,  besides  the  mechanical  obstruction  of 
the  stone,  there  is  an  inflammatory  process,  or  the  inflammation  may  occur 
primarily  without  any  previous  impaction  of  the  calculus.  Eiedel  depicts 
these  processes,  which  take  place  with  particular  frequency  as  follows :  So  long 
as  the  stones  in  the  gall  bladder  remain  there  without  exciting  any  secondary 
change,  and  so  long  as  the  bile  flows  freely  around  them,  in  and  out,  there  are 
no  clinical  symptoms,  although  there  is  very  often  a  gradual  development  of 
what  is  called  dropsy  of  the  gall  bladder.  If  a  stone  enters  the  neck  of  the 
bladder  and  there  increases  in  size,  or  if  the  cystic  duct  becomes  obstructed  by 


BILIARY   CALCULI  675 

the  swelling  of  ils  membrane/ then  the  entrance  of  the  bile  into  the  gall  blad- 
der is  impeded.  The  constituents  of  the  bile  which  is  in  it  are  absorbed,  and 
the  contents  of  the  gall  bladder  change  to  a  yellowish  serum,  which  may  finally 

be  almost  colorless.  This  process  often  goes  on  without  any  symptoms,  but 
frequently  there  are  slight  suggestions  of  chronic  inflammation.    The  wall  of 

the  gall  hladder  becomes  thickened;  there  may  be  a  gradual  formation  of 
manifold  adhesions  between  the  serous  coat  of  the  gall  bladder  and  the  neigh- 
boring parts,  such  as  the  omentum,  duodenum,  or  transverse  colon;  and  these 
adhesions  are  in  many  cases  the  cause  of  the  mild  and  indefinite  pains  and 
other  unpleasant  sensations  of  which  many  patients  with  gallstones  complain 
for  a  long  time  previous  to  their  first  genuine  attack.  When  a  gall  bladder 
has  been  changed  in  this  way,  there  is  liability  to  frequent  and  sudden  acute 
inflammatory  symptoms;  acute  calculous  cholecystitis  is  the  true  anatomical 
basis  of  biliary  colic.  These  inflammatory  gallstone  attacks  are  sometimes 
mild  and  of  short  duration,  but,  as  a  rule,  they  last  longer  than  the  attacks 
due  to  impaction  alone.  They  may  last  several  days,  and  are  often  associated 
with  elevations  of  temperature  and  signs  of  peritoneal  irritation.  The  excit- 
ing cause  of  these  acute  inflammations,  which  often  recur  or  show  exacerba- 
tions, is  probably  some  infectious  agent  derived  from  the  intestine  (Bacterium 
coli),  or  occasionally,  perhaps,  from  the  tonsils  or  from  some  other  place,  and 
entering  the  gall  bladder  by  way  of  the  blood  (diplococci,  streptococci).  Fre- 
quently, in  these  attacks,  there  is  no  migration  and  expulsion  of  the  calculi 
into  the  intestine,  and  Riedel  classifies  them  as  "  unsuccessful  gallstone  colic." 
They  are,  of  course,  as  a  rule,  not  associated  with  jaundice.  If,  however,  the 
stone,  situated  at  the  neck  of  the  gall  bladder,  is  small  and  the  cystic  duct 
patent,  the  stone  is  pushed  on  by  the  pressure  of  the  inflammatory  exudation 
which  collects  behind  it.  We  have  now  the  pain  due  to  the  inflammation  and 
also  that  due  to  the  incarceration  of  the  stone,  and  as  soon  as  the  stone  reaches 
the  common  duct,  and  for  a  time  blocks  the  discharge  of  bile,  we  have  ob- 
structive jaundice.  If  the  stone  is  successfully  driven  through  the  common 
duct  into  the  duodenum,  the  pain  and  inflammation  usually  promptly  cease. 
By  careful  search  we  may  find  one  or  more  stones  in  the  feces.  In  brief,  we 
have  to  deal  with  a  so-called  "  successful "  attack  of  biliary  colic.  The  dis- 
tinction between  unsuccessful  and  successful  attacks  is,  of  course,  not  always 
self-evident;  but  it  should  be  noted  that,  according  to  Eiedel,  unsuccessful 
attacks  are  much  more  frequent  than  the  successful.  It  is  true  that  in  the 
successful  attacks  there  is  always  jaundice,  and  in  the  unsuccessful  attacks 
there  is  usually  no  jaundice,  yet  this  criterion  is  not  absolute,  because,  as 
Riedel  was  the  first  to  point  out,  jaundice  may  occasionally  be  present  in  the 
unsuccessful  attacks.  In  such  a  case  the  jaundice,  of  course,  is  not  due  to 
closure  of  the  common  duct  by  a  stone — that  is,  it  is  not  lithogenous,  but  it  is 
inflammatory.  The  catarrhal  inflammation  of  the  gall  bladder  may  sometimes 
extend  to  the  bile  ducts  and  produce  jaundice,  because  of  inflammatory  swell- 
ing of  the  common  or  hepatic  duct. 

These  mechanical  and  reflex  processes  and  this  simple  cholecystitis  or 
cholangitis  (inflammation  of  the  bile  ducts)  do  not  by  any  means  comprise 
all  of  the  pathology  of  cholelithiasis.  In  many  cases  there  is  not  a  simple 
cholecystitis  or  cholangitis,  but  a  purulent  inflammation,  which  is  either  puru- 
lent from  the  start  or  a  sequel  to  a  serous  exudation.    That  bacteria  are  factors 


676  DISEASES   OF   THE   DIGESTIVE   ORGANS 

in  this  process  there  can  be  no  doubt.  The  condition  now  presented  is  no 
longer  a  simple  attack  of  colic,  but  a  far  more  severe  and  persistent  constitu- 
tional disturbance,  associated  with  pain  in  the  hepatic  region,  vomiting,  pos- 
sibly jaundice,  and  very  likely  signs  of  enlargemeiit  of  the  gall  bladder  and  the 
liver.  There  are  high  fever  (often  accompanied  with  rigors),  general  prostra- 
tion, and  cerebral  symptoms.  In  milder  cases  there  is  only  a  purulent  chole- 
cystitis. In  the  severer  cases  there  is  a  purulent  diffuse  cholangitis  alone,  or 
combined  with  purulent  inflammation  of  the  gall  bladder.  To  enumerate  here 
all  the  possibilities  of  the  condition  is  impossible.  Even  severe  derangement 
of  this  sort  is  not  incompatible  with  spontaneous  recovery,  but  in  some 
cases,  if  it  is  too  late  for  surgical  aid,  there  is  general  septic  infection  and 
death. 

A  number  of  other  sequela?  of  gallstones  may  develop  as  a  result  of  the 
impaction  of  the  stone  in  the  bile  ducts,  be  it  in  the  cystic  or  in  the  common 
duct.  If  the  stone  lodges  in  the  cystic  duct,  there  usually  develops  a  large, 
often  pear-shaped  and  palpable  tumor  of  the  gall  bladder,  the  so-called  dropsy 
of  the  gall  bladder.  If  the  stone  lodges  in  the  common  duct  there  is  usually 
long-continued  jaundice  with  biliary  congestion  in  the  liver,  which  may  finally 
lead  to  the  so-called  secondary  biliary  cirrhosis  of  the  liver.  As  a  result  of 
secondary  enlargement  of  the  common  bile  duct,  slight  changes  in  position  of 
the  stone,  etc.,  the  passage  of  bile  may  again  become  free  for  a  longer  or  a 
shorter  time.  This  explains  the  frequent  variations  in  the  intensity  of  the 
jaundice  despite  a  continuous  impaction  of  the  calculus  in  the  common  duct. 
Quite  frequently,  even  without  actual  suppuration,  an  intermittent  fever  de- 
velops as  a  result  of  secondary  infection  (fievre  hepatique  intermittante) .  We 
may  only  assume  the  presence  of  advanced  suppuration  when  severe  general 
septic  symptoms  are  present.  These  occur  especially  when  there  is  a  consider- 
able pressure  necrosis  of  the  surrounding  tissue.  This  immediately  opens  the 
door  to  inflammatory  germs,  and  results  in  secondary  suppuration,  which  may 
be  either  diffuse  or  localized.  In  the  worst  cases  there  may  be  purulent 
phlebitis  of  an  abdominal  vein,  with  metastatic  abscesses  in  other  organs. 
Those  cases  without  actual  perforation  occasion  merely  chronic  inflammatory 
adhesions  and  contractions  in  the  vicinity  of  the  bile  duct. 

Precisely  similar  consequences  may,  however,  arise  from  stones  which  are 
situated  in  the  gall  bladder  itself  (usually  at  its  neck),  with  a  consequent 
suppurative  infection  of  the  neighboring  parts.  Perforation  into  the  ab- 
dominal cavity  leads  to  purulent  peritonitis.  If  adhesions  have  already  been 
formed,  as  is  usually  the  case,  there  may  he  perforation  in  any  one  of  many 
directions,  either  outward  with  escape  of  the  pus  and  often  the  gallstones,  and 
perhaps  with  the  formation  of  a  biliary  fistula,  or  into  the  transverse  colon,  or 
more  rarely  into  the  stomach,  the  portal  vein,  or  the  urinary  tract ;  but  chief 
in  relative  frequency  and  importance  is  perforation  from  the  neck  of  the  gall 
bladder  into  the  duodenum,  for  this,  as  Virchow  and  Fiedler  have  pointed  out, 
is  the  most  common  way  by  which  large  gallstones  reach  the  intestine  and 
come  to  be  discharged  with  the  feces.  Many  of  these  processes  may,  under 
favorable  circumstances,  lead  to  spontaneous  recovery  from  cholelithiasis.  The 
gall  bladder,  under  the  influence  of  suppuration,  may  finally  completely  shrivel 
up,  perhaps  retaining  in  its  folds  one  or  more  calculi ;  but  much  of tener,  if 
there  is  no  prompt  surgical  intervention,  the  termination  is  unfavorable.     The 


BILIARY   CALCULI  077 

associated  clinical  conditions  arc  manifold  and  they  cannol  be  sketched  in  de- 
tail, and  the  end  may  come  in  an  acute  and  stormy  manner,  or  after  a  long 
illness  marked  by  many  fluctuations.  Still,  we  feel  bound  to  emphasize,  in 
closing,  that  the  frequency  of  these  many  grave  results  of  cholelithiasis  which 
we  have  mentioned  must  not  be  overestimated.  In  comparison  with  tin;  ex- 
tremely great  number  of  gallstones  which  produce  either  no  symptoms  at  all, 
or  none  which  suggest  danger  to  life,  the  severe  cases  of  purulent  inflammation 
after  cholelithiasis  are  few.  Another  severe,  but  fortunately  likewise  very  rare, 
sequel  of  large  gallstones  is  intestinal  obstruction  from  impaction  of  the  stone 
in  the  intestine.     This  has  already  been  referred  to   (page  615). 

Diagnosis. — It  is  evident  from  what  has  been  already  said  that  often  the 
diagnosis  of  cholelithiasis  is  easy  and  indubitable,  while  in  other  cases  the 
symptoms  and  course  of  the  disease  are  obscure  and  ambiguous.  The  attacks 
of  colic  are  certainly  the  most  characteristic  symptom.  We  should  therefore 
make  it  a  rule,  in  case  of  severe  paroxysmal  pain  in  the  region  of  the  stomach 
or  liver,  to  think  of  the  possibility  of  gallstones,  and  to  try  to  discover  by  a 
most  careful  inquiry  if  the  pains  can  be  explained  by  a  cholelithiasis.  The 
aphorism  of  Pel  applies,  above  all,  to  gallstones :  "  Qui  bene  interrogat  bene 
diagnoscit ! "  The  main  points  to  be  elicited  are  the  sudden  onset  of  the  pain 
in  the  later  afternoon  hours  or  at  night  without  particular  cause,  their  great 
severity,  their  relatively  short  duration,  their  association  with  vomiting  and 
chills,  and  their  radiation  to  the  back  and  shoulders.  Furthermore,  we  must 
investigate  the  occurrence  of  previous  attacks,  a  possible  hereditary  predispo- 
sition, and  the  presence  of  special  etiological  factors,  such  as  pregnancy 
[typhoid  fever],  etc.  If  an  attack  of  this  sort  is  associated  in  even  a  slight 
degree  with  jaundice,  the  diagnosis  is  usually  perfectly  clear.  If  there  is  no 
jaundice — and  frequently  there  is  none — the  diagnosis  is  less  certain,  but  still 
it  can  often  enough  be  correctly  suspected  because  of  the  general  character  of 
the  painful  attack,  and  the  subsequent  period  of  complete  freedom  from  pain, 
as  distinguished  from  the  pains  of  gastric  ulcer. 

In  our  objective  examination  we  must  first  look  for  local  tenderness  in  the 
region  of  the  gall  bladder,  and  then,  above  all,  the  existence  of  a  palpable 
tumor  of  the  gall  bladder  or  an  enlargement  of  the  liver.  In  examining  it 
is  best  to  place  the  left  hand  behind  the  right  lumbar  region  of  the  patient, 
and  by  pressure  to  try  to  push  the  liver  forward  while  deep  palpation  is  care- 
fully made  with  the  right  hand.  The  gall  bladder  often  only  becomes  pal- 
pable on  deep  inspiration.  The  liver  itself  may  be  unchanged  or  enlarged 
on  account  of  biliary  obstruction  or  inflammatory  swelling.  As  has  been  men- 
tioned, a  corset  liver  is  often  found  in  cholelithiasis.  Occasionally  that  por- 
tion of  the  liver  which  is  over  the  gall  bladder  is  unusually  enlarged  down- 
ward (so-called  Eiedel's  lobe).  Sometimes  the  neck  of  the  gall  bladder  is 
considerably  elongated,  so  that  the  gall  bladder  itself  forms  an  elongated, 
freely  movable  tumor,  that  may  easily  be  confused  with  a  movable  kidney,  or 
even  with  a  movable  carcinoma  of  the  pylorus  or  intestine. 

After  we  have  decided  that  an  existing  attack  of  pain  is  the  result  of  gall- 
stone disease,  we  must  then  decide  further  whether  we  have  to  deal  with  a 
simple  colic  or  with  an  inflammatory  complication,  such  as  cholecystitis, 
cholangitis,  or  pericystitis.  In  this  regard  the  most  important  differential 
points  are  the  duration  of  the  attack,  the  presence  of  fever,  the  local  rigidity 
43 


678  DISEASES   OF  THE   DIGESTIVE   ORGANS 

of  the  abdominal  walls  [and  the  ribs],  and  the  sensitiveness  to  pressure,  the 
general  condition,  the  vomiting,  etc. 

In  a  certain  number  of  cases,  to  be  sure,  it  will  not  be  possible  to  get  be- 
yond a  mere  suspicion  that  there  are  gallstones,  and  occasionally  it  will  not 
be  entirely  possible  to  avoid  confusion  with  intestinal  colic,  renal  colic,  pan- 
creatic colic,  the  pains  of  a  movable  kidney,  and  purely  nervous  visceral  neu- 
ralgia; yes,  even  with  arteriosclerotic  and  anginose  attacks,  and  with  the 
gastric  crises  of  tabes.  The  diagnosis  is  also  particularly  difficult  when  the 
attack  is  not  a  well-developed  one  with  characteristic  symptoms,  but  is  more 
indefinite  and  suggests  cardialgia,  dyspepsia,  and  similar  conditions.  A  care- 
ful and  thorough  examination  of  all  the  organs  that  might  be  involved,  such 
as  the  stomach  and  kidneys,  may  in  many  cases  aid  us;  and  often  the  truth 
is  revealed  by  the  further  course  of  the  disease,  but  many  cases  remain  obscure. 
The  hope  that  gallstones  might  be  recognized  during  life  by  means  of  the 
Eontgen  rays  has  only  been  fulfilled  in  isolated  instances. 

We  must  say  a  word  about  finding  the  gallstones  in  the  feces.  Of  course 
the  discovery  of  the  corpus  delicti  in  the  evacuations  after  an  attack  of  colic 
makes  the  diagnosis  absolute.  They  are  to  be  searched  for  by  mixing  the 
stools  with  water,  and  then  passing  them  through  a  sieve.  But,  as  we  have 
pointed  out  above,  the  "  unsuccessful "  attacks  of  biliary  colic  are  probably 
much  more  frequent  than  the  "  successful."  Perhaps  some  gallstones  may 
also  become  disorganized  in  the  intestine.  We  cannot,  therefore,  be  surprised 
that  in  many  cases  of  cholelithiasis  no  stones  can  be  found  in  the  dejecta,  and 
Riedel  is  right  in  maintaining  that  it  is  not  worth  while  to  search  for  the 
stones  except  in  those  attacks  which  are  associated  with  jaundice — that  is,  those 
that  are  not  unlikely  to  be  "  successful.'*'.  It  should  be  pointed  out  further  that 
we  should  be  on  our  guard  not  to  mistake  for  gallstones  hardened  portions  of 
feces — for  instance,  compacted  vegetable  matter. 

Often  the  diagnosis  is  very  difficult  in  cases  of  severe  and  long-continued 
purulent  inflammation,  originating  from  gallstones.  If  there  are  such  symp- 
toms as  indicate  a  peritonitis  localized  in  the  hepatic  region,  associated  with 
fever  and  rigors,  and  suggesting  circumscribed  suppuration,  we  must  always 
consider  the  possibility  of  gallstones  being  the  primary  cause.  We  should 
make  a  careful  local  examination  and  consider  the  general  conditions,  such 
as  age  and  sex,  and  we  shall  often  be  greatly  helped  by  inquiring  carefully 
into  the  previous  health  of  the  patient — e.  g.,  with  regard  to  any  characteristic 
colic.  It  must  be  confessed  that  it  will  not  always  be  possible  to  avoid  con- 
fusion between  this  and  other  suppurative  processes,  particularly  those  origi- 
nating from  old  gastric  and  duodenal  ulcers,  from  an  abnormally  situated 
appendix,  or  from  suppurating  echinococci.  No  special  diagnostic  rules  can 
be  formulated,  for  the  symptoms  are  peculiar  in  almost  every  single  case. 
Even  when  we  are  able  to  make  a  correct  diagnosis  of  cholelithiasis  we  are 
often  unable  to  estimate  the  exact  condition,  the  extent  of  the  secondary  in- 
flammation, the  number  and  the  situation  of  the  stones,  or  the  presence  of 
secondary  adhesions. 

Prognosis. — The  prognosis  of  gallstones  must  really  be  termed  doubtful 
in  every  case,  that  is,  if  we  provisionally  exclude  the  possibility  of  cure  by 
surgical  means.  The  presence  of  gallstones,  as  the  reader  already  knows,  may 
entail  a  number  of  dangerous  sequels,  and  we  can  never  foretell  whether  the 


BILIARY  CALCULI  079 

patient  will  suffer  from  these  or  escape  them;  still,  there  is  no  doubt  that  in 
some  cases,  when  the  stones  are  small,  or  after  perforation  and  emptying  of 
the  gall  bladder  into  the  small  intestine,  there  ma}'  be  a  spontaneous  and  per- 
manent recovery,  while  in  other  cases  there  may  he  disturbances  of  the  most 
varied  kind,  persistent,  or  constantly  recurrent,  and  ye1  never  absolutely 
serious.  There  is  no  occasion  for  describing  here  a  second  time  the  number- 
less possibilities  of  cholelithiasis  and  their  prognostic  significance. 

There  is  one  important  symptom  which  is  interesting  from  the  standpoint 
of  general  pathology  and  which  must  be  noted  here — viz.,  the  development, 
subsequent  to  cholelithiasis,  of  cancer  of  the  gall  bladder  and  bile  ducts. 
This  possibility  is,  of  course,  of  great  clinical  importance,  and  agrees  with 
the  general  observation  that  persistent  mechanical  irritation  of  the  mucous 
membrane  and  scar  formations  may  occasion  the  development  of  carcinoma. 
The  formation  of  secondary  cancer  after  cholelithiasis  is  precisely  analogous 
to  the  growth  of  cancer  after  ulcer  of  the  stomach,  or  secondarily  to  stone  in 
the  kidney. 

Treatment. — Our  means  of  efficient  prophylaxis  against  the  formation  of 
gallstones  are  very  limited.  The  most  we  can  assume  is  that  an  entirely  suit- 
able regimen,  and  particularly  the  avoidance  of  any  tight  lacing  or  similar 
mechanical  interference  with  the  excretion  of  bile,  will  prevent  or  at  least 
delay  the  development  of  any  tendency  to  the  formation  of  calculi.  If  gall- 
stones have  been  once  formed,  our  task  as  physicians  consists  merely  in  mod- 
erating the  disturbance  which  they  produce;  in  guiding,  so  far  as  possible, 
all  sequela?  to  a  favorable  termination,  and  finally  in  effecting  the  removal  of 
the  stones  from  the  body,  so  far  as  this  is  within  our  power. 

If  the  symptoms  of  the  patient  remain  comparatively  slight,  and  especially 
if  the  diagnosis  of  gallstones  has  not  yet  been  absolutely  established,  energetic 
treatment  is  not  demanded.  We  regard  it  as  important  that  in  such  cases,  as 
soon  as  we  conceive  the  possibility  of  cholelithiasis,  the  patients  should  enter 
upon  a  proper  rest  cure.  Very  often  female  patients  of  this  sort  are  regarded 
as  nervous,  are  sent  into  all  sorts  of  health  resorts,  and  treated  with  electricity 
and  massage,  and,  of  course,  without  success.  Instead  we  should  induce  such 
a  patient  to  spend  a  few  weeks  of  complete  rest  in  bed,  or,  at  any  rate,  lying 
on  a  sofa  with  easy  clothing;  prescribe  a  cautious  and  nourishing  diet,  and 
the  regular  application  of  warm  poultices  upon  the  hepatic  region,  and  ad- 
minister before  breakfast  and  in  the  middle  of  the  forenoon  a  half  pint  of 
warm  Carlsbad  Miihlbrunnen  water.  We  may  then  hope  for  a  satisfactory 
improvement  in  the  symptoms  due,  in  our  judgment,  to  the  cessation  of  the 
slight  inflammatory  irritation.  Often  patients  of  this  sort  are  sent  to  Carls- 
bad. We  will  not  deny  that  Carlsbad  water  may  have  some  favorable  influence 
upon  cholelithiasis,  but  we  believe  that  the  exertion  of  the  journey  and  the 
promenades  and  other  activities  in  which  the  patients  are  apt  to  indulge  after 
their  arrival,  are  often  serious  drawbacks.  That  Carlsbad  water,  as  such,  is 
of  real  value  in  expelling  the  stones  or  in  actually  dissolving  ( ! )  them,  we 
find  it  difficult  to  believe. 

Whenever  there  is  a  well-marked  attack  of  biliary  colic  we  have  special  in- 
dications for  treatment.  Of  course,  in  this  case  also,  we  must  immediately 
enjoin  complete  rest  in  bed. 

The  pain  demands  the  prompt  employment  of  narcotics,  particularly  of 


680  DISEASES  OF  THE  DIGESTIVE  ORGANS 

morphin  or  opium.  If  the  suffering  is  extreme,  a  subcutaneous  injection  of 
morphin  is  by  far  the  best  and  quickest  remedy,  but  the  internal  use  of  opium 
is  also  to  be  recommended.  We  may  give  every  two  or  three  hours  15  or  20 
drops  of  the  tincture,  or  0.5  to  1  gr.  of  powdered  opium  (gm.  0.03  to  0.05).1 
The  use  of  opium  suppositories  or  small  enemata  (20  to  30  drops  of  tincture 
of  opium  in  5  drachms  [gm.  20]  of  tepid  water)  is  often  very  effective.  Other 
narcotics,  such  as  chloral  or  belladonna,  are  scarcely  ever  necessary,  but  we 
may  sometimes  combine  extract  of  belladonna,  which  is  much  praised  by  many 
physicians,  with  the  opium.  Of  external  applications  upon  the  hepatic  region 
the  best  is  a  warm  or  hot  poultice.  It  is  exceptional  for  the  patient  to  prefer 
an  ice  bag.  Usually  gentle  rubbing  of  the  hepatic  region  with  chloroform  oil 
(a  mixture  of  equal  parts  of  chloroform  and  olive  oil)  does  good.  In  a  few 
cases  the  patient  experiences  relief  from  a  prolonged  warm  bath.  If  there  is 
violent  vomiting  we  give  tincture  of  opium,  bromid  of  potassium,  cocain,  or 
bits  of  ice.  If  there  is  marked  collapse,  such  stimulants  must  be  employed  as 
wine,  strong  black  coffee,  or  even  injections  of  camphor.  When  the  acute 
symptoms  have  ceased,  we  must  still  persist  for  some  time  in  a  cautious  diet 
and  in  bodily  quiet,  and  it  is  often  well  to  prescribe  a  gentle  laxative,  such  as 
Carlsbad  salts  or  rhubarb. 

When  the  attack  is  completely  over,  the  question  arises  how  to  guard 
against  the  occurrence  of  others.  The  answer  to  this  question  depends  mainly 
upon  the  view  we  take  of  the  present  attack,  whether  we  regard  it  as  a  "  suc- 
cessful "  or  an  "  unsuccessful "  one.  If  the  attack  was  successful — that  is, 
if  calculi  were  found  in  the  intestinal  evacuations  after  it — we  may  hope  that 
in  case  there  are  more  stones  present  they  also  may  be  discharged.  How  far 
we  are  able  to  hasten  this  process  by  artificial  measures  is  a  difficult  question. 
We  must  adopt  here,  as  is  so  frequently  the  case,  the  purely  empirical  stand- 
point. Under  this  heading,  a  course  of  waters  at  Carlsbad  or  similar  watering 
places  (Homburg,  Ems,  Tarasp,  Mergentheim,  Neuenahr,  Bertrich,  Vichy, 
etc.)  must  be  given  primary  consideration.  If  the  patient  cannot  visit  a 
watering  place,  a  methodical  course  may  be  prescribed  at  home.  Thus,  0.5  to 
1  pint  of  warmed  Carlsbad  Miihlbrunnen  water  may  be  slowly  taken  every 
morning  on  an  empty  stomach  and  also  every  afternoon. 

Of  the  other  remedies  recommended  for  cholelithiasis,  we  would  mention 
turpentine,  formerly  frequently  used,  but  now  only  rarely.  This  may  be  used 
in  the  form  of  what  is  called  Durande's  remedy;  that  is,  a  mixture  of  ether 
and  turpentine  in  the  proportion  of  3  to  2,  of  which  two  or  three  times 
a  day  20  to  30  drops  are  given;  salicylate  of  sodium,  of  which  we  have  often 
given,  per  rectum,  daily  0.5  to  1  drachm  (gm.  2  to  4),  in  combination  with 
bicarbonate  of  sodium.  Finally,  a  number  of  drugs  have  been  recently  manu- 
factured and  frequently  used.  Among  these  are  chologen  (a  mixture  of 
podophyllin  and  calomel),  cholelysin  (oleate  of  sodium),  and  probilin.  The 
administration  of  large  doses  of  olive  oil  has  been  repeatedly  recommended. 
Three  to  seven  ounces  (gm.  100  to  200)  are  given  in  divided  doses  daily  with 

1  [When  giving  repeated  doses  of  opium  for  biliary  or  renal  colic,  it  should  be  remembered 
that  the  pain  will  cease  abruptly  as  soon  as  the  stone  ceases  to  obstruct  the  passage,  and  that 
severe  toxic  effects  of  the  drug  may  then  appear.  In  bilious  colic  the  distance  to  be  traversed 
by  the  stone  is  relatively  short,  and  in  that  affection,  especially,  the  inhalation  of  ether  of  chloro- 
form is  sometimes  the  best,  and,  indeed,  the  imperative  treatment.] 


SUPPURATIVA  HEPATITIS  081 

lemon  juice.  [Most  of  the  oil  is  passed  in  lumps,  which  have  a  superficial  re- 
semblance to  gallstones,  and  are  sometimes  called  such.  |  All  of  these  remedies 
appear  at  times  to  have  a  certain  virtue,  perhaps  because  they  usually  act 
as  cathartics.     They  are,  however,  of  no  great  value. 

In  all  cases  where  the  attacks  occur  very  frequently  and  are  associated 
with  such  severe  symptoms  that  the  patients  are  constantly  miserable,  we  are 
justified  in  advising  operation.  In  recent  times  the  surgical  treatment  of 
cholelithiasis  has  achieved  many  brilliant  cures.  If  one  considers  the  possible 
dangers  of  the  disease  itself,  it  is  easy  to  understand  why  some  surgeons  al- 
most always  recommend  operative  interference  whenever  the  presence  of  gall- 
stones has  been  demonstrated.  Still,  we  must  consider  that  the  circumstances 
in  practice  may  prevail  over  purely  theoretical  considerations,  however  lucid 
the  latter  may  be.  Many  patients  will  not  consent  to  an  operation  after  a 
single  brief  attack,  which,  although  painful,  has  ended  in  apparently  complete 
recovery,  and  the  conscientious  physician  will  consider  in  any  actual  case  the 
indisputable  dangers  of  the  operation  and  the  possible  doubt  as  to  diagnosis. 
I  am  very  loath  to  advise  operation  to  patients  with  severe  chronic  jaundice, 
as  I  have  often  seen  an  unfavorable  outcome  in  such  cases  as  the  result  of 
uncontrollable  hemorrhage  (hemorrhagic  diathesis)  ! 

We  must  therefore  carefully  consider  the  surgical  indications  in  each  in- 
dividual case,  and  in  all  mild  cases  first  try  to  improve  the  condition  of  the 
patient  by  other  means,  such  as  a  rest  cure,  a  course  of  waters  at  Carlsbad, 
etc.  If  no  result  is  obtained  by  these  palliative  measures,  then  the  question 
of  operation  must  naturally  be  given-  closer  attention.  An  operation  is  neces- 
sary when  the  symptoms  indicate  a  purulent  cholecystitis  or  a  localized 
abscess,  due  to  gallstones.  It  would  probably  be  better  if  such  complications 
of  cholelithiasis  were  avoided  by  anticipatory  surgical  interference,  but  this 
desirable  result  will  never  be  attained  in  practice,  because  in  many  cases  the 
purulent  infection  of  the  gall  bladder  or  the  bile  ducts  occurs  without  having 
been  preceded  by  any  marked  symptoms.  In  circumscribed  suppurations, 
surgical  intervention  often  not  only  saves  life  but  works  a  permanent  cure, 
unless  the  purulent  infection  has  already  extended  to  the  bile  ducts  of  the 
liver  itself,  or  has  led  to  general  pyaemia.  We  cannot  in  this  place  enter  into 
all  the  particulars  of  the  surgical  treatment  of  gallstones  or  the  various  opera- 
tive methods.     Complete  information  will  be  found  in  surgical  monographs. 


CHAPTER    III 

SUPPUPvATIVE    HEPATITIS 

{Hepatic  Abscess) 

iEtiology. — Exclusive  of  traumatism  there  are  two  ways  by  which  bacteria 
may  penetrate  into  the  liver,  there  to  excite  a  suppurative  inflammation — 
namely,  by  the  blood  and  through  the  bile  ducts.  In  the  circulatory  system  the 
main  route  is  by  way  of  the  portal  vein,  by  which  pyogenic  organisms  from  the 
intestines  reach  the  liver.  This  explains  why  many  ulcerative  processes  in 
the  intestines,  such  as  severe  dysentery,  are  followed  by  hepatic  abscess,  and  why 


682  DISEASES  OF  THE   DIGESTIVE  ORGANS 

other  suppurative  processes  within  the  portal  system,  particularly  the  suppura- 
tive thrombophlebitis  after  appendicular  inflammations  (q.v.)  may  have  a 
similar  sequel.  In  general  pyaemia  the  germs  must  take  a  very  circuitous  route 
in  order  to  reach  the  liver.  They  must,  on  leaving  the  primary  abscesses,  first 
enter  the  veins  and  the  lungs,  and  then  gain  the  liver  by  way  of  the  hepatic 
artery.  It  has  been  well  known  for  a  long  time  that  suppurating  wounds  of 
the  head  are  followed  by  hepatic  abscess  with  comparative  frequency.  We 
have  observed  fatal  suppurative  hepatitis  subsequent  to  a  fetid  bronchitis.  Per- 
haps it  may  exceptionally  happen  that  infectious  matter  enters  the  hepatic 
veins  by  "  retrogressive  embolism  "  from  the  vena  cava. 

The  germs  which  make  their  way  into  the  liver  from  the  bile  ducts  invariably 
originate  in  the  intestine.  In  these  cases  the  hepatic  inflammation  is  almost 
always  preceded  by  disease  of  the  biliary  passages.  The  most  frequent  cause 
by  far  of  this  variety  of  hepatic  abscess  is  the  formation  of  gallstones  in  the 
gall  bladder  and  in  the  liver.  This  has  been  fully  discussed  in  the  preceding 
chapter. 

.  Among  us,  hepatic  abscesses  are  rarely  occasioned  in  other  ways  than  those 
indicated ;  but  in  the  tropics  it  is  said  that  quite  a  large  number  of  apparently 
primary  hepatic  abscesses  are  met  with.  Their  origin  is  likewise  to  be  attrib- 
uted to  the  entrance  of  infectious  material  from  the  intestine.  Most  fre- 
quently, these  liver  abscesses  develop  after  a  tropical  amoebic  dysentery,  and 
often  after  apparently  mild  cases.  Bacillary  dysentery,  it  must  be  mentioned, 
almost  never  produces  a  liver  abscess.  The  amoebic  abscesses  are  found  chiefly 
in  males,  and  much  more  rarely  in  those  who  are  natives  of  the  tropics  than  in 
those  who  have  immigrated  thereto. 

Pathology. — The  smallest  and  "as  yet  imperfectly  developed  embolic 
abscesses  best  illustrate  the  mode  of  formation.  We  find  the  blood  vessels 
choked  with  micrococci,  and  the  cells  of  the  surrounding  parenchyma  void  of 
nuclei  and  in  process  of  disintegration.  Along  the  course  of  the  blood  vessels 
nuclei  are  very  abundant.  These  are  due  to  white  corpuscles  which  have  es- 
caped through  the  vascular  walls.  The  cells  and  the  liquid  exudation  rapidly 
increase,  and  there  is  complete  destruction  of  the  hepatic  parenchyma,  and  the 
formation  of  an  abscess  in  its  place.  This  extends  in  all  directions.  Large 
abscesses  may  at  last  involve  an  entire  lobe.  The  tropical  liver  abscesses  are 
situated  almost  without  exception  in  the  right  lobe  of  the  liver.  In  other  cases 
the  suppurative  process  is  limited  by  encapsulation.  Sometimes  quite  large 
portions  of  the  liver  become  necrotic  and  slough  off,  under  the  influence 
of  what  is  called  "  sequestrating "  suppuration.  We  almost  invariably  find 
some  shreds  of  hepatic  tissue  in  the  pus  of  hepatic  abscesses.  When  hepatic 
abscess  has  been  occasioned  by  gallstones,  the  suppuration  is  usually  due 
to  direct  extension  of  the  process  from  the  bile  ducts  to  the  parenchyma 
of  the  liver.  Not  infrequently  gallstones  are  found  in  the  pus  of  such 
cases. 

Small  abscesses  may  perhaps  be  absorbed,  but  they  are  in  most  cases  merely 
symptomatic  of  pyaemia  or  some  such  disease,  which  is  itself  incurable.  Larger 
abscesses  may  point  into  neighboring  organs.  If  they  are  discharged  into  the 
abdominal  cavity,  diffuse  peritonitis  follows.  The  most  favorable  termination, 
and  one  repeatedly  observed,  is  perforation  through  the  abdominal  walls,  after 
these  walls  and  the  liver  have  been  joined  by  adhesions.    They  may  also  break 


SUPPURATIVE   HEPATITIS  G83 

into  the  pleural  cavity,  the  pericardium,  the  intestine,  and  the  pelvis  of  the  right 

kidney. 

Clinical  History. — An  ahsolutely  complete  clinical  description  of  hepatic 
abscess  is  impossible,  because,  as  we  have  seen,  it  may  be  a  symptom  of  such 
diverse  pathological  processes.  Hepatic  abscesses  are  often  found  postmortem 
which  had  given  no  previous  indication  of  their  presence;  this  is  frequently  true 
in  pyaemia.  In  other  cases  there  are  symptoms,  in  part  directly  referable  to  the 
seat  of  inflammation,  and  in  part  due  to  its  influence  upon  neighboring  organs. 
In  recent  times,  the  pathology  of  tropical  liver  abscess  has  been  particularly 
well  elaborated. 

Enlargement  of  the  liver  can  almost  always  be  made  out  by  percussion  and 
usually  also  by  palpation.  It  is  the  result  of  swelling  and  hyperaemia  involving 
the  entire  organ.  Of  particular  importance  is  the  percussion  of  the  upper  bor- 
der of  the  liver  to  determine  its  height  and  the  dome-shaped  bulging  of  the 
right  lobe.  Extensive  abscesses  may  give  much  more  definite  signs  of  their 
presence,  however,  if  situated  on  the  anterior  surface  of  the  organ.  They  are 
sometimes  felt  through  the  abdominal  walls  as  hemispherical  and  actually  fluc- 
tuating tumors.  It  is  not  so  very  rare  for  tropical  hepatic  abscess  to  attain 
these  dimensions. 

Pain  in  the  right  hypochondrium,  although  it  may  be  entirely  absent  when 
the  abscesses  are  small,  even  if  they  are  numerous,  is  often  violent  and  per- 
sistent when  the  abscess  is  large.  It  is  excited  by  the  tension  of  the  peritoneal 
covering  of  the  liver,  or  by  perihepatitis.  The  pain  often  radiates — and  with 
especial  frequency  into  the  neighborhood  of  the  right  shoulder.  The  exact 
determination  of  the  tenderness  on  palpation  is  also  important. 

The  course  of  the  fever  may  prove  a  strong  diagnostic  point.  When  the 
abscess  is  chronic  and  encapsulated  there  may,  it  is  true,  be  no  fever  whatever ; 
but,  as  a  rule,  fever  does  exist,  and  it  often  presents  a  very  characteristic  inter- 
mittent character.  There  are  great  elevations,  usually  ushered  in  by  a  chill, 
and  succeeded  by  deep  depressions  of  temperature  accompanied  by  perspiration. 
If  the  hepatic  trouble  is  merely  a  symptom  of  general  pyaemia,  then  the  fever  is 
to  be  ascribed  to  the  latter ;  but  if  there  are  signs  of  a  severe  local  hepatic  disease, 
such  as  pain,  enlargement,  and  perhaps  jaundice,  and  if  these  febrile  attacks 
come  on  at  irregular  intervals,  we  should  always  consider  the  possibility  of 
abscess  of  the  liver.  In  the  cases  of  large  tropical  abscess  this  sort  of  fever  is 
the  rule.  It  is  most  frequent  with  us  in  cases  of  purulent  pylephlebitis  and  of 
abscess  excited  by  gallstones.  The  "  fievre  intermittent e  hepatique  "  of  the 
French  is  in  most  instances  due  to  the  presence  of  gallstones  in  the  liver,  with 
secondary  suppuration  and  abscess  formation. 

Among  the  secondary  symptoms  of  hepatic  abscess  jaundice  is  prominent. 
It  is  not  invariably  present,  however,  occurring  only  when  the  abscess  has  com- 
pressed some  large  biliary  duct,  and  has  thus  given  occasion  to  the  absorption 
of  bile  by  the  lymphatics,  or  when  an  extensive  cholangitis  has  simultaneously 
developed,  sufficient  to  cause  jaundice.  In  rare  instances  the  abscess  compresses 
the  portal  vein  and  thus  causes  ascites.  There  may  be  pulmonary  symptoms  of 
considerable  importance,  even  when  there  are  no  actual  pulmonary  complica- 
tions. This  is  because  the  right  half  of  the  diaphragm  is  crowded  up  by  ab- 
scesses projecting  from  the  convex  surface  of  the  liver.  Compression  of  the 
cardia  occasionally  produce  persistent  difficulty  in  deglutition.     Hiccough  is 


684  DISEASES   OF   THE   DIGESTIVE   ORGANS 

sometimes  a  source  of  distress,  and  it  may  be  due  to  the  pressure  of  the  abscess 
upon  the  stomach.  A  distressing  reflex  cough  may  also  occasionally  occur. 
Vomiting  is  also  a  rather  common  and  often  very  troublesome  symptom.  The 
occurrence  of  a  leucocytosis  is  worth  noting. 

There  is  almost  always  great  constitutional  disturbance.  The  patient  has 
no  appetite,  and  loses  flesh,  particularly  if  there  are  frequent  febrile  exacerba- 
tions. Often  there  are  severe  nervous  attacks.  Very  exceptionally,  the  disease 
remains  latent  for  a  long  time,  and  does  not  disturb  the  general  health  to  any 
great  extent. 

The  course  of  the  disease  depends  mainly  upon  the  nature  of  the  original 
disturbance.  Severe  pyemic  cases,  in  which  hepatic  abscesses  develop,  are  gen- 
erally brief,  and  are  almost  invariably  fatal.  Abscesses  due  to  gallstones,  and 
the  large  abscesses  which  are  apparently  idiopathic,  are  generally  chronic,  last- 
ing for  weeks,  or  even  for  many  months.  Cases  exhibit  manifold  diversities, 
according  to  the  position,  size,  number,  and  sequelae  of  the  abscesses.  Among 
the  possible  results,  we  would  once  more  call  attention  to  perforation  into  neigh- 
boring organs.  If  the  pus  is  discharged  externally,  recovery  may  ensue ;  as  also 
if  the  pus  reaches  the  intestinal  canal  or  the  bronchi,  which  seldom  happens. 
Perforation  into  the  abdominal  cavity  always  excites  a  fatal  acute  peritonitis. 
As  a  general  rule,  hepatic  abscess  finally  proves  fatal,  recovery  being  excep- 
tional. Death  is  due  either  to  the  gradual  loss  of  strength  or  to  some  compli- 
cation. 

Treatment. — Local  bleeding,  counterirritation,  purgatives,  and  emetics  are 
among  the  remedies  which  are  advocated,  but  we  can  hardly  expect  them  to 
exert  much  influence  upon  a  hepatic  abscess.  The  best  way  is  to  treat  the  case 
purely  symptomatically,  seeking  to  keep  up  the  patient's  strength  and  mitigate 
his  suffering  until,  if  we  are  very  fortunate,  we  have  a  chance  for  operative  inter- 
ference. When  once  the  other  symptoms  are  reenforced  by  the  discovery  on 
palpation  of  a  fluctuating  tumor,  the  diagnosis  is  established,  and  the  pus 
should  be  evacuated  and  the  cavity  drained.  Particulars  about  the  operation 
should  be  sought  in  works  on  surgery.  More  than  one  case  of  the  large  tropical 
abscess  has  been  cured  in  this  way;  but  the  cases  which  are  most  common 
among  us — namely,  embolic  abscesses  and  those  excited  by  gallstones — hardly 
ever  afford  any  opportunity  for  surgical  interference. 


CHAPTER    IV 

CIRRHOSIS    OF    THE    LIVER 

{Chronic  Diffuse  Interstitial  Hepatitis.     Laennec's  Cirrhosis.     Gin-drinker's  Liver. 

Hobnailed  Liver) 

iEtiology  and  Pathology. — Cirrhosis  of  the  liver  is  usually  defined  as  a 
diffuse  interstitial  inflammation,  chronic  in  duration,  and  resulting  in  a  sec- 
ondary atrophy  of  the  true  hepatic  parenchyma.  Weigert's  careful  study,  how- 
ever, of  the  analogous  processes  of  "  chronic  interstitial  nephritis  "  has  shown 
that  at  least  a  large  part  of  the  changes  which  take  place  in  the  connective 
tissue  are  not  primary,  but  secondary,  and  the  consequence  of  a  primary  de- 
struction of  the  genuine  renal  parenchyma.     In  our  opinion  we  must  adopt  a 


CIRRHOSIS   OF  THE   LIVER  685 

similar  point  of  view  for  hepatic  cirrhosis.  We  feel,  therefore,  that  in  mosi 
cases  of  hepatic  cirrhosis  the  origin  of  the  disease  consists  of  a  primary  injury 
and  consequent  partial  destruction  of  the  hepatic  cells,  whereupon  follow  a 
secondary  proliferation  and  final  contraction  of  the  interstitial  tissue,  just  as 
is  seen  in  lesions  of  the  parenchyma  of  the  kidneys,  spinal  cord,  and  heart. 

Such  a  conception  would  he  extremely  compatible  with  one  fact  about  the 
a3tiology  of  the  disease — namely,  that  chronic  alcoholism  is  universally  regarded 
as  a  potent  predisposing  cause.  Hence  the  English  name,  "  gin-drinker's  liver." 
The  harmful  influence  of  alcohol  can  be  appreciated  if  we  remember  that  on 
being  absorbed  it  is  carried  directly  by  the  blood  vessels  through  the  portal  vein 
to  the  liver.  We  assume  that  the  poison  exerts  a  specific  injurious  influence 
upon  the  hepatic  cells  proper,  impairing  their  nutrition,  and  finally  causing 
their  destruction.  That  the  disease  attacks  the  periphery  of  the  lobules  and 
the  interlobular  connective  tissue  is  easily  intelligible.  It  is  well  known  that 
the  capillary  anastomoses  of  the  portal  vein  are  situated  between  the  lobules. 

Hepatic  cirrhosis  is  most  common  in  those  who  drink  distilled  liquors,  while 
excessive  indulgence  in  less  strongly  alcoholic  beverages,  such  as  wine  and  beer, 
leads  less  frequently  to  cirrhosis.  Still,  we  have  repeatedly  seen  the  disease  in 
beer  drinkers. 

Until  now,  attempts  to  produce  experimentally  a  hepatic  cirrhosis  in  ani- 
mals by  chronic  alcohol  poisoning  have  given  contradictory  results.  The  inter- 
esting fact  discovered  by  Bauer  is,  however,  worthy  of  mention — viz.,  that 
after  the  administration  of  large  quantities  of  alcohol  in  dogs,  alcohol  and  also 
albumen  (  !)  can  be  demonstrated  in  the  bile. 

The  abuse  of  alcohol  is  surely  the  chief  but  by  no  means  the  only  cause  of 
cirrhosis.  The  disease  sometimes  attacks  persons  in  whose  case  no  such  astiology 
is  possible.  In  such- instances  we  are  seldom  able  to  demonstrate  the  real  cause. 
The  excessive  use  of  spices,  and  other  analogous  substances,  has  sometimes 
been  regarded  as  causative.  It  is  also  said  that  malaria  and  the  acute  infectious 
diseases  sometimes  leave  behind  them  a  tendency  to  cirrhosis.  In  our  opinion 
such  cases  are  due  to  the  long-continued  action  of  chemical  agents,  about  which 
we  do  not  as  yet  possess  any  accurate  knowledge,  which  are  conveyed  from  the 
intestine,  or,  perhaps,  in  some  instances,  also  from  the  blood  to  the  liver.  These 
cases  of  "  genuine  hepatic  cirrhosis  "  are  analogous  to  the  not  infrequent  cases 
of  "  genuine  interstitial  nephritis  "  of  unknown  origin.  Perhaps  in  many  in- 
stances, also,  there  is  a  constitutional  and  excessive  sensitiveness  of  the  hepatic 
cells  to  the  injurious  influences  to  which  they  are  exposed  while  performing  their 
normal  functions. — The  form  of  cirrhosis  which  follows  diseases  of  the  bile, 
ducts  (biliary  cirrhosis  as  distinguished  from  portal  hepatic  cirrhosis),  and 
also  "  syphilitic  cirrhosis,"  will  receive  separate  consideration.  The  liver 
changes  in  diabetes  mellitus  will  be  considered  in  the  discussion  of  this  disease. 

Cirrhosis  of  the  liver  is  seen  much  oftener  in  men  than  in  women,  and  usu- 
ally occurs  in  middle  life.  This  is  in  harmony  with  the  fact  that  the  chief  cause 
is  the  abuse  of  alcohol. 

The  anatomical  changes  are  generally  divided,  without  regard  to  the  way  in 
which  they  are  brought  about,  into  two  stages.  In  the  first  stage  the  liver  is 
uniformly  enlarged,  resistant,  with  its  edge  blunt  and  its  surface  at  first  per- 
fectly smooth,  but  later  presenting  little  dimples.  On  section,  the  increased  con- 
sistence, or  "interstitial  induration"  of  the  liver,  can  be  readily  perceived. 


686  DISEASES   OF  THE   DIGESTIVE   ORGANS 

The  acini  are  separated  from  one  another  by  a  relatively  thick  hand  of  grayish- 
red  interstitial  tissue,  and  are  at  first  readily  distinguishable.  Later  on,  the 
interstitial  hyperplasia  invades  the  acini  themselves,  and  they  cease  to  be  dis- 
cernible. If  there  is  a  marked  fatty  infiltration  of  the  liver  cells,  the  liver  on 
section  presents  a  distinct  yellowish  color.  The  microscope  shows  that  the 
cause  of  this  increase  in  size  and  firmness  of  the  organ  is  due  exclusively  to 
the  abundant  cellular  infiltration  and  the  new  formation  of  connective  tissue 
between  the  individual  lobules.  Very  frequently  we  find  newly  formed  bile 
capillaries  in  the  interstitial  connective  tissue.  The  neighboring  cells  of  the 
parenchyma  exhibit  signs  of  disintegration,  undergoing  either  simple  atrophy 
or  else  fatty  degeneration. 

The  second  stage  corresponds  with  the  process  of  contraction  of  the  newly 
formed  connective  tissue,  but  in  this  stage  the  destruction  of  the  proper  hepatic 
tissue  has  already  assumed  grave  proportions.  Under  this  process  of  contrac- 
tion the  liver  undergoes  progressive  atrophy,  and  its  surface  becomes  mammil- 
lated.  The  size  of  the  nodules  varies.  The  size  of  the  whole  organ  may  be 
reduced  one  half,  or  even  more.  Frequently  its  general  contour  is  considerably 
modified.  Often  the  diminution  of  the  size  of  the  liver  is  confined  mainly  to 
the  left  lobe.  The  serous  coat  of  the  liver  is  usually  thickened  and  rendered 
opaque ;  the  hepatic  tissue  feels  very  resistant  and  cuts  with  difficulty,  often  with 
a  grating  sound;  the  color  of  the  cut  surface  is  usually  a  rather  light  yellow 
(/cippos  =  yellow).  Upon  microscopic  examination,  we  find  merely  vestiges  of 
parenchyma,  embracing  which  are  wide,  firm  bands  of  connective  tissue.  Even 
within  the  acini  there  is  decided  interstitial  hyperplasia  along  the  blood  vessels. 
The  hepatic  cells  exhibit  various  stages  of  fatty  degeneration  and  simple 
atrophy.  Brown  masses  of  jrigment  are  often  found  here  and  there,  which  have 
been  left  behind  lyy  the  hepatic  cells  now  destroj^ed.  Eegenerative  changes  can 
also  be  detected  quite  frequently.  The  most  common  of  these  is  the  formation 
of  small  biliary  passages  in  the  broad  bands  of  interstitial  tissue. 

Although  this  division  of  hepatic  cirrhosis  into  two  successive  "  stages  "  is 
useful  for  a  schematic  understanding  of  the  disease,  it  must  be  emphasized 
that  such  a  division  does  not  always  correspond  to  the  actual  conditions.  Per- 
haps, as  in  chronic  nephritis  (q.  v.),  it  depends  on  the  kind  and  intensity  of  the 
active  harmful  influence  as  to  whether  we  shall  find  a  large  liver  with  a  smooth 
surface  (analogous  to  the  kidney  of  diffuse  nephritis)  or  a  small  liver  with  a 
granular  surface  (analogous  to  the  secondarily  contracted  kidney).  In  many 
cases  there  seems  to  be  no  so-called  "  first  stage  "  at  all,  and  the  previously 
normal  liver  is  directly  transformed  into  a  contracted  liver,  perhaps  comparable 
to  the  kidney  of  genuine  interstitial  nephritis. 

Clinical  History. — The  onset  of  the  disease  is  usually  insidious.  At  autop- 
sies quite  an  advanced  stage  of  cirrhosis  is  sometimes  found,  to  which  not  a 
single  clinical  symptom  had  pointed ;  and  it  is  often  observed  that  the  duration 
of  unambiguous  symptoms  is  much  shorter  than  the  degree  of  anatomical  change 
discovered  postmortem  would  have  led  us  to  expect. 

Cirrhotic  disease  of  the  liver  may  also  be  compensated  for,  for  a  long  time, 
by  the  organism.  In  such  cases  we  occasionally  find,  on  examination  of  the 
liver,  that  it  is  distinctly  enlarged  and  hardened  without  the  patient  showing 
any  particular  symptoms  of  the  disease. 

Very  often,  to  be  sure,  certain  prodromata  appear  long  before  the  genuine 


CIRRHOSIS  OF  THE   LIVER  G87 

cirrhotic  symptoms;  but  there  is  generally  room  for  doubt  whether  these 
prodromata  are  excited  by  the  incipient  hepatic  disease  or  whether  they  are 
not  due  to  other  coincident  affections,  such  as  the  chronic  gastric  or  intestinal 
catarrh  which  drunkards  so  often  have.    There  arc  anorexia,  nausea,  epigastric 

uneasiness,  eructations,  constipation,  and  sometimes  vomiting.  There  is  evi- 
dent constitutional  disturbance  in  many  cases,  but  in  others  the  strength  is 
unimpaired.  The  severer  symptoms  usually  date  from  the  time  when  disturb- 
ance of  the  portal  circulation  arises.  We  have  already  stated  that  the  diseased 
process  is  most  active  in  the  interlobular  connective  tissue — that  is,  where  the 
portal  capillaries  are  situated.  When  the  contraction  of  the  connective  tissue 
has  resulted  in  the  destruction  of  a  large  number  of  these  portal  capillaries 
and  the  minute  veins  from  which  they  spring,  the  portal  circulation  is  in- 
evitably impeded,  and  there  arises  a  passive  congestion  of  the  whole  portal 
system.    The  signs  of  this  are  soon  manifest. 

The  stasis  in  the  veins  of  the  peritoneum  is,  as  a  rule,  the  first  to  attract 
attention,  from  the  ascites  which  it  occasions.  The  distention  of  the  abdomen 
and  the  sensation  of  weight  and  pressure  due  to  this  effusion  are  often  the 
first  things  which  excite  the  patient's  attention  and  lead  him  to  seek  medical 
advice.  Later  on,  the  ascites  sometimes  becomes  enormous,  causing  immense 
swelling  and  extreme  tension  of  the  abdominal  walls,  and,  of  course,  propor- 
tionate discomfort.  Proper  nursing  and  internal  treatment  may  diminish  the 
ascitic  effusion,  and  it  occasionally  disappears  entirely.  It  quite  often  re- 
mains nearly  uniform,  until  finally,  for  some  reason,  there  is  a  change  for  the 
worse. 

Next  to  ascites,  the  most  important  symptom  of  portal  obstruction  is  en- 
largement of  the  spleen,  which  is  due  both  to  the  increased  amount  of  blood  in 
the  organ  and  to  a  diffuse  hyperplasia  of  its  tissues.  As  a  rule,  the  increase 
in  size  is  considerable,  amounting  sometimes  to  two  or  three  times  the  normal 
dimensions.  It  is  not  very  exceptional  to  find  a  well-marked  splenic  tumor 
in  hepatic  cirrhosis  even  before  there  is  any  ascites.  In  such  cases  the  splenic 
tumor  is  not  due  at  all  to  portal  congestion  but  to  other,  perhaps  toxic,  influ- 
ences, just  as  in  biliary  cirrhosis  (vide  infra).  At  any  rate  the  discovery  of 
splenic  tumor  is  invariably  of  great  diagnostic  importance,  although  it  is  often 
no  easy  matter  to  make  out  the  size  of  the  spleen,  inasmuch  as  both  percussion 
and  palpation  are  rendered  very  difficult  by  the  presence  of  ascites.  On  the 
whole,  palpation  is  the  more  reliable.  Pain  or  other  subjective  symptoms  are 
rarely  observed.  Exceptionally,  there  is  no  enlargement  of  the  spleen.  This 
may  be  due  to  the  firmness  and  thickness  of  its  capsule,  or  to  the  general 
marantic  condition  of  the  patient. 

The  venous  congestion  of  the  stomach  and  intestines  excites  catarrh,  which 
is  evinced  by  anorexia,  nausea,  and  irregularity  of  the  bowels.  Usually  there 
is  quite  obstinate  constipation,  but  there  may  be  persistent  diarrhea.  None  of 
these  symptoms  occupies  the  foreground  of  the  clinical  picture,  however,  both 
because  such  symptoms  are  frequent  in  all  grave  chronic  diseases  and  because 
many  patients  have  had  digestive  derangements  long  before  these  severer 
troubles  began.  In  less  frequent  but  more  important  cases,  the  congestion  in 
the  gastric  and  intestinal  mucous  membranes  reaches  so  extreme  a  degree  that 
hemorrhages  occur.  If  the  hemorrhage  is  slight  and  comes  from  capillaries, 
there  is  diarrhea  with  blood-stained  stools,  or  vomiting,  the  vomitus  being 


688  DISEASES   OF   THE   DIGESTIVE   ORGANS 

dark-colored.  Probably  the  tendency  to  hemorrhage  is  aggravated  by  the  gen- 
eral cachexia  or  by  the  alcoholism.  Of  more  importance  is  the  vomiting  of 
large  amounts  of  pure  blood.  This,  as  the  author  knows  from  repeated  ob- 
servations, may  be  sufficient  of  itself  to  endanger  life.  Such  cases  have  more 
than  once  led  to  the  incorrect  diagnosis  of  gastric  ulcer,  but  at  autopsy  we 
usually  find  well-marked  varices  in  the  oesophagus,  due  to  passive  congestion. 
The  severe  hemorrhage  is  occasioned  by  the  bursting  of  a  varix.  We  surmise 
that  similar  conditions,  probably  mostly  in  the  rectum,  cause  the  severe  in- 
testinal hemorrhages  which  are  sometimes  seen.  Profuse  surface  hemorrhages 
by  diapedesis  may  occur  without  varix  or  ulceration.  These  depend  upon  a 
form  of  hemorrhagic  diathesis  due  to  changes  in  the  walls  of  the  capillaries. 

There  is  sometimes  a  slight  jaundice  in  ordinary  cirrhosis,  which  is  due  to 
the  existence  of  duodenal  catarrh,  or  perhaps  to  catarrh  of  the  smaller  bile 
ducts.  In  many  cases,  however,  there  is  no  jaundice  at  all,  or  scarcely  any. 
Not  infrequently  then,  however,  the  skin  shows  a  peculiar  dark,  dirty-yellowish 
color,  which  is  very  characteristic  of  chronic  hepatic  disease. 

The  above  signs  of  portal  obstruction  will  often  render  the  diagnosis  of 
hepatic  disease  extremely  probable,  but  we  should  always  endeavor  to  confirm 
our  opinion  by  physical  examination  of  the  liver.  In  the  later  stages  of  the 
disease,  and  particularly  if  there  be  great  ascites,  our  efforts  may  be  fruitless ; 
but  at  first,  or  after  paracentesis  has  been  performed,  percussion  and  palpation 
may  yield  valuable  information.  In  the  earliest  stages  the  liver  is  usually 
large.  Hepatic  dullness  reaches  some  way  below  the  edge  of  the  ribs,  and  we 
can  often  feel  the  lower  edge  and  anterior  surface  of  the  organ.  Later  on  we 
find  the  surface  irregular  and  rough.  If  we  can  feel  these  little  nodules  or 
prominences  through  the  abdominal  walls,  as  we  sometimes  can,  of  course  the 
diagnosis  of  cirrhosis  of  the  liver  is  nearly  certain.  As  already  mentioned,  it 
often  happens  that  irregularities  are  already  to  be  felt  upon  the  surface  of  the 
organ  while  it  still  remains  hypertrophic.  The  demonstration  of  atrophy  by 
percussion  in  the  later  stages  of  the  disease  is  less  reliable.  The  ascites  often 
interferes  with  such  an  attempt.  We  may  also  be  misled  by  coils  of  intestine 
distended  with  gas  and  perhaps  lying  in  front  of  the  liver.  If,  however,  after 
guarding  against  error,  we  constantly  find  the  area  of  hepatic  dullness  dimin- 
ished, the  sign  has  some  value.  Moreover,  it  is  not  infrequently  possible  to 
make  out  by  palpation  that  the  liver,  although  reduced  in  size,  is  hard  and 
uneven.  This  is  easier  after  the  removal  of  ascitic  fluid,  when  the  abdominal 
walls  are  lax,  and  also  if  the  attachments  of  the  liver  have  been  relaxed  so  that 
it  sinks  downward.  If  the  atrophied  liver  cannot  be  directly  felt,  I  have  at 
times  been  struck  in  palpation  by  the  "  emptiness  of  the  right  hypochondrium  " 
— i.  e.,  the  possibility  of  reaching  without  resistance  high  up  under  the  right 
costal  arch. 

General  nutrition  is  usually  much  impaired  in  the  later  stages  of  the  dis- 
ease. At  first  the  patient  may  retain  vestiges  of  his  former  corpulence,  but 
finally  he  grows  emaciated.  Anasarca  may  exceptionally  occur  toward  the 
close,  but  there  is  frequently  considerable  oedema  of  the  lower  extremities,  and 
even  of  the  scrotum  and  the  dependent  portions  of  the  abdominal  walls.  The 
cause  of  this  is  a  purely  local  one — the  pressure  of  the  ascites  impedes  the  re- 
turn of  blood  from  the  lower  limbs  to  the  heart.  Thus  arises  a  condition 
which  is  characteristic  of  portal  obstruction  in  general,  and  hepatic  cirrhosis 


CIRRHOSIS   OF  THE   LIVER  689 

in  particular,  and  has  been  termed  "  oedema  of  the  lower  half  of  the  body." 
There  is  ascites  with  oedema  of  the  loins,  the  scrotum,  and  the  lower  extremi- 
ties; while  the  upper  extremities,  the  upper  half  of  the  trunk,  and  the  face 
are  entirely  free  from  oedema. 

Occasionally  there  are  ecchymoses  into  the  skin,  the  mucous  membranes, 
the  retina,  and  other  parts.  These  are  probably  due  to  malnutrition  of  the 
vascular  walls.  The  gastric  and  intestinal  hemorrhages  have  been  already 
discussed. 

In  uncomplicated  cases  of  the  disease  there  is  no  fever.  The  pulse,  even 
when  there  are  no  cardiac  complications,  is  small  and  often  somewhat  rapid. 
Eespi ration  may  be  much  embarrassed  as  a  result  of  the  upward  pressure  of 
the  diaphragm. 

At  first  the  urine  presents  no  characteristic  changes.  When  the  ascites  has 
become  considerable,  and  there  is  oedema,  the  urine  grows  scanty,  dark,  and 
concentrated,  and  often  has  an  abundant  sediment  of  urates.  The  frequently 
large  amount  of  urobilin  in  the  urine  is  worthy  of  mention.  This  is  best 
demonstrated  by  the  Schlesinger  test — viz.,  fluorescence  of  the  urine  on  addition 
of  an  equal  amount  of  a  ten-per-cent  solution  of  zinc  acetate  in  absolute  alco- 
hol. The  demonstration  of  the  presence  of  urobilin  is  not  without  significance 
in  the  diagnosis  of  hepatic  cirrhosis  (P.  K.  Pel),  as  we  also  can  testify.  An 
exact  explanation  of  urobilinuria  in  liver  disease  is  as  yet  not  possible.  It  is 
generally  assumed  that  the  diseased  liver  cells  are  no  longer  able  to  dispose  of 
the  urobilin  absorbed  from  the  intestine.  It  must  also  be  mentioned  that  some 
observers  have  found  a  diminished  amount  of  urea  in  the  urine,  and  have 
attempted  to  attribute  this  to  a  disturbance  of  the  urea-forming  function  of 
the  liver.  More  recent  observations,  however,  have  not  confirmed  this  conten- 
tion. Frequently,  comparatively  large  quantities  of  ammonia  have  been 
found  in  the  urine.  This  is  probably  due  to  an  increased  acid  formation  in 
the  blood,  and  not  to  a  diminution  in  the  formation  of  urea.  The  statements 
of  Bouchard  relative  to  the  increased  toxicity  of  the  urine  in  hepatic  disease, 
in  consequence  of  the  diminished  poison-neutralizing  function  of  the  liver, 
require  further  verification.  Glycosuria  and  alimentary  glycosuria  occur  oc- 
casionally, but  by  no  means  regularly.  Worthy  of  note,  too,  is  the  assertion 
of  H.  Strauss  and  others,  that  levulosuria  results  more  readily  in  patients 
with  hepatic  disease  after  the  administration  of  levulose  than  it  does  in  healthy 
persons.     This  also  requires  further  investigation. 

It  remains  for  us  to  describe  briefly  the  collateral  circulation  which  may  be 
developed  in  cirrhosis,  so  as  to  enable  the  blood  of  the  portal  system  to  reach 
the  systemic  veins.  The  clinical  history  of  the  disease  does  not  indicate  that 
this  attempt  at  compensation  is  very  successful.  We  may  have:  1.  Communi- 
cations between  the  veins  of  the  mesentery  and  of  the  abdominal  walls.  2. 
Communications  between  the  coronary  vein  of  the  stomach  and  the  veins  of 
Glisson's   capsule   on   the   one   hand   and   the   phrenic   veins    on   the   other. 

3.  Anastomoses  between  the  internal  hemorrhoidal  and  the  hypogastric  veins. 

4.  As  pointed  out  by  Baumgarten,  enlargement  of  the  not  yet  completely 
obliterated  umbilical  vein  in  the  ligamentum  teres.  Through  all  these  the 
blood  may  flow  from  the  portal  system  into  the  veins  of  the  abdominal  walls 
— that  is,  in  the  reverse  of  the  normal  direction.  Then  in  a  few  exceptional 
cases  the  veins  around  the  navel  become  varicose,  a  phenomenon  which  has 


690  DISEASES   OF   THE   DIGESTIVE   ORGANS 

been  termed  the  "  caput  Medusae."  Much  more  frequent  and  more  important 
is  the  finding  of  unnaturally  distended  and  tortuous  veins  in  the  skin  of  the 
abdominal  walls  when  there  is  ascites.  These  veins  usually  extend  upward 
from  the  neighborhood  of  Poupart's  ligament.  This  phenomenon,  aside  from 
possible  anastomoses  between  the  subcutaneous  veins  and  the  portal  tributaries 
(vide  supra),  is  due  to  the  fact  that  because  of  the  ascites  the  flow  of  venous 
blood  from  the  lower  extremities  through  the  iliac  veins  is  impeded,  and  con- 
sequently a  part  of  the  venous  blood  takes  its  course  through  the  inferior  and 
superior  epigastric  veins  to  the  mammary  veins. 

The  complications  of  hepatic  cirrhosis  which  are  seen  in  many  cases  are 
probably  due  in  part  to  the  same  influences  (alcoholism)  which  occasion  the 
cirrhosis.  In  this  list  belong,  for  example,  cardiac  hypertrophy,  intestinal 
nephritis,  and  chronic  pachymeningitis.  Of  special  interest,  because  of  its 
diagnostic  and  therapeutic  importance,  is  the  combination  of  hepatic  cirrhosis 
with  tuberculous  peritonitis.  As  we  have  already  seen,  hepatic  cirrhosis  is  prob- 
ably in  most  cases  the  primary  disease,  and  occasions  a  predisposition  to  the 
development  of  tuberculous  peritonitis.  The  clinical  picture  in  these  cases  is 
a  combination  of  the  symptoms  of  hepatic  cirrhosis,  such  as  a  palpable  granular 
liver,  splenic  tumor,  and  yellowish  complexion,  with  the  symptoms  of  tuber- 
culosis, such  as  irregular  distention  and  tenderness  of  the  abdomen,  persistent 
fever,  and  emaciation.  If  we  consider  the  setiology  (alcoholism),  we  may, 
therefore,  sometimes  make  a  complete  diagnosis  of  this  combination,  particu- 
larly if  at  the  same  time  the  tubercular  inflammation  attacks  other  serous 
membranes,  such  as  the  pleura,  or  if  there  are  other  signs  of  a  tubercular  in- 
fection (lungs,  etc.). 

As  to  the  general  course  of  cirrhosis,  its  duration  cannot  easily  be  deter- 
mined because  the  onset  is  usually  insidious.  As  a  rule,  the  disease  lasts  one 
to  three  years,  or  rarely  longer.  In  many  cases  the  symptoms  are  insignificant 
for  the  first  six  to  eighteen  months.  Then  the  disorder  takes  on  a  severer 
form,  perhaps  rather  suddenly.  Ascites  appears,  for  example.  These  graver 
symptoms  persist,  until  after  a  few  months  the  patient  dies.  The  course  of 
the  disease  reminds  one  of  cardiac  cases,  where  for  a  long  while  the  compen- 
satory changes  avert  any  distress,  until  on  a  sudden  the  circulatory  disturb- 
ances become  pronounced  and  persist  to  the  end.  To  be  sure,  in  hepatic  cir- 
rhosis very  marked  symptoms  (extreme  ascites)  may  for  a  time  completely 
disappear. 

Prognosis. — The  prognosis  is  always  unfavorable,  at  least  when  the  symp- 
toms have  once  become  well  marked.  It  may  be  that  in  the  earlier  stages  the 
disease  can  be  checked  or  even  permanently  cured,  but  even  this  is  open  to 
doubt.    No  case  recovers  in  which  the  diagnosis  of  cirrhosis  is  certain. 

Death  is  due  either  to  intercurrent  disease,  or  more  often  to  gradually  in- 
creasing exhaustion.  In  some  few  cases  severe  cerebral  symptoms  suddenly 
appear:  there  are  coma,  general  convulsions,  and  delirium,  and  these  usually 
are  soon  fatal.  Just  how  these  nervous  phenomena  originate  we  do  not  cer- 
tainly know  (see  the  chapter  on  Acute  Yellow  Atrophy  of  the  Liver). 

Diagnosis. — The  diagnosis  of  hepatic  cirrhosis  is  not  usually  self-evident. 
It  may  be  made  with  some  positiveness  if  a  patient  who  has  a  previous  history 
of  alcoholic  excess  gradually  develops  ascites  and  splenic  tumor,  and  if  upon 
palpation  we  find  the  liver  unnaturally  firm  and  hard,  either  enlarged  or 


CIRRHOSIS   OF   THE   LIVER  691 

shrunken,  perhaps  with  a  roughened  surface,  and  in  any  case  distinctly  to  be 
felt;  yet  in  palpating  the  granular  surface  one  is  very  liable  to  errors,  and  par- 
ticularly the  separate  kernels  of  fat  in  the  panniculus  adiposus  of  the  abdomen 

are  apt  to  be  mistaken  by  inexperienced  observers  for  irregularities  in  the 
surface  of  the  liver.  The  difficulties  in  the  percussion  of  the  liver  have  been 
already  indicated.  Often  a  patient  does  not  come  under  observation  until  a 
considerable  ascitic  effusion  has  already  taken  place,  so  that  physical  examina- 
tion of  the  liver  and  spleen  is  rendered  very  difficult,  if  not  impossible.  Then 
we  must  first  exclude  any  general  disturbance  of  circulation  as  a  cause  of  the 
ascites.  If  the  heart,  lungs,  and  kidneys  are  found  to  be  normal,  and  if  there 
is  no  oedema  in  the  upper  half  of  the  body,  it  is  very  probable  that  there  is  a 
local  derangement  of  the  portal  circulation,  particularly  if  the  patient  is  pos- 
itive that  the  abdominal  enlargement  was  the  first  evidence  of  dropsy ;  but  we 
have  still  to  determine  whether  the  cause  of  this  derangement  is  cirrhosis  of 
the  liver.  This  may  be  assumed  to  be  the  case  if  the  whole  course  of  the 
disease  warrants  the  assumption,  and  if  the  history  furnishes  that  most  fre- 
quent of  all  serological  factors,  chronic  alcoholism.  Otherwise  we  must  be 
cautious,  for  portal  obstruction  with  precisely  similar  results  may  be  due  to 
other  causes — such  as  the  external  pressure  of  tumors  or  portal  thrombosis. 
Many  forms  of  hepatic  syphilis  (q.  v.)  cannot  be  differentiated  from  cirrhosis 
by  mere  clinical  observation  of  the  hepatic  disorder.  Here  it  is  only  the 
aetiology  and  the  demonstration  of  other  signs  of  syphilis  that  can  justify  the 
assumption  that  the  disease  in  hand  is  of  specific  origin.  It  is  often  a  great 
aid  in  diagnosis  to  examine  the  liver  directly  after  tapping.  The  abdominal 
walls  are  then  relaxed  and  soft,  so  that  the  liver  may  be  made  out  very  dis- 
tinctly. It  should  be  borne  in  mind  that  irregularities  of  considerable  size 
are  more  frequent  in  hepatic  syphilis  ("lobulated  liver"),  while  cirrhosis  is 
suggested  by  a  more  uniform  granulation. 

It  is  also  very  difficult  in  many  instances  to  exclude  chronic  peritonitis. 
The  aetiology  may  aid  us.  Other  points  are,  that  in  chronic  peritonitis  there 
may  be  tenderness  on  pressure,  the  abdominal  distention  is  less  uniform,  and 
there  is  no  enlargement  of  the  spleen.  Another  point  is  that  the  specific 
gravity  of  a  simple  ascites  due  to  passive  congestion  is  often  below  1.015,  while 
an  inflammatory  exudation  usually  reaches  higher  figures.  The  albumen 
content  of  an.  inflammatory  exudation  is  generally  decidedly  higher  than  that 
of  a  transudate.  As  a  boundary  figure,  four  per  cent  may  be  taken,  though 
exceptions  in  both  directions  may  occur.  Finally,  the  Eivalt  test  deserves 
consideration  (vide  supra,  page  355).  Hemorrhagic  ascites,  as  a  rule,  indi- 
cates tubercular  or  cancerous  peritonitis.  But  even  if  an  isolated  transudate 
in  the  abdominal  cavity  has  been  demonstrated,  a  false  assumption  of  hepatic 
disease  not  infrequently  occurs,  through  the  circumstance  that  occasionally 
in  heart  disease,  particularly  in  obliteration  of  the  pericardium  and  in  mitral 
stenosis,  an  isolated  ascites  may  develop.  We  have  already  discussed  this 
question  (cf.  pages  402  and  448). 

The  combination  of  hepatic  cirrhosis  and  chronic  peritoneal  tuberculosis 
(vide  supra)  may  be  diagnosticated  with  a  certain  probability  if,  besides 
symptoms  of  cirrhosis  and  peritoneal  disturbance,  there  are  definite  indications 
of  a  tubercular  affection;  such  are  a  phthisical  constitution,  persistent  fever, 
and  the  existence  of  a  tubercular  disease  in  some  other  organ,  particularly 


692  DISEASES  OF  THE  DIGESTIVE  ORGANS 

the  pleura.  The  lymphocyte  content  of  the  exudate  is  also  of  diagnostic 
importance  (cf.  page  361). 

Treatment. — In  treating  hepatic  cirrhosis  the  first  necessity  is  a  strict 
regulation  of  the  diet.  The  earlier  in  the  disease  proper  diagnostic  rules  are 
followed,  the  more  likelihood  of  benefit.  The  most  important  principle  in 
regulating  the  diet  is  to  avoid  all  ingesta  which  in  any  way  might  irritate  or 
damage  the  hepatic  cells.  We  forbid,  therefore,  all  alcoholic  beverages,  or  at 
most  allow  very  small  amounts  merely  to  stimulate  the  appetite.  We  likewise 
forbid  sharp  spices,  pepper,  mustard,  horse-radish,  onions,  and  similar  arti- 
cles. In  general,  the  amount  of  meat  should  be  limited.  We  may  allow  milk, 
buttermilk,  eggs,  vegetables,  and  cereals.  In  suitable  cases  we  may  try  the 
prescription  of  an  exclusive  milk  diet  for  some  weeks.  Quite  a  number  of 
authors  report  favorable  results  from  a  milk  cure  of  this  sort,  but  the  indi- 
vidual peculiarities  of  every  case  must  be  considered. 

If  the  disease  has  already  developed  we  must  resign  ourselves  to  merely 
symptomatic  treatment.  The  benefit  which  iodid  of  potassium  is  said  to 
exercise  in  hepatic  cirrhosis  is  very  doubtful,  and  is  probably  based  merely 
upon  cases  of  syphilitic  disease  of  the  liver. 

The  symptomatic  treatment  of  hepatic  cirrhosis  has  to  deal  mainly  with  the 
disturbances  due  to  portal  congestion,  and  the  associated  gastrointestinal  ca- 
tarrh. In  such  cases  experience  sbows  that  the  best  results  are  obtained  by  the 
cautious  use  for  a  considerable  time  of  laxatives.  In  early  cases  we  should 
resort  first  to  salines,  particularly  Carlsbad  salts.  We  may  prescribe  artificial 
Carlsbad  salts,  dissolved  in  warm  water,  or  the  genuine  Carlsbad  water  to  be 
drunk  at  all  times.  If  the  patient's  circumstances  permit  we  may  even  recom- 
mend in  suitable  cases  a  visit  to  Carlsbad.  Other  appropriate  health  resorts 
are  Marienbad,  Kissingen,  and  Neuenahr.  If  the  saline  remedies  are  ill-borne 
we  employ  vegetable  laxatives,  such  as  rhubarb  and  aloes.  In  case  there  is 
already  a  considerable  degree  of  ascites,  good  results  may  sometimes  be  ob- 
tained by  administering  drastic  purgatives,  among  which  gamboge  has  earned 
a  special  reputation.  Many  observers  have  seen  benefit  from  calomel,  giving 
three  times  a  day  3  gr.  (gm.  0.2)  for  a  period  of  two  to  three  days.  Calomel 
may  be  given  repeatedly  in  this  way  at  intervals  of  from  five  to  eight  days. 
Of  course,  caution  is  necessary  in  its  employment.  Probably  it  does  good  both 
as  a  laxative  and  also  as  a  diuretic.  Sasaki,  in  Japan,  has  seen  excellent  results 
in  hepatic  cirrhosis  from  the  administration  of  cream  of  tartar  in  considerable 
doses,  2  to  4  drachms  (gm.  10  to  15)  a  day,  associated  with  a  nourishing  diet, 
including  milk  and  scraped  raw  meat.  After  all,  however,  laxatives  should  not 
be  employed  if  they  disturb  the  digestive  apparatus. 

If  ascites  has  already  developed,  we  may  administer  diuretics  besides  the 
drastic  purgatives;  trial  may  be  made,  first  of  all,  with  diuretin,  theophyllin, 
caffein;  further,  with  acetate  of  potassium  or  sodium,  squills,  the  species 
diuretics  of  the  German  Pharmacopoeia,  dog-rose  tea,  bean  tea,  etc.  English 
authorities  recommend  the  balsam  and  the  resin  of  copaiba  as  particularly 
efficient  in  the  various  forms  of  ascites.  The  dose  is  about  15  minims  (gm.  1) 
a  day.  The  best  mode  of  administration  is  in  gelatin  capsules.  Pure  urea 
(2.5  to  4  drachms  [gm.  10  to  15]  daily,  dissolved  in  water)  has  also  been  rec- 
ommended. We  dare  not  place  too  much  hope  in  all  these  remedies.  If  the 
heart  is  feeble,  digitalis  may  cause  a  decided  increase  in  the  amount  of  urine, 


BILIARY   CIRRHOSIS   AND   HYPERTROPHIC   CIRRHOSIS   OF    LIVER    693 

and  it  is  also  worth  while  to  try  a  combination  of  digitalis  with  calomel  or 
with  other  diuretics. 

If  the  ascites  is  so  excessive  as  to  occasion  much  local  discomfort  and  to 
impede  respiration,  the  removal  of  the  fluid  by  paracentesis  may  afford  relief. 
The  details  of  this  proceeding  were  given  in  the  last  section.  Many  physicians 
recommend  tapping  as  early  as  possible,  before  it  is  absolutely  necessary.  The 
relief  is  said  to  be  more  lasting  in  that  case;  but  this  proposal  has  by  no  means 
met  with  universal  assent,  and,  as  a  rule,  the  physician  will  not  tap  until  the 
abdominal  tension,  the  dyspncea,  and  other  symptoms  occasioned  by  the  ascites 
render  it  necessary.  Unfortunately,  the  relief  is  only  temporary,  for  the  fluid 
collects  again  with  great  rapidity  after  tapping;  yet  it  is  sometimes  possible 
to  dslay  the  reaccumulation  for  a  considerable  time  by  compressing  the  ab- 
domen with  an  elastic  bandage,  and  by  using  the  above-mentioned  remedies 
(diuretics  and  digitalis)  directly  after  tapping. 

We  have  finally  to  consider  the  ingenious  suggestion  of  Talma  to  assist 
in  the  establishment  of  a  collateral  circulation  between  the  portal  tributaries 
and  the  veins  of  the  abdominal  wall,  by  suturing  the  omentum  and  the  spleen, 
also,  if  necessary,  to  the  anterior  abdominal  wall.  This  Talma-Drummond 
operation  has  already  been  frequently  carried  out  in  hepatic  cirrhosis  as  well 
as  in  other  diseases  of  the  liver  with  portal  obstruction  (syphilis  of  the  liver, 
portal  thrombosis,  etc.).  Sometimes  the  result  has  been  apparently  satis- 
factory, inasmuch  as  after  the  operation  the  ascites  did  not  return  imme- 
diately and  the  patients  felt  much  improved.  In  suitable  cases,  therefore, 
we  may  advise  an  operative  procedure  of  this  kind. 


CHAPTER    V 

BILIARY    CIRRHOSIS    AND    HYPERTROPHIC    CIRRHOSIS    OF    THE    LIVER 

•  There  are  two  forms  of  cirrhosis  which  differ  in  many  respects  from  the 
disease  just  described:  they  are  called  biliary  cirrhosis  and  hypertrophic 
cirrhosis  of  the  liver.  Charcot  and  Hanot  were  the  first  to  call  attention  to 
them.  Since  then  the  literature  of  the  subject  has  become  quite  extensive,  but 
all  doubts  and  differences  of  opinion  are  not  yet  settled. 

1.     SECONDARY    BILIARY    CIRRHOSIS    OF    THE    LIVER 

Whenever  there  is  retention  of  bile  in  the  liver  for  any  length  of  time,  no 
matter  what  causes  it,  certain  changes  result.  The  small  and  the  medium-sized 
bile  ducts  become  distended,  and  granules  of  pigment  are  deposited,  both  in 
the  interlobular  connective  tissue  and  within  the  acini  themselves.  Besides 
this,  however,  and  undoubtedly  because  of  the  noxious  influence  of  the  retained 
bile,  the  hepatic  cells  not  infrequently  undergo  destructive  changes.  In  ac- 
cordance with  the  general  rule,  connective  tissue  gradually  fills  the  gaps  thus 
left  in  the  parenchyma,  and,  more  than  this,  the  interstitial  hyperplasia  is  so 
great  as  to  increase  the  size  of  the  organ.  If,  therefore,  there  is  persistent  ob- 
struction of  the  common  duct  by  a  gallstone,  or  a  cicatricial  stenosis,  or  a 
tumor  pressing  from  without  upon  the  duct,  the  liver  will,  in  all  such  cases,  be 
44 


694  DISEASES   OF   THE   DIGESTIVE   ORGANS 

found  to  be  larger,  firmer,  and  richer  in  fibrous  tissue  than  normal — in  a  word, 
"  cirrhotic."  Hence  this  condition  does  not  represent  an  independent  disease, 
but  is  a  result  of  chronic  biliary  retention,  in  whatever  way  occasioned.  It  is 
appropriately  termed  "  secondary  biliary  cirrhosis."  That  retention  is  really 
the  cause  of  this  change  has  been  j>roved  by  experiments,  for  it  has  been  shown 
that  ligature  of  the  common  duct  in  animals  causes  well-marked  biliary  cir- 
rhosis. 

2.     PRIMARY  HYPERTROPHIC   OR  BILIARY  CIRRHOSIS 

The  secondary  cirrhosis  just  described  is  due  to  occlusion  of  the  large  bile 
ducts.  There  is  also  a  not  very  common  (at  least  in  Germany,  though  more 
frequent  in  Holland)  primary  form  of  biliary  cirrhosis,  usually  known  as 
hypertrophic  cirrhosis.  French  authors  have  given  it  the  name  of  "  cirrhose 
hypertrophique  satis  ascite  avec  ictere,"  out  of  regard  to  its  most  important 
clinical  symptom.  That  there  is  an  essential  difference  between  this  form 
and  the  ordinary  "  atrophic  "  cirrhosis  of  Laennec  is  manifested  by  tbe  clinical 
behavior  of  the  disease. 

The  specific  cause  of  hypertrophic  biliary  hepatic  cirrhosis  is  as  yet  entirely 
unknown.  We  can  merely  surmise  that  we  have  to  do  with  a  chronic  inflam- 
matory process,  excited  by  some  toxic  or  infectious  agent,  and  that  the  process 
probably  originates  in  the  small  bile  ducts  of  the  liver.  The  disease  occurs 
most  frequently  in  younger  individuals,  between  the  ages  of  twenty  and  thirty. 
Sometimes  this  disorder  attacks  hard  drinkers,  but  they  are  not  by  any  means 
its  only  victims.  While,  in  the  common  form  of  cirrhosis,  ascites  is  usually  the 
earliest  grave  symptom  of  disease,  in  hypertrophic  cirrhosis  a  slight  jaundice 
generally  appears  simultaneously  with  the  first  indefinite  symptoms  of  pressure 
in  the  region  of  the  liver,  languor,  and  anorexia.  This  jaundice  rapidly  in- 
creases, and  persists  throughout  the  illness.  It  is  worth  mentioning  that, 
despite  the  most  extreme  icterus  and  bile-colored  urine,  the  stools  in  biliary 
cirrhosis  are,  as  a  rule,  not  entirely  decolorized.  In  ordinary  cirrhosis  there 
may  be,  as  we  have  said,  hardly  any  jaundice,  or,  at  any  rate,  it  is  a  rather  late 
symptom,  and  even  then  it  is  seldom  extreme.  On  the  other  hand,  ascites,  as  a 
rule,  is  slight  or  absent  in  hypertrophic  cirrhosis.  It  is  true  that  there  have 
been  cases  with  great  ascitic  effusion,  but  it  never  comes  till  the  disease  is 
quite  far  advanced. 

On  physical  examination  the  liver  is  usually  found  to  be  considerably  en- 
larged, and  its  surface  is  smooth,  as  a  rule,  or  rarely  it  displays  some  low  eleva- 
tions, due,  perhaps,  to  variations  in  the  fullness  of  the  blood  vessels.  In  general 
there  is  said  to  be  this  important  difference  between  the  ordinary  (atrophic) 
and  the  hypertrophic  forms,  that  in  the  latter  the  newly  formed  connective 
tissue  evinces  little  tendency  to  contraction,  so  that  the  liver  remains  large, 
even  late  in  the  course  of  the  disease,  and  does  not  shrink.  This  is  certainly 
true  of  the  majority  of  cases,  so  that  after  an  illness  of  two  or  three  years  the 
liver  is  still  found  to  be  large  and  smooth ;  but  further  observations  are  neces- 
sary in  order  to  determine  whether  there  may  not  sometimes  be  contraction 
toward  the  end  of  the  disease. 

Along  with  the  chronic  jaundice  and  the  marked  enlargement  of  the  liver 
there  is  a  third  important  symptom — viz.,  chronic  splenic  tumor,  usually  of 


BILIARY   CIRRHOSIS   AND   HYPERTROPHIC   CIRRHOSIS   OF   LIVER    695 

considerable  size.  As  there  are  no  indication-  of  portal  obstruction,  we  must 
conclude  that  the  spleen  is  not  enlarged  from  passive  congestion,  as  is  usually 
the  case  in  ordinary  alcoholic  cirrhosis,  but  as  the  result  of  hyperplasia;  and 
post-mortem  examinations  confirm  this  conclusion.  The  origin  of  the  hyper- 
plasia is  not  clear.  In  one  case  we  found  not  only  splenic  tumor  but  a  distinct 
hyperplasia  of  many  mesenteric  and  peritoneal  lymph-glands;  which  suggests 
the  possibility  of  infectious  influences.  A  corroborative  fact  is  that  not  in- 
frequently the  entire  course  of  the  disease  will  be  marked  by  slight  elevations 
of  temperature.  Longer  fever  periods  with  intermittent  higher  elevations  of 
temperature  also  occasionally  occur.  The  other  symptoms  of  the  disease  are 
in  part  the  direct  result  of  the  jaundice,  such  as  the  slow  pulse,  the  itching, 
and  the  changes  in  the  urine ;  while  others,  such  as  languor  and  weakness,  are 
the  results  of  the  constitutional  disturbance.  The  dejections,  as  already  men- 
tioned, are  not  always  colorless  and  fatty,  as  in  case  of  obstruction  of  the  large 
bile  ducts.  Many  patients  have  a  noticeable  tendency  to  hemorrhage,  particu- 
larly to  frequent  epistaxis,  hemorrhage  from  the  gums  into  the  skin,  and  to 
hematemesis.  In  the  case  mentioned  above,  the  fatal  termination  was  due  to 
constantly  repeated  and  profuse  hemorrhages  from  the  stomach,  for  which  the 
autopsy  disclosed  no  anatomical  cause  in  the  stomach  or  intestine.  It  seemed 
as  if  the  hemorrhages  had  taken  place  by  diapedesis. 

The  entire  duration  of  the  disease  is  about  two  or  three  years;  but  it  may 
last  much  longer.  The  prognosis  is  almost  always  bad.  Occasionally  a  case 
will  exhibit  marked  temporary  improvement  or  an  apparent  arrest  of  the  dis- 
ease, so  that,  in  spite  of  the  size  of  the  liver,  the  patient  is  able  to  do  light 
work.  Death  comes,  when  there  are  none  of  the  above-mentioned  hemorrhages, 
as  a  result  of  gradual  exhaustion,  or  is  suddenly  ushered  in  by  coma,  convul- 
sions, and  other  grave  nervous  symptoms,  usually  ascribed  to  cholasmia  (vide 
infra) . 

That  a  chronic  hepatic  disease  of  so  peculiar  a  nature  should  be  marked  by 
peculiar  anatomical  changes  would  seem  certain,  even  from  clinical  observa- 
tion. In  general,  this  view  is  confirmed,  although  further  and  careful  inves- 
tigations are  much  needed.  Upon  microscopic  examination  there  is  always 
found  an  abundant  new  growth  of  a  tissue  containing  many  cellular  elements, 
surrounding  the  small  bile  ducts  of  the  liver.  In  other  particulars  the  histo- 
logical changes  are  very  similar  to  those  of  ordinary  hepatic  cirrhosis.  The 
new  growth  of  connective  tissue  is  found  in  the  interior  of  the  hepatic  lobules, 
but  this  can  scarcely  be  regarded  as  a  radical  difference.  Still,  one  gets  the 
impression  that  the  entire  pathological  process  of  hypertrophic  cirrhosis  orig- 
inates in  the  bile  ducts  and.  the  tissues  surrounding  them,  while  the  changes 
of  ordinary  alcoholic  hepatic  cirrhosis  start  from  the  branches  of  the  portal 
vein.  The  absence  of  contraction  in  the  new  tissue  of  hypertrophic  cirrhosis 
seems  to  be  consonant  with  the  fact  that  the  anatomical  changes  suggest  hyper- 
plasia rather  than  inflammation  (compare  the  changes  in  the  spleen  and  the 
lymph-glands). 

The  diagnosis  of  hypertrophic  cirrhosis  can  sometimes  be  made  with  con- 
siderable positiveness,  and  sometimes  can  merely  be  regarded  as  probable.  The 
gradual  development  and  persistence  of  jaundice  and  the  presence  of  an  en- 
larged liver  and  spleen,  but  usually  without  marked  ascites,  would  suggest  the 
disease  strongly,  especially  if  long-continued  observation  enabled  us  to  exclude 


696  DISEASES   OF   THE   DIGESTIVE   ORGANS 

carcinoma  and  other  diseases.  Sometimes,  however,  it  is  very  difficult  to  de- 
cide whether  the  biliary  cirrhosis  is  primary  or  secondary,  for  the  conditions 
giving  rise  to  secondary  biliary  cirrhosis  (occlusion  of  the  bile  ducts  from 
scars,  new  growths,  or  calculi)  may  be  obscure.  A  careful  investigation  into 
the  history  of  the  case  with  regard  to  biliary  colic  and  similar  symptoms  might 
be  decisive.  Other  factors  are  the  general  course  of  the  disease  and  the  pres- 
ence of  a  splenic  tumor,  unaccompanied  by  ascites.  An  enlarged  spleen  is 
scarcely  ever  seen  in  this  way  in  ordinary  chronic  jaundice  of  obstructive  origin. 

The  prognosis  of  biliary  cirrhosis  of  the  liver  is  most  unfavorable,  although 
the  duration  of  the  disease  may  in  some  cases  extend  over  a  period  of  many 
years. 

The  treatment  should  conform  to  the  principles  laid  down  in  the  chapters 
on  jaundice  and  ordinary  cirrhosis  of  the  liver.  Sacharjin  has  lately  recom- 
mended the  persistent  use  of  small  doses  of  calomel — 1  gr.  (gm.  0.06)  several 
times  a  day.    I  personally  have  never  seen  any  distinct  benefit  from  it. 


CHAPTER    VI 
ACUTE    YELLOW    ATROPHY    OF    THE    LIVER 

^Etiology. — Acute  fatty  degeneration  of  the  liver  occurs  both  as  a  primary 
disease  and  as  secondary  to  other  hepatic  disorders,  or  as  a  symptom  of  con- 
stitutional diseases.  Secondary  acute  fatty  degeneration  in  rare  instances 
accompanies  severe  acute  infectious  diseases,  such  as  typhoid  fever,  recurrent 
fever,  septicaemia,  and  puerperal  disease.  It  also  appears,  with  equal  rarity, 
in  the  course  of  cirrhosis  of  the  liver  or  of  persistent  biliary  retention,  and 
it  is  a  constant  phenomenon  in  acute  phosphorus  poisoning.  Indeed,  the 
effects  of  phosphorus  resemble  the  symptoms  of  primary  acute  yellow  atrophy 
in  many  ways  so  closely,  even  postmortem,  that  formerly  the  two  were  often 
confounded. 

Primary  acute  yellow  atrophy  of  the  liver  is  a  very  rare  but  extremely 
severe  disease  which  almost  invariably  leads  to  speedy  death.  There  is  gen- 
erally no  determinable  cause,  and  its  victims  are  struck  down  in  blooming 
health.  It  is  most  common  in  young  adult  life  between  the  fifteenth  and 
thirty -fifth  year.  Children  and  elderly  people  have  been  occasionally  attacked. 
Females  are  much  more  liable  to  the  disease  than  males,  and  pregnancy  in- 
creases the  predisposition  to  it. 

As  we  have  said,  we  cannot,  as  a  rule,  find  any  exciting  cause.  It  is  stated 
that  sometimes  the  onset  has  been  preceded  by  some  violent  emotional  excite- 
ment, or  excess  in  alcohol,  or  the  like;  but  how  important  these  factors  may 
be  is  not  at  all  clear. 

It  is  an  interesting  fact  that  sometimes  the  disease  becomes  rather  more 
frequent  than  usual,  and  endemic.  For  instance,  several  members  of  one 
family  may  be  attacked.  This  fact,  the  whole  course  of  the  disease,  and  the 
pathological  appearances,  seem  to  place  the  disease  in  the  category  of  acute 
infectious  diseases.  It  must  be  confessed  that  as  ygt  we  know  nothing  about 
the  intimate  nature  of  the  infection.  / 


ACUTE   YELLOW   ATROPHY   OF   THE   LIVER  697 

Pathology. — The  chief  change  found  postmortem  is  in  the  liver,  and  it  has 
determined  the  name  given  to  the  disease. 

The  liver  is  much  atrophied,  sometimes  being  only  one  half  or  one  third 
its  normal  size.  This  makes  its  capsule  often  seem  contracted  and  wrinkled. 
The  organ  is  usually  soft  and  flabby,  so  that  in  some  places  it  seems  as  if  the 
finger  could  be  pressed  into  it.  The  color  of  the  surface,  and  for  the  most 
part  of  the  cross-section  also,  is  yellow,  like  ochre  or  saffron;  but  the  cut  sur- 
face may  be  particolored,  having  red  and  yellow  spots  interspersed.  Hence 
the  names  "  red  atrophy  "  and  "  yellow  atrophy."  The  arrangement  and  rela- 
tive extent  of  these  patches  may  vary  exceedingly.  The  red  places  look  as  if 
they  had  collapsed,  and  seem  tougher  than  the  yellow.  They  correspond,  as 
we  shall  soon  see,  to  the  more  advanced  stages  of  the  affection,  while  the  yel- 
low spots  have  undergone  less  change.  The  lobules  are,  as  a  rule,  no  longer 
distinguishable  by  the  naked  eye.  Such  lobules  as  can  still  be  made  out 
seem  abnormally  small  and  have  a  gray  periphery. 

On  microscopic  examination,  we  find  that  the  essential  change  is  an  in- 
tense and  uniform  fatty  degeneration  of  the  hepatic  cells,  affecting  the  entire 
parenchyma.  Only  a  few  cells  still  retain  their  normal  condition.  The  others 
are  filled  with  large  and  small  fat  globules,  and  many  are  already  suffering 
evident  disintegration  and  absorption.  Where  the  degeneration  is  furthest 
advanced,  fat,  detritus,  and  pigment  alone  remain.  Inasmuch  as  the  lym- 
phatics readily  absorb  and  remove  the  fatty  and  albuminoid  granules,  there  is 
finally  little  left  except  blood  vessels  and  connective  tissue.  The  blood  vessels 
are  frequently  quite  congested,  and  thus  occasion  that  red  color  which  the 
naked  eye  detects  in  the  more  advanced,  broken-down  portions.  Frerichs 
made  an  interesting  discovery,  which  deserves  mention,  of  the  existence  of 
leucin  and  tyrosin  crystals  both  in  the  parenchyma  and  in  the  blood  vessels. 
Bilirubin  crystals  also  are  sometimes  found  in  the  detritus,  and  more  rarely 
in  the  interior  of  the  hepatic  cells. 

ISTot  only  the  liver,. but  many  other  organs  present  fatty  degeneration:  the 
heart,  in  particular,  the  kidneys,  and  rarely  the  muscles;  but  the  process  is 
always  most  intense  in  the  liver.  The  skin  (vide  infra)  and  most  of  the  vis- 
cera are  evidently  tinged  with  jaundice. 

Acute  splenic  tumor  is  invariably  present.  This  suggests  that  the  disease 
may  be  infectious.  That  the  disease  is  a  constitutional  one  is  also  to  be  in- 
ferred from  the  numerous  ecchymoses  in  the  skin  and  the  interior  of  the  body, 
especially  in  the  mucous  membrane  of  the  stomach  and  intestines,  in  the 
serous  membranes,  in  the  pelvis  of  the  kidneys  and  the  kidneys  themselves, 
and  more  rarely  in  the  brain  and  heart.  This,  again,  is  like  the  grave  septic 
diseases.  The  blood  itself  is  dark,  with  few  clots.  Leucin  and  tyrosin  have 
repeatedly  been  detected  in  it.  The  peritoneum  and  other  serous  cavities 
sometimes  contain  a  considerable  amount  of  serum. 

Clinical  History. — The  disease  is  usually  divided  into  two  stages,  the  first 
of  which  corresponds  to  the  milder  prodromal  symptoms,  the  second  to  those 
severe  symptoms  which  are  alone  characteristic.  In  many  instances,  however, 
the  first  period  is  wanting,  or  is  so  brief  that  the  patient  is  plunged  almost 
without  warning  into  the  gravest  condition. 

The  prodromata  in  most  cases  consist  of  constitutional  disturbances  and 
mild  gastrointestinal  symptoms.     The  patient  is  languid,  without  appetite, 


698  DISEASES   OF   THE   DIGESTIVE   ORGANS 

and  disinclined  to  exertion.  There  are  headache,  nausea,  vomiting,  slight 
pains  in  the  gastrohepatic  region,  and  sometimes  moderate  fever.  In  a  few 
days  jaundice  usually  appears.  This  is  almost  invariably  taken  for  an 
ordinary  catarrhal  attack. 

After  some  days,  or  it  may  be  weeks,  the  second  stage  begins.  The  chief 
characteristic  of  this  is  the  occurrence  of  grave  nervous  symptoms.  First 
there  is  violent  headache,  with  sleeplessness  and  marked  restlessness.  The  in- 
tellect is  usually  somewhat  dulled  even  now,  and  articulation  is  slow  and 
clumsy.  The  mental  confusion  usually  advances  very  rapidly  to  a  noisy  and 
violent  delirium.  The  excitement  becomes  at  times  maniacal.  The  patient  is 
very  restless,  and  he  can  hardly  be  kept  in  bed.  Often  there  are  convulsive 
twitchings  of  individual  muscles,  and  there  may  be  typical  epileptiform  at- 
tacks, but  this  is  not  common.  After  one  or  two  days,  or  rarely  longer,  the 
excitement  abates,  and  is  followed  by  sopor,  which  soon  passes  into  deep  coma. 
At  death  the  patient  is  usually  perfectly  unconscious.  It  is  exceptional  for 
the  excited  stage  to  be  wanting;  in  such  cases  the  first  nervous  symptom  is 
sopor. 

The  cause  of  the  nervous  symptoms  has  not  been  explained  in  a  way  to 
silence  discussion.  The  same  theories  which  have  been  set  up  to  account  for 
the  grave  form  of  jaundice  in  general  (see  Appendix  to  this  chapter)  have 
also  been  employed  to  elucidate  the  nervous  phenomena  of  acute  yellow 
atrophy.  It  might  also  be  that  the  primary  specific  processes  of  infection  or 
intoxication  are  factors. 

The  jaundice,  which  is  present  even  in  the  first  stage,  afterwards  usually 
deepens.  The  urine  contains  bile  pigment,  and  many  investigators  have  also 
found  bile  acids  in  it.  If  these  latter  are  present,  it  suggests  that  the  jaundice 
is  not  (as  was  formerly  believed)  hematogenous — that  is,  the  result  of  a 
destruction  of  red  blood  corpuscles  and  the  transformation  of  their  pig- 
ment into  biliary  coloring  matter — but  is  due  rather  to  a  retention  of 
bile.  Just  how  this  retention  arises  we  do  not  yet  know  definitely.  The 
obstruction  cannot  be  in  the  large  bile  ducts,  for  the  gall  bladder  is  usu- 
ally found  empty.  Hence  the  cause  of  the  retention  of  bile  and  of  the 
jaundice  is  probably  a  derangement  of  the  smaller  biliary  passages  within 
the  liver.  We  should  add  that  in  a  few  rare  cases  there  has  been  little  or  no 
jaundice. 

On  physical  examination  of  the  liver  during  the  last  stage  of  the  disease 
there  is  usually  a  striking  diminution  of  hepatic  dullness,  corresponding  to 
the  atrophy  of  the  organ.  Generally  the  first  change  to  be  detected  is  a  con- 
traction of  the  left  lobe,  as  shown  by  the  development  of  tympanitic  reso- 
nance in  the  epigastrium.  At  the  commencement  of  the  illness  the  hepatic 
dullness  is  normal  or  slightly  increased  in  area.  If  the  disease  proves  very 
rapidly  fatal  the  organ  may  never  become  very  small.  In  most  cases,  though 
by  no  means  in  all,  there  are  pain  and  tenderness  in  the  hepatic  region,  but 
these  are  seldom  so  great  as  in  phosphorous  poisoning. 

The  enlargement  of  the  spleen  has  been  already  mentioned  as  an  almost 
constant  symptom  of  the  disease.  Even  during  life  some  increase  of  the  area 
of  splenic  dullness  can  usually  be  made  out,  and  sometimes  the  spleen  can  be 
felt  under  the  edge  of  the  ribs. 

The  occurrence  of  the  hemorrhages,  which  have  already  been  referred  to 


ACUTE   YELLOW   ATROPHY   OF   THE    LIVER 


G99 


under  the  pathological  lesions,  can  often  be  demonstrated  during  life.  The 
cutaneous  ecchymoses  can,  of  course,  be  seen,  and  the  hemorrhages  in  the 
mucous  membranes  may  give  rise  to  hematemesis,  bloody  stools,  bleeding 
from  the  female  genitals,  or  epistaxis.  The  hemorrhages  are  due  probably 
to  the  impaired  nutrition  and  diminished  resisting  power  of  the  vascular  walls 
occasioned  by  the  grave  constitutional  disturbance. 

The  condition  of  the  urine  in  acute  yellow  atrophy  is  very  interesting. 
The  amount  is  either  normal  or  slightly  diminished,  and  the  specific  gravity 
is  somewhat  increased.  Often  there  is  a  trace  of  albumen.  We  have  already 
mentioned  the  presence  of  bile  pigment.  The  point  of  chief  interest,  however, 
is  one  that  Frerichs  discovered  and  various  others  have  since  confirmed — 
namely,  the  great  diminution  of  urea  and  the  appearance  in  its  place  of  other 
substances,  which  are  likewise  the  products  of  the  decomposition  of  albu- 
minoid matter,  and  represent,  in  all  probability,  the  first  steps  in  the  forma- 
tion of  urea.  This  explains,  above  all,  the  increased  amount  of  ammonia  in 
the  urine,  and  the  presence  of  leucin  and  tyrosin 
in  the  same.  The  characteristic  crystals  of  the 
latter  can  sometimes  be  detected  by  the  microscope 
in  the  urinary  sediment  (see  Fig.  90).  The  crys- 
tals may  also  sometimes  be  obtained  by  allowing 
a  drop  of  the  fresh  urine  to  evaporate  slowly  upon 
an  object  glass.  The  proper  way,  however,  to 
demonstrate  these  crystals  is  to  precipitate  the 
urine  with  basic  acetate  of  lead,  to  remove  the 
lead  from  the  filtrate  by  means  of  sulphureted 
hydrogen,  and  then  to  evaporate  the  filtrate 
thus  obtained  to  the  point  of  crystallization. 
There  are  some  other  abnormal  constituents 
to  be  found  in  the  urine  besides  leucin  and  tyrosin,  but  what  their  sig- 
nificance is  we  do  not  know.  Among  these  are  sarcolactic  acid,  oxymandelic 
(paraoxyphenjdglycolic)  acid,  peptonoid  substances,  and  large  amounts  of 
kreatin. 

It  at  once  suggests  itself  that  this  disappearance  of  urea  and  appearance 
of  ammonia,  leucin,  and  tyrosin,  which  are  regarded  as  preparatory  stages  in 
the  formation  of  urea,  gives  valuable  support  to  Meissner's  and  Von  Schroder's 
idea  that  this  substance  is  manufactured  in  the  liver. 

As  to  the  other  organs  little  need  he  said.  Vomiting  is  very  frequent  in  the 
second  stage,  as  well  as  in  the  first.  It  usually  ushers  in  the  severe  cerebral 
symptoms.  The  stools  are,  as  a  rule,  clay-colored,  as  is  usual  in  jaundice.  There 
is  generally  constipation.  The  pulse  is  rapid,  often  reaching  140  to  160  beats 
per  minute,  and  is  also  small  and  compressible.  It  is  this  acceleration  of  the 
pulse,  contrasting  with  its  usual  slowness  during  the  first  stage,  which,  along 
with  the  vomiting,  announces  the  onset  of  dangerous  symptoms.  The  pulmo- 
nary signs  are  seldom  marked,  although  there  may  be  bronchitis  or  a  pneumonia 
due  to  the  inhalation  of  foreign  substances.  During  the  coma  which  precedes 
death  respiration  is  usually  hurried,  and  often  deep  and  noisy.  Sometimes  it  is 
irregular. 

The  temperature  is  at  first  approximately  normal  or  slightly  elevated. 
Toward  the  fatal  termination  there  may  be  a  subnormal  temperature  or  the 


Fig.  90. — a.  Leucin  crystals. 
b.  Tyrosin  crystals. 


700  DISEASES   OF   THE   DIGESTIVE   ORGANS 

temperature  rises  before  death,  and  even  sometimes  grows  higher  after  death, 
reaching  107.5°  F.  (42°  C.)  or  more. 

In  case  the  disease  attacks  a  pregnant  woman,  abortion  or  premature  deliv- 
ery is  almost  certain  to  occur. 

The  entire  duration  of  the  disease  depends  mainly  upon  the  length  of  the 
first  stage.  This  may  be  wholly  absent,  or  may  be  brief,  or  may  occupy  several 
weeks.  The  duration  of  the  second  stage,  reckoning  from  the  occurrence  of 
grave  cerebral  symptoms,  is  generally  only  a  few  days  (two  to  four),  rarely  a 
week.  The  termination  is  almost  invariably  fatal.  In  a  few  cases  recovery  has 
been  observed. 

Diagnosis. — The  diagnosis  cannot  be  made  till  the  second  stage.  The 
symptoms  of  the  first  stage  are  indistinguishable  from  those  of  simple  catarrhal 
jaundice.  With  the  development  of  the  grave  symptoms  all  doubt  usually  van- 
ishes. The  general  course  of  the  disease,  the  deep  jaundice,  the  cerebral  dis- 
turbances, the  cutaneous  ecchymoses,  and  the  character  of  the  urine,  form  a 
clinical  picture  resembling  no  other  disease.  The  only  cases  where  there  can 
be  any  uncertainty  about  the  diagnosis  are  the  exceptional  ones  in  which  there 
is  no  jaundice.  It  is  of  practical  importance  to  distinguish  this  disease  from 
acute  phosphorous  poisoning  (q.v.).  The  differential  diagnosis  is  to  be  made 
from  the  history  of  the  case  and  from  the  following  factors : 

ACUTE   YELLOW   ATROPHY   OF    THE 

LIVER  PHOSPHOROUS   POISONING 

1.  Prodromes  are  usually  present,  1.  Prodromes  are  almost  always 
but  may  be  absent.  present. 

2.  Jaundice  develops  early,  some-  2.  Jaundice  does  not  appear  until 
times  becomes  marked.  rather  late,  and  it  may  be  slight  to 

the  end. 

3.  Liver  seldom  enlarged,  becomes  3.  Liver  much  enlarged  until 
atrophic  from  the  start;  pain  in  he-      death,  and  very  painful. 

patic  region  not  the  rule. 

4.  Maniacal    delirium    very    fre-  4.  Seldom  marked  delirium, 
quent. 

5.  Not  infrequently  fever,  some-  5.  Not  infrequently  fever  is  ab- 
times  high  fever.  sent  throughout. 

6.  Leucin  and  tyrosin  often  found  6.  Leucin  and  tyrosin  found  in 
in  the  urine.  urine  exceptionally. 

7.  Spleen  often  enlarged.  7.  Usually  no  enlargement  of  the 

spleen. 

Treatment. — From  what  has  been  said,  it  may  be  gathered  that  the  treat- 
ment of  acute  yellow  atrophy  of  the  liver  is  almost  hopeless.  Usually  laxatives 
are  employed,  particularly  calomel.  The  nervous  symptoms  are  combated  by 
an  ice  cap  and  baths  and  narcotics;  the  vomiting,  by  opium  and  bits  of  ice; 
and  the  cardiac  weakness,  by  stimulants. 


ACUTE   YELLOW   ATROPHY   OF   THE   LIVER  701 

APPENDIX 
PERNICIOUS   JAUNDICE.     CHOUEMIA   AND   ACHOLIA 

Reference  has  been  repeatedly  made  in  the  preceding  chapters  to  the  possi- 
bility of  the  sudden  supervention  of  grave  nervous  derangements  in  the  course 
of  various  hepatic  diseases.  These  nervous  symptoms  resemble  one  another  so 
much  in  the  different  instances  of  their  occurrence  that  we  are  forced  to  believe 
them  always  due  to  the  same  cause. 

These  symptoms  are  relatively  most  frequent  when  there  is  chronic  biliary 
retention.  Whether  this  retention  be  the  result,  for  example,  of  obstruction  of 
the  common  or  the  hepatic  duct,  or  of  stenosis  of  the  biliary  passages  from  a 
carcinoma  involving  the  opening  of  the  common  duct  into  the  duodenum  or 
that  duct  itself,  the  patient  may  quite  suddenly  fall  into  a  condition  which  in 
many  respects  corresponds  to  the  second  stage  of  acute  yellow  atrophy  just 
described.  Grave  cerebral  disturbances  declare  themselves,  with  delirium, 
convulsions,  and  coma.  There  are  hemorrhages  into  the  skin  and  into  the 
mucous  membranes,  and  in  a  few  clays  the  patient  dies.  Usually  the  end  is 
attended  with  high  fever.  We  have  ourselves  seen  a  temperature  of  107.4°  F. 
(41.9°  C.)  in  a  case  of  cancer  at  the  duodenal  extremity  of  the  common  duct. 
It  is  this  group  of  symptoms  which  is  usually  termed  pernicious  jaundice;  but 
almost  precisely  similar  phenomena  may  suddenly  appear  in  hepatic  cirrhosis, 
when  there  is  no  great  degree  of  jaundice,  if  any. 

Exactly  what  produces  these  grave  results  in  acute  yellow  atrophy  and  the 
other  disorders  just  enumerated,  we  are  not  quite  certain.  Three  theories 
have  been  propounded  in  explanation.  The  first  theory,  the  latest  champion  of 
which  is  Leyden,  attributes  pernicious  jaundice  to  cholsemia — that  is,  to  the 
accumulation  in  the  blood  of  the  constituents  of  bile,  and  in  particular  of  the 
biliary  acids,  as  a  result  of  absorption.  This  accumulation,  it  is  said,  is  pro- 
moted by  the  paralyzing  effect  of  the  jaundice  upon  the  activity  of  the  kidneys. 
Opposed  to  this  theory  is  the  fact  that  these  same  symptoms  may  occur  when 
there  is  no  marked  hepatogenous  jaundice.  Furthermore,  it  is  doubtful  if  the 
constituents  of  the  bile,  especially  the  bile  acids,  can  accumulate  in  such  quan- 
tity in  the  blood  that  they  can  produce  toxic  effects. 

Bouchard  and  other  French  physicians  ascribe  to  the  liver  the  function  of 
rendering  harmless  the  products  of  the  decay  of  albuminous  matters  developing 
in  the  intestine,  which  may  be  absorbed  and  enter  the  circulation.  Destruction 
of  the  hepatic  cells  would  consequently  lead  to  autointoxication  with  these  intes- 
tinal ptomains.    In  Germany  this  doctrine  has  gained  few  adherents. 

The  view  which  we  are  most  inclined  to  accept  was  first  brought  forward  by 
Frerichs.  He  has  given  to  the  group  of  symptoms  under  discussion  the  name  of 
acholia.  These  symptoms  he  ascribes  to  the  pernicious  influence  of  those  sub- 
stances which  under  normal  conditions  are  manufactured  by  the  liver  into  bile, 
but  which  in  such  cases  accumulate  in  the  blood  and  the  tissues.  As  Frerichs 
himself  has  said,  and  we  believe  very  justly,  this  view  should  be  extended  to 
include  all  other  metabolic  functions  of  the  liver  (urea  production  from  am- 
monia and  carbon  dioxid,  formation  of  carbohydrates  from  albumen,  conver- 
sion of  glycogen  into  sugar,  etc.).     There  is  no  doubt  that  the  processes  of 


702  DISEASES   OF   THE   DIGESTIVE   ORGANS 

metamorphosis  are  very  active  in  the  liver.  That  these  should  be  incomplete 
when  there  is  a  severe  anatomical  lesion  of  the  liver,  or  when  there  is  persistent 
biliary,  obstruction,  is  very  likely,  and  this  limitation  of  activity  might  occasion 
an  accumulation  of  all  sorts  of  material  in  the  blood.  We  may,  therefore,  regard 
acholia,  using  the  word  as  Frerichs  does,  as  entirely  analogous  to  uraemia,  which 
latter  appears  not  only  in  diseases  of  the  kidney  but  also  when  the  ureters  are 
obstructed.  In  this  sense  the  name  cholaeinia  would  be  preferable  to  the  term 
acholia,  to  represent  a  condition  analogous  to  uraemia — taking  the  word  cholas- 
mia  to  mean  the  intoxication  of  the  blood  with  all  sorts  of  substances  due  to 
the  imperfect  metamorphosis  going  on  in  the  liver  (hepatic  autointoxication), 
and  not,  as  Leyden  formerly  held,  the  saturation  of  the  blood  with  the  com- 
pletely formed  components  of  the  bile. 

The  termination  of  cholasmia  is  almost  always  unfavorable.  Only  in  excep- 
tional cases  have  the  symptoms  disappeared  after  the  occurrence  of  a  profuse 
diuresis  or  marked  catharsis.  This  suggests  the  indicated  therapy — viz.,  cathar- 
sis, diuresis,  hypodermoclysis,  etc.  At  the  post-mortem  examination  of  cho- 
laemic  patients  there  is  usually  found  marked  fatty  degeneration  of  the  hepatic 
parenchyma  as  the  anatomical  expression  of  its  suspended  function. 


CHAPTEE    VII 

ICTERUS    NEONATORUM 

(Jaundice  of  the  Newborn) 

Frequently  the  normal  red  color  of  the  skin  in  children  changes  on  the 
second,  third,  or  fourth  day  after  birth  to  a  distinctly  yellow,  jaundiced  hue. 
The  yellow  tinge  is  deeper  on  the  face  and  trunk  than  on  the  extremities.  There 
are  no  special  digestive  or  constitutional  disturbances.  Still,  it  may  be  taken 
for  the  rule  that  weaklings  and  premature  infants  more  often  present  this  jaun- 
dice than  do  vigorous  babes.  The  abnormal  hue  is  almost  certain  to  vanish  in 
&  week  or  two,  and  leave  no  sequela?.  The  termination  is  unfavorable  in  those 
instances  alone  where  there  is  some  special  complication,  not  directly  connected 
with  the  jaundice  as  such. 

The  aetiology  is  a  disputed  matter.  A  large  number  of  theories  of  all  sorts 
have  been  set  up,  no  one  of  which  to  this  day  has  gained  universal  acceptance. 
Formerly  there  was  considerable  tendency  to  regard  the  jaundice  as  hematoge- 
nous— that  is,  as  due  to  the  transformation  of  the  pigment  of  broken-down 
blood  corpuscles  into  bile  pigment.  Points  which  seemed  to  support  this  view 
are  the  light  (not  jaundiced)  color  of  the  urine  and  the  yellow  color  of  the 
stools  (from  bile).  But  more  accurate  examination  has  shown  that  the  urine 
does  contain  biliary  pigment,  as  do  also  the  kidneys  of  such  infants  as  happen  to 
die  during  the  existence  of  the  jaundice ;  and  the  biliary  acids  have  been  clearly 
shown  to  be  present  in  the  serous  transudations.  It  is  therefore  assumed  at 
present  by  most  authors  that  icterus  neonatorum  is  hepatogenous ;  but  how  the 
biliary  retention  and  consequent  absorption  are  caused  we  do  not  know.  Per- 
haps the  bile  is  not  ejected  properly,  from  weakness,  or  the  ducts  may  be  nar- 
row, or  temporarily  plugged  by  desquamated  epithelium.    Birch-Hirschfeld  has 


SYPHILIS   OF   THE   LIVER  703 

called  attention  to  the  fact  that  after  birth  there  Le  a  tendency  to  considerable 

passive  congestion  of  the  liver,  with  resultant  ccdema  of  Glisson's  capsule  and 
pressure  upon  the  interlobular  bile  ducts.  Probably  more  importance,  however, 
attaches  to  a  circumstance  which  Hofmeier  has  noted,  that  in  the  first  days 
after  birth  many  red  corpuscles  are  disintegrated,  and  consequently  there  is  a 
comparatively  large  secretion  of  bile.  This  might  easily  lead  to  congestion  of 
the  smallest  bile  ducts  and  so  to  icterus ;  but  it  should  be  said  this  view  has  its 
opponents.  Quincke  has  an  entirely  different  explanation  of  icterus  neona- 
torum. He  goes  back  to  an  old  theory  enunciated  by  Peter  Frank.  According 
to  this,  the  jaundice  of  the  newborn  is  due  to  the  absorption  by  the  intestine 
of  a  large  amount  of  biliary  coloring  matter  from  the  meconium  in  the  large 
intestine.  Now,  if  the  ductus  venosus  remains  open  for  some  little  time  after 
birth,  as  it  often  does,  this  biliary  pigment  is  carried  not  to  the  liver,  but  by 
means  of  the  vena  cava  inferior  directly  into  the  systemic  circulation.  The 
meconium  is  rich  in  bile  pigment,  and  moreover  there  is  an  abundant  secretion 
of  biliary  coloring  matter  in  the  newborn,  and  in  them  bilirubin  is  not  changed 
into  urobilin  in  the  intestine,  and  finally  the  renal  secretion  of  the  newborn 
is  at  first  very  scanty.  Consequently,  the  absorption  of  the  bile  pigment  from 
the  intestine  results  in  jaundice. 

It  is  well  to  mention  in  conclusion  that  in  very  rare  instances  there  is  com- 
plete congenital  stenosis,  or  even  entire  absence,  of  the  larger  bile  ducts.  Then 
deep  jaundice  comes  on  soon  after  birth,  and  is  persistent.  The  children  become 
extremely  emaciated,  and,  after  a  few  weeks,  inevitably  perish. 


CHAPTEE    VIII 
SYPHILIS    OF    THE    LIVER 

iEtiology  and  Pathology. — Syphilitic  disease  of  the  liver  occurs  both  when 
the  syphilis  is  acquired  and  when  it  is  congenital.  Congenital  syphilitic  disease 
of  the  liver  may  be  diffuse  or  localized,  and  it  causes  a  cellular  infiltration  in 
either  case.  If  the  changes  are  extensive,  the  organ  is  hard  and  considerably 
enlarged ;  or,  if  the  newly  formed  connective  tissue  has  undergone  contraction, 
the  liver  is  smaller  than  normal,  and  its  surface  is  uneven.  In  some  cases  of 
hereditary  syphilis,  distinct  gummata  of  considerable  size  have  been  observed. 

In  acquired  syphilis,  hepatic  disease  is  one  of  the  so-called  tertiary  symp- 
toms, and  does  not  usually  develop,  at  least  to  any  great  extent,  until  several 
days  after  infection.  Indeed,  it  may  be  a  very  late  result.  It  may  take  the 
form  either  of  a  diffuse  syphilitic  hepatitis,  or  of  circumscribed  gummata  or 
syphilomata.  The  diffuse  hepatitis  does  not  present  essentially  different  ana- 
tomical appearances  from  those  of  ordinary  cirrhosis,  although  in  syphilis  the 
changes  are  seldom  so  uniformly  distributed  throughout  the  organ.  The  gum- 
mata are  the  most  characteristic,  and  the  most  important  clinically.  They 
may  form  separate  tumors  the  size  of  an  apple  or  even  larger.  The  convex 
surface  of  the  organ,  particularly  that  portion  near  the  suspensory  ligament, 
seems  to  be  a  favorite  location  for  the  new  growth.  The  same  is  true  of  the 
porta  hepatis,  where  Glisson's  capsule  enters  the  liver.     At  the  autopsy  the 


704  DISEASES  OF  THE  DIGESTIVE  ORGANS 

gummata  have  in  most  cases  already  begun  to  undergo  contraction.  If  so,  the 
liver  is  usually  smaller  than  normal,  and  traversed  in  various  directions  by 
deep  furrows,  which  divide  it  into  lobes.  These  furrows  are  due  to  firm  cica- 
tricial bands,  among  the  fibers  of  which  we  may  sometimes  find  necrotic  and 
cheesy  vestiges  of  the  gumma  proper.  Often  there  is  evident  syphilitic  endar- 
teritis in  the  smaller  and  sometimes  also  in  the  larger  branches  of  the  hepatic 
artery  and  portal  vein. 

Clinical  History. — Circumscribed  syphilitic  changes  in  the  liver  often  give 
rise  to  no  symptoms  whatever.  It  is  only  when  the  disease  comes  to  disturb  the 
portal  circulation  that  a  series  of  symptoms  results,  which,  for  evident  reasons,, 
may  be  analogous  in  all  essential  points  to  the  effects  of  ordinary  cirrhosis. 
Whenever  the  syphilitic  growths  contract  so  as  to  obliterate  a  large  number  of 
branches  of  the  portal  vein,  or  whenever  a  gumma  happens  to  be  so  situated  as 
to  compress  the  trunk  of  the  portal  vein  itself,  then  the  well-known  results  of 
portal  obstruction  are  inevitable,  the  chief  being  ascites  and  enlargement  of  the 
spleen.  The  disturbance  of  circulation  often  gives  rise  also  to  anorexia  and 
digestive  disorders.  We  once  observed  severe  gastric  and  intestinal  hemor- 
rhages without  gross  changes  in  the  corresponding  mucous  membranes — i.  e., 
hemorrhage  by  diapedesis.  Experience  shows  jaundice  to  be  rare  in  hepatic 
syphilis,  but  it  may  appear  when  the  lesions  involve  the  larger  bile  ducts  or  a 
considerable  number  of  the  smaller  biliary  passages.  It  deserves  mention  that 
hepatic  syphilis  quite  often  causes  severe  pain,  sometimes  over  the  entire  region 
of  the  liver  and  sometimes  in  just  one  spot.  Pain  is  by  no  means  felt  in  every 
case.    With  the  pain  there  may  be  great  tenderness  on  pressure. 

On  physical  examination  of  the  liver  the  results  vary  according  to  the  form 
and  the  stage  of  the  disorder.  Sometimes  the  larger  gummata  may  be  plainly 
felt  through  the  abdominal  walls,  usually  as  flattened  hemispheres.  Frequently, 
also,  we  can  feel  the  edge  of  the  enlarged  organ,  and  can  detect  that  the  edge  is- 
less  sharp  than  normal.  In  other  instances  the  separate  elevations  and  promi- 
nences can  be  made  out.  The  area  of  dullness  on  percussion  of  course  varies 
in  different  cases. 

The  course  of  the  disease  is  usually  tedious,  and  it  may  occupy  many  years. 
Probably,  too,  lesions  exist  in  many  cases  long  before  there  are  any  symptoms. 
Just  as  in  cirrhosis,  ascites  is  usually  the  first  thing  to  attract  the  patient's  at- 
tention. Improvement  and  temporary  arrest  of  the  disease  are  more  frequent 
than  in  ordinary  cirrhosis.  Still,  in  most  cases,  if  the  lesions  are  at  all  exten- 
sive, the  termination  is  unfavorable. 

Of  practical  importance  is  a  form  of  syphilis  of  the  liver,  which,  however, 
has  been  little  studied  pathologically,  and  the  course  of  which  is  more  acute  and 
is  associated  with  a  continuous  remittent  fever.  Persistent  febrile  conditions 
of  doubtful  origin  have  been  repeatedly  observed  in  which  an  enlargement  of 
the  liver  was  demonstrable,  and  in  which,  after  the  administration  of  iodid  of 
potassium,  recovery  ensued.  These  cases  are  explained  on  the  basis  of  a  gumma 
formation  in  the  liver.  We  once  observed  a  case  of  syphilis  of  the  liver  com- 
plicated by  tuberculosis  of  the  peritoneum — an  interesting  analogy  to  the  com- 
bination of  hepatic  cirrhosis  and  peritoneal  tuberculosis  (vide  supra,  page  670). 

Diagnosis. — The  diagnosis  is  not  always  easy.  Usually  the  objective 
changes  in  the  liver,  the  ascites,  and  the  enlarged  spleen,  indicate  hepatic  trou- 
ble, but  we  are  often  unable  to  determine  just  what  the  trouble  is.    Naturally, 


CANCER  OF  THE   LIVER  AND   BILE   DUCTS  705 

the  {Etiological  factors  are  of  great  importance.  In  a  toper  we  would  think- 
rather  of  the  common  form  of  cirrhosis.  If  there  is  a  syphilitic  history,  or  if 
we  find  scars  in  the  throat,  irregularities  in  the  surface  of  the  hones,  or  other 
signs  of  a  specific  dyscrasia,  we  would  naturally  ascribe  the  hepatic  disorder  to 
the  same  cause.  As  to  special  signs,  if  the  prominences  on  the  liver  are  rather 
large  in  contrast  to  the  smaller  granulations  of  common  cirrhosis,  syphilis  is 
somewhat  more  probable.  Severe  pain  in  the  right  hypochondrium  also  sug- 
gests syphilis  rather  than  cirrhosis.  It  should  also  be  considered  that  the 
course  of  hepatic  syphilis  is  usually  much  more  protracted  than  that  of  ordi- 
nary hepatic  cirrhosis. 

Treatment. — Specific  treatment  should  first  be  tried.  Mercury  and  potas- 
sium iodid  should  both  be  given,  but  probably  the  iodid  is  the  more  valuable  of 
the  two.  These  remedies  can  be  successful  only  when  the  gummata  are  still  in 
process  of  formation.  Our  therapeutic  efforts  produce  no  impression  upon  the 
cicatricial  bands,  the  contraction  of  which  is  the  main  cause  of  derangement. 
Indeed,  even  the  absorption  of  gummata  may  not  always  have  a  favorable  influ- 
ence upon  the  patient,  because  of  the  mechanical  disturbance  due  to  the  conse- 
quent cicatricial  change.  Hence,  in  general,  the  results  of  antisyphilitic  treat- 
ment are  not  very  satisfactory.  Only  in  the  above-mentioned  rare  cases  of 
tertiary  syphilitic  fever  with  gumma  formation  in  the  liver  has  the  iodid  of 
potassium  usually  any  very  good  effect. 

For  symptomatic  treatment,  the  reader  is  referred  to  the  chapter  on  Cir- 
rhosis of  the  Liver. 


CHAPTER    IX 
CANCER    OF    THE    LIVER   AND    BILE    DUCTS 

etiology  and  Pathology. — Primary  cancer  of  the  liver  is  very  rare,  but 
secondary  or  metastatic  cancer  of  this  organ  is  met  with  often.  The  chief  ex- 
planation of  this  latter  fact  is  the  slowness  of  the  blood  current  in  the  liver, 
which  favors  the  deposition  of  the  cancerous  germs  suspended  in  the  blood. 

Secondary  hepatic  cancer  may  be  a  sequel  to  primary  cancer  of  any  organ. 
It  is  most  often  seen,  however,  when  the  primary  growth  lies  within  the  portal 
system,  in  the  stomach,  intestines,  rectum,  oesophagus,  or  pancreas.  In  some 
instances  the  projection  of  the  primary  growth  into  the  lumen  of  a  branch  of 
the  portal  vein  has  been  directly  demonstrated,  thus  furnishing  an  obvious 
source  for  metastasis.  The  secondary  cancers  in  the  liver  may  be  very  numer- 
ous. They  are  found  both  within  the  organ  and  upon  its  surface.  If  superficial, 
they  form  flattened  protuberances,  which  are  often  dimpled  in  the  middle.  If 
the  new  growth  is  extensive,  the  liver  may  be  greatly  enlarged,  so  as  to  occupy 
a  great  part  of  the  abdominal  cavity. 

As  we  have  said,  primary  cancer  of  the  liver  is  very  unusual.  It  may  occur 
either  in  the  form  of  separate  large  nodules,  or  as  a  more  diffuse  cancerous 
infiltration  pervading  the  greater  part  of  the  organ.  Histologically  consid- 
ered, the  primary  growths  are  of  cylindrical-cell  carcinoma,  apparently  orig- 
inating from  the  epithelium  of  the  minute  bile  ducts,  but  also,  according  to 
some  authors,  sometimes  starting  from  the  cells  of  the  parenchyma. 


706  DISEASES   OF   THE   DIGESTIVE   ORGANS 

Primary  cancer  of  the  larger  bile  ducts  is  of  more  frequent  occurrence  than 
genuine  primary  hepatic  cancer,  and  therefore  it  is  of  more  importance  clin- 
ically. The  gall  bladder  may  also  be  the  seat  of  primary  carcinoma.  From 
these  sources  may  proceed  abundant  metastatic  growths  in  the  liver  itself. 

As  to  the  aetiology  of  hepatic  cancer  we  can  be  brief.  The  disease  is  most 
frequent  in  advanced  life,  from  forty  to  sixty,  following  in  this  the  general 
rule  for  cancer.  Of  special  exciting  causes,  there  is  only  one  to  be  mentioned 
— that  is,  biliary  calculi.  As  we  have  already  remarked,  the  formation  of 
cancer  subsequent  to  cholelithiasis  has  been  observed  so  many  times  that  mere 
coincidence  is  out  of  the  question. 

Clinical  History.  Diagnosis. — Many  small  nodules  of  cancer,  as  well  as 
large  masses  which  are  favorably  situated,  may  exist  in  the  liver  without  ex- 
citing any  symptoms.  If  there  is  an  undoubted  primary  cancer  in  another 
organ,  such  as  the  stomach,  we  must  alwa^ys  remember  the  possibility  of 
metastatic  growths  in  the  liver,  but  they  cannot  be  proved  to  exist  unless  they 
alter  appreciably  the  size  or  shape  of  the  organ.  Sometimes  their  existence 
may  be  inferred  when  we  observe  either  ascites  and  enlargement  of  the  spleen 
from  pressure  on  the  portal  vein,  or  jaundice  from  pressure  on  the  bile  ducts. 

On  palpation  we  are  often  able  to  make  out  plainly  one  or  more  tumors  in 
hepatic  cancer.  These  tumors  are  in  the  region  of  the  liver,  and  they  are  di- 
rectly connected  with  it,  as  we  can  prove  by  marking  out  its  limits  by  percus- 
sion and  palpation.  Another  characteristic  sign  is  that  almost  all  hepatic 
tumors  can  be  felt  to  move  with  respiration,  on  account  of  the  inspiratory 
depression  of  the  diaphragm  pushing  down  the  liver  and  all  that  is  joined  to  it. 
Percussion  over  a  hepatic  tumor  almost  invariably  gives  flatness,  in  contrast 
to  the  muffled  tympanitic  resonance  of  many  gastric  tumors. 

The  most  characteristic  condition  is  not  a  very  rare  one ;  in  it  the  liver  is 
the  seat  of  a  very  large  number  of  cancerous  nodules.  In  such  cases  the  organ 
is  usually  much  enlarged.  Often  we  can  detect  by  mere  inspection  a  great, 
irregular  prominence  in  the  hepatic  region,  pressing,  forward  the  flabby, 
atrophied  walls  of  the  abdomen,  reaching  down  to  the  level  of  the  umbilicus, 
or  even  lower,  and  moving  with  respiration.  On  palpation  we  can  feel  most 
of  the  anterior  surface  of  the  liver,  and  the  separate  cancerous  nodules  scat- 
tered over  it.  These  usually  are  as  large  as  walnuts,  or  even  apples,  and  they 
are  often  umbilicated.  The  lower  or  anterior  margin  of  the  liver  can  often 
be  made  out  plainly,  and  it  also  is  often  the  seat  of  nodules ;  and  we  can  some- 
times feel  nodules  on  the  lower  surface  of  the  organ. 

The  other  clinical  phenomenon  in  hepatic  cancer  have  several  causes:  (1) 
The  primary  disease,  such  as  cancer  of  the  stomach;  (2)  the  general  cancerous 
cachexia,  as  shown  by  languor,  emaciation,  and  possibly  a  slight  oedema  of  the 
ankles;  and  (3)  the  possible  compression  of  the  blood  vessels  or  bile  ducts. 
Compression  of  the  portal  vein  produces  a  moderate  or  even  a  large  ascitic 
effusion.  Even  in  these  instances  the  spleen  is  seldom  much  enlarged  as  a 
result  of  the  passive  congestion,  because  the  universal  emaciation  and  anaemia 
counteract  the  tendency  to  increase  in  size.  Jaundice  is  relatively  more  fre- 
quent in  cancer  of  the  liver  than  is  ascites.  It  is  caused  by  compression  either 
of  the  hepatic  duct  or  of  the  minuter  bile  ducts.  On  the  other  hand,  however, 
we  can  easily  see  that  hepatic  cancer  may  exist  without  producing  either  icterus 
or  ascites. 


ECHINOCOCCUS   OF   THE   LIVER  707 

The  differential  diagnosis  of  hepatic  cancer  from  cancer  in  other  organs  is 
sometimes  extremely  difficult.  This  is  particularly  true  of  pyloric  cancer,  and 
especially  so  when  the  pylorus  has  become  adherent  to  the  liver,  which  often 
is  the  case.  Cancers  of  the  omentum  and  of  the  colon  sometimes  simulate 
hepatic  cancer,  but  they  seldom  move  so  decidedly  in  respiration  as  do  hepatic 
tumors.  Given  a  new  growth  in  the  liver,  it  is  usually  comparatively  easy  to 
distinguish  between  carcinoma  and  other  tumors.  In  case  of  syphilitic  new 
growths,  we  have  to  consider  the  previous  history  and  other  signs  of  syphilis, 
also  the  eventual  contractions  and  diminution  in  size  of  the  liver,  the  usually 
longer  duration  of  the  disease,  and  the  general  condition  of  the  patient. 
Echinococci  have,  as  -a  rule,  a  much  more  regular  shape,  like  a  flattened  ball ; 
they  seldom  occasion  marked  cachexia,  and  also  have  a  much  longer  clinical 
history.  Large  abscesses  are  very  rare  in  our  climate,  and  they  can  usually  be 
recognized  by  special  objective  conditions.  Moreover,  they  cause  fever  (rigors), 
which  is  exceptional  in  carcinoma.  Other  primary  tumors  of  the  liver,  such  as 
sarcoma  and  adenoma,  are  very  rare,  and  therefore  of  no  great  clinical  im- 
portance. There  is,  however,  one  rare  but  important  tumor  of  the  liver  which 
we  must  mention — viz.,  melanotic  sarcoma,  which  may  appear  as  a  secondary 
growth  in  the  liver.  It  may  be  of  enormous  extent,  either  diffuse  or  nodular, 
and  secondary  to  melanotic  sarcoma  of  the  choroid  or  of  the  skin. 

When  we  have  decided  that  cancer  of  the  liver  is  present,  the  question 
arises :  Is  it  primary  or  secondary  ?  In  the  first  place,  primary  cancer  here  is 
so  rare  that  the  probabilities  are  in  favor  of  a  secondary  growth.  Not  infre- 
quently the  primary  tumor  cannot  be  detected  during  life.  Thus  a  small 
cancer  of  the  stomach,  or  a  flat  oesophageal  cancer,  or  carcinoma  of  the  pan- 
creas, are  all  easily  overlooked.  Cancer  in  the  rectum  may  be  detected  by 
digital  examination.  If  we  find  many  nodules  in  the  liver  and  no  primary 
trouble  elsewhere,  then  there  comes  the  possibility  that  there  is  primary  cancer 
in  the  gall  bladder  or  the  bile  ducts.  In  rare  instances  palpation  may  discover 
the  gall  bladder  in  a  state  of  cancerous  degeneration  close  underneath  the 
liver;  but  usually  the  viscus  will  be  small  and  contracted,  and  the  flat  and 
ulcerating  growth  is  not  noticeable  except  from  the  inside.  It  is  particularly 
in  those  cases  of  hepatic  cancer  in  which  there  is  at  an  early  period  great  and 
persistent  icterus,  without  evidence  of  carcinoma  in  any  other  organ,  that  we 
should  be  most  apt  to  think  of  primary  cancer  of  the  bile  ducts. 

The  duration  of  hepatic  cancer  is  usually  not  prolonged.  The  first  decided 
evidences  of  its  existence  no  sooner  present  themselves  than  marasmus  and 
cachexia  rapidly  develop.  The  fatal  end  comes  in  a  few  months,  or  at  latest 
within  a  year. 

The  prognosis  is  hopeless.  Treatment  can  avail  only  to  alleviate  somewhat 
the  patient's  sufferings. 

CHAPTEE   X 

ECHINOCOCCUS    OF    THE    LIVER 

Natural  History  and  Pathology. — Inasmuch  as  it  is  the  liver  which  suffers 
most  frequently  from  invasions  of  the  echinococcus,  we  will  mere  state  the 
main  general  points  relative  to  the  troubles  produced  by  this  parasite. 


708 


DISEASES   OF   THE   DIGESTIVE   ORGANS 


The  taenia  echinococcus  (see  Fig.  91)  is  a  small  tapeworm  about  4  mm. 
long,  and  composed  of  four  joints.  It  inhabits  the  intestinal  canal  of  the 
dog.  The  head  is  small  and  bears  a  beak  which  is  pro- 
vided with  some  thirty  to  forty  hooklets,  arranged  in 
two  rows.  Behind  the  circle  of  hooklets  are  four  suck- 
ers. The  last  joint  of  the  tsenia  is  by  far  the  largest, 
and  contains  some  five  hundred  eggs.  Man  is  infected 
by  ingestion  of  the  eggs.  The  great  frequency  of  the 
echinococcus  in  Iceland  is  explained  by  the  close  in- 
timacy of  the  Icelanders  with  their  clogs.  In  Ger- 
many the  echinococcus  is  most  frequent  in  Mecklen- 
burg and  Pomerania. 

If  a  human  being  has  become  infected,  the  embryo 
pierces  the  intestinal  wall,  and  is  carried  with  the  blood 
current  or  the  lymph  current  to  some  remote  organ. 
Most  of  the  eggs  no  doubt  are  destroyed  in  the  stomach, 
as  may  be  inferred  from  the  fact  that  multiple  echino- 
cocci  are  much  less  frequent  than  solitary  individuals. 
In  a  great  majority  of  cases  the  embryo  passes  through 
a  branch  of  the  portal  vein  into  the  liver  and  there  fas- 
tens itself;  but  the  echinococcus  may  be  developed  in 
other  organs — including  the  lungs  {vide  Vol.  I),  the 
bones,  the  brain,  the  kidneys,  and  the  heart.  A  hyda- 
tid cyst  develops  from  the  embryo,  and  is  filled  with  a 
nonalbuminous  fluid.  The  cyst  is  composed  of  an  ex- 
ternal cuticle  of  laminated  structure,  and  an  inner, 
parenchymatous  layer,  which  contains  muscular  fibers 
and  blood  vessels.  Surrounding  the  cyst,  as  it  lies  in 
the  infested  organ,  there  is  gradually  developed  a  thick 
capsule  of  connective  tissue. 
After  the  cyst  has  continued  its  growth  for  some  four  to  six  months,  being 
now  about  the  size  of  a  walnut,  there  are  generated  upon  the  inner  surface  of 
the  capsule,  from  the  parenchymatous  layer,  so-called  breeding  capsules,  con- 
taining numbers  of  echinococcus  heads,  or 
" scolices."  Each  scolex  has  four  suckers 
and  a  circlet  of  hooks.  It  can  draw  itself 
into  the  breeding  capsule  and  also  produce  a 
prominence  upon  the  outer  surface  of  the 
latter  (see  Figs.  92,  93,  and' 94).  The  num- 
ber of  new-formed  scolices  in  an  echinococ- 
cus is  very  great.  The  sac  grows  very  slowly 
up  to  about  the  size  of  a  fist,  or  even  larger ; 
its  wall  has  a  pale  yellow  color,  is  trans- 
parent, and  displays  an  extremely  char- 
acteristic laminated  structure.     The  firmly 

attached  breeding  capsules  are  visible  from  the  outside  through  the  walls  as 
minute  points. 

The  primary  cyst  often  gives  rise  to  secondary  "  daughter  vesicles."  and 
these  to  "  granddaughter  vesicles."     Some  of  these  are  formed  in  the  cuticle, 


Fig.  91. — (From  Heller.) 
Taenia  echinococcus,  en- 
larged. Above,  at  the 
right,  echinococcus,  of 
natural  size. 


Fig.  92.  Fig.  93. 

Figs.  92  and  93.  —  (From  Helleh.) 
Echinococcus  scolices,  drawn  in  and 
turned  outward. 


> 


ECHINOCOCCUS   OF  THE   LIVER  709 

others  from  the  breeding  capsules.  In  man  they  generally  grow  inward — 
that  is,  are  endogenous  (echinococcus  hydatidosus) — and  finally  become  de- 
tached. Hundreds  of  them  may  sometimes  be  found  free  in  the  liquid  con- 
tents of  the  cyst.  In  animals  the  daughter  vesicles  are  more  often  exogenous 
(echinococcus  veterinorum  seu  granulosus) .  A  peculiar  kind  of  echinococcus, 
which  was  formerly  regarded  as  a  kind  of  new  growth,  is 
that  called  by  Virchow  echinococcus  multilocularis.   This  M^ 

is  a  resistant  tumor  containing  much  connective  tissue, 
and  permeated  with  numerous  small  alveoli.     The  gelat- 
inous  contents    of   the    alveoli    consist    of    echinococcus       "^\  nJ 
vesicles.     The  growth  probably  originates  from  a  single          '  v)          J\   ^"" 
germ,   which  by   persistent   exogenous   proliferation    in- 
vades the  lymph  vessels   (perhaps  also  the  blood  vessels        J& 
and  the  bile  ducts).                                                                                _ 

The  growth  of  a  hydatid  cyst  is  very  slow,  and  it  may  hookkt.s. 

continue  for  years.     At  last,  however,  the  echinococcus 
dies.     The  cyst  then  undergoes  considerable  though  gradual  contraction,  and 
both  walls  and  contents  become  fatty  degenerated  and  calcified.     In  the  mor- 
tar-like detritus  it  is  usually  possible  to  find  some  characteristic  hooklets. 

Clinical  Symptoms. — As  long  as  the  cyst  in  the  liver  retains  moderate 
dimensions,  there  is  usually  no  discomfort.  Frequently  the  cysts  perish  and 
become  calcified  without  having  ever  attracted  attention,  and  are  found  post- 
mortem merely  by  accident. 

If  the  cyst  becomes  very  large,  it  causes  a  sensation  of  pressure  and  pain 
in  the  hepatic  region.  In  rare  instances  unusually  large  cysts,  if  situated  on 
the  convex  surface  of  the  liver,  may  crowd  up  the  diaphragm  so  as  to  compress 
the  lower  portions  of  the  lung  and  induce  dyspnoea.  In  such  cases  we  find  on 
the  anterior  or  posterior  wall  of  the  thorax  an  abnormal  protuberance,  with 
dullness  and  diminished  respiratory  murmur.  If  a  large  echinococcus  grows 
downward  into  the  abdominal  cavity  it  occasions  pressure,  tension,  and  pain 
in  the  abdomen.  Compression  of  the  portal  vein  may  lead  to  ascites,  and 
compression  of  the  bile  duct,  in  rare  cases,  to  jaundice.  The  tumor  can  usu- 
ally be  made  out  with  ease  by  inspection  and  palpation.  It  is  approximately 
hemispherical,  smooth,  not  tender,  and  feels  rather  firm  and  elastic.  There 
is  often  a  sense  of  fluctuation,  while  the  so-called  hydatid  thrill — to  be  elicited 
by  quick  pushes  with  the  flat  of  the  hand — is  recognized  distinctly  in  but  few 
cases. 

The  condition  may  be  complicated  (1)  by  rupture  of  the  echinococcus  sac 
into  neighboring  parts,  and  (2)  by  secondary  suppuration.  Both  occurrences 
may  be  apparently  spontaneous,  or  the  result  of  traumatic  influences. 

Of  the  possible  directions  in  which  rupture  may  take  place,  penetration  of 
the  pleural  cavity  should  be  particularly  mentioned.  It  usually  results  in  an 
acute  empyema.  Here  we  have  to  do  partly  with  secondary  infection  occa- 
sioned by  pyogenic  bacteria,  and  partly,  also,  as  it  seems,  with  the  influence  of 
toxic  substances  (toxalbumens),  which  are  present  in  the  echinococcus  fluid 
(vide  infra).  Penetration  into  the  lungs  with  rupture  of  the  echinococcus 
sac  leads  to  severe  pulmonary  symptoms.  The  patient  may  cough  up  constitu- 
ents of  the  bile  and  small  echinococcus  vesicles,  or  portions  of  the  same.  Per- 
foration into  the  abdominal  cavity  occasions  purulent  peritonitis.  If  viable 
45 


710  DISEASES   OF   THE   DIGESTIVE   ORGANS 

daughter  vesicles  are  set  free  in  the  abdominal  cavity,  they  may  settle  on  some 
fresh  spot  and  continue  to  grow.  As  extreme  exceptions  are  to  be  mentioned 
rupture  of  the  echinococcus  sac  into  the  pericardium,  the  bile  ducts,  the  in- 
testine, the  vena  cava,  and  the  pelvis  of  the  kidney. 

Suppuration  of  an  echinococcus  in  the  liver  (developing  occasionally  after 
injuries,  acute  infectious  diseases,  etc.)  leads  to  the  clinical  symptoms  of 
hepatic  abscess — increasing  tenderness  and  fluctuation  of  the  tumor,  fever, 
aggravation  of  the  constitutional  symptoms,  etc.  Perforation  of  tbe  abscess 
into  neighboring  structures  may  occur  in  the  same  way  as  above  mentioned. 
Spontaneous  recovery  is  possible,  but  infrequent.  In  general,  suppuration 
of  an  echinococcus  sac  is  a  dangerous  condition,  unless  'there  is  surgical  in- 
terference. 

We  must  devote  a  few  words  to  ecliinococcus  rnultil ocularis  of  the  liver. 
As  has  been  said,  the  tumor  in  this  case  is  large,  very  firm  and  hard,  and  with 
a  surface  which  is  either  smooth  or  rough.  Tenderness  on  pressure  is  ex- 
ceptional. On  the  other  hand,  there  is  a  feeling  of  painful  distention  in  the 
hepatic  region.  Comparatively  often  (H.  Vierordt)  there  is  jaundice,  which 
may  be  extreme.  In  other  cases  the  picture  rather  of  a  chronic  portal  ob- 
struction develops  (ascites,  splenic  enlargement,  etc.).  The  bodily  condition 
is  fairly  good  for  a  long  while,  but  later  gradually  increasing  weakness  de- 
velops. Secondary  suppuration  in  the  interior  of  the  tumor  also  leads  to  fever 
and  rapid  loss  of  strength.  The  disease  lasts  two  to  three  years,  sometimes, 
much  longer. 

Diagnosis. — The  diagnosis  of  echinococcus  of  the  liver  depends  chiefly 
upon  the  demonstration  of  a  very  slowly  developing  tumor  in  the  liver,  hemi- 
spherical, fluctuating,  and  painless,  with  no  marked  influence  at  first  upon 
the  general  health.  If  the  patient  comes  from  a  country  where  the  echino- 
coccus is  particularly  frequent,  of  course  this  renders  the  diagnosis  easier. 
Formerly  it  was  the  custom  to  aspirate  the  tumor  for  diagnostic  purposes. 
In  this  way  we  can,  in  many  cases,  obtain  from  the  interior  of  the  sac  a  light 
yellow  nonalbuminous  fluid,  which  often  contains  sugar  and  succinic  acid, 
and  in  it  sometimes,  but  of  course  not  invariably,  are  found  upon  microscopic 
examination  the  characteristic  hooklets,  or  little  pieces  of  the  laminated  mem- 
brane. Lately,  however,  physicians  have  become  much  more  cautious  about 
puncturing  echinococcus  cysts,  because  the  procedure  is  sometimes  followed 
by  symptoms  which  are  probably  due  to  the  poisonous  influence  of  the  escap- 
ing contents  of  the  cyst  (vide  supra).  Not  infrequently  after  puncture  there 
occurs  urticaria  or  severe  toxic  symptoms,  such  as  collapse,  vomiting,  dysp- 
noea, diarrhea,  chills,  and  epileptiform  attacks ;  and  these  may  even  prove 
quickly  fatal,  although  occurrences  of  this  sort  are  infrequent.  They  have 
brought  great  discredit  upon  the  practice  of  aspiration  for  diagnostic  pur- 
poses in  case  of  echinococcus. 

The  interesting  fact  that  an  eosinophilia  occurs  in  the  blood  of  patients 
with  echinococcus  disease,  as  in  infections  with  other  animal  parasites  (tasnia, 
etc.),  is  of  considerable  diagnostic  significance. 

The  diagnosis  of  the  multilocular  echinococcus  of  the  liver  is  always  very 
difficult.  The  large  hard  tumor  can  be  differentiated  from  carcinoma  of  the 
liver  by  the  longer  duration  of  the  illness  and  the  slighter  constitutional  in- 
volvement.    On  the  other  hand,  the  differential  diagnosis  from  certain  forms 


CIRCULATORY   DISTURBANCES   IN   THE   LIVER  711 

of  cirrhosis  and  syphilis  of  the  liver  is  for  a  long  time  often  impossible. 
Decisive  for  echinocoecus  in  some  cases  is  the  perforation  of  the  parasitic 
new  growth  through  the  diaphragm  into  the  lung.  This  results  in  persistent 
chest  symptoms — pain,  cough,  expectoration,  and  generally  the  discharge  of 
a  very  characteristic  peculiar,  bile-stained,  ochre-yellow  sputum. 

Treatment.— Inasmuch  as  internal  remedies,  such  as  iodin  and  mercury, 
are  absolutely  useless,  the  only  treatment  of  echinocoecus  is  by  surgical  means. 
In  case  the  echinocoecus  tumor  causes  little  if  any  discomfort,  the  patient  is 
usually  loath  to  consent  to  an  operation,  but  it  should  be  recommended  in  all 
cases,  for  it  protects  the  patient  from  the  possibility  of  later  dangerous  de- 
velopments, and  in  itself  is  no  grave  matter.  A  description  of  the  many 
methods  of  surgical  treatment  will  be  found  in  the  text-books  on  surgery.  In 
multilocular  echinocoecus  cysts,  surgical  treatment  is  impossible.  The  therapy 
must  therefore  be  purely  symptomatic  (puncture  for  the  ascites,  etc.). 


CHAPTEE    XI 
CIRCULATORY   DISTURBANCES    IN   THE    LIVER 

1.  Hepatic  Anaemia. — Hepatic  ansemia  is  seldom  extreme  except  in  cases 
of  profound  general  ansemia,  and  it  has  no  clinical  importance,  so  far  as  we 
are  aware. 

2.  Passive  Congestion. — Passive  congestion  of  the  liver  is  of  frequent  oc- 
currence and  is  of  importance.  It  may  arise  subsequent  to  any  disorder 
which  disturbs  the  systemic  circulation.  It  is  oftenest  seen  in  connection  with 
heart  disease,  particularly  mitral  disease.  It  also  follows  pulmonary  em- 
physema and  chronic  processes  which  result  in  contraction  of  the  lungs.  The 
liver  is  enlarged  and  engorged.  The  hepatic  veins  being  situated  in  the  center 
of  the  lobules,  this  central  portion  becomes  darkly  pigmented,  while  the 
periphery  of  the  lobules  seems  lighter  colored.  The  peripheral  cells  may  even 
appear  distinctly  yellow,  from  a  fatty  infiltration  which  is  not  infrequent. 
In  this  way  the  cut  surface  comes  to  present  that  variegated  appearance  which 
has  led  to  the  name  of  "  nutmeg  liver/'  If  the  venous  stasis  be  persistent, 
there  is  considerable  atrophy  of  the  hepatic  parenchyma,  involving  especially 
the  cells  near  the  center  of  each  lobule.  Thus  the  liver  is  somewhat  reduced 
in  size  in  spite  of  the  secondary  increase  of  connective  tissue,  and  its  surface 
may  become  slightly  granular.  This  is  the  "  atrophic  nutmeg  liver  "  or  "  con- 
tracted liver  due  to  passive  congestion." 

The  clinical  phenomena  are  chiefly  those  caused  by  the  hepatic  enlarge- 
ment. If  chronic  cardiac  disease,  emphysema,  or  some  analogous  trouble  has 
occasioned  congestion  of  the  liver,  the  area  of  hepatic  dullness  is  increased, 
and  frequently  we  can  feel  the  edge  or  even  a  portion  of  the  anterior  surface. 
In  well-developed  cases  the  liver  reaches  a  hand's-breadth  or  more  below  the 
ribs  on  the  right  side.  If  there  is  also  tricuspid  regurgitation  (q.v.),  the 
liver  is  usually  much  enlarged  and  can  be  felt  to  pulsate  distinctly  if  the  palm 
of  the  hand  is  laid  upon  it.  Not  infrequently  in  passive  congestion  of  the 
liver  there  is  jaundice,  which  may  be  slight  or  quite  well  marked.    This  is  per- 


712  DISEASES   OF   THE   DIGESTIVE   ORGANS 

haps  due  to  the  pressure  exerted  by  the  distended  blood  vessels  upon  the  small 
bile  ducts  in  the  liver,  and  perhaps  also  to  the  secretion  of  a  particularly 
viscid  bile  containing  less  water  than  normal,  and  tending  to  stagnate.  As 
we  have  already  mentioned,  the  peculiar  mixture  of  jaundice  and  cyanosis  in 
the  complexion  of  many  cardiac  patients,  is  very  characteristic.  The  sec- 
ondary cirrhosis  of  the  congested  liver  leads  to  ascites.  We  may  suspect  this 
condition  of  the  liver  in  all  cases  of  heart  disease  in  which  ascites  is  par- 
ticularly well  marked,  in  comparison  with  the  slight  cedema  in  other  portions 
of  the  body. 

Quite  often  the  congestion,  if  great,  produces  subjective  disturbances. 
There  is  a  feeling  of  pressure  and  weight  in  the  hepatic  region,  and  if  the  cap- 
sule of  the  organ  is  tightly  stretched  there  may  be  actual  pain. 

The  prognosis  and  treatment  depend,  of  course,  upon  the  primary  dis- 
order. 

3.  Active  Hypersemia. — About  active  hyperasmia  of  the  liver  we  have  little 
definite  information.  Formerly  there  was  a  great  deal  said  about  it,  as  one 
of  the  conditions  in  "  abdominal  plethora."  Active  hyperasmia  is  most  fre- 
quently assumed  to  exist  in  case  of  those  who  are  good  livers  and  of  sedentary 
habit.  In  such,  we  are  told,  the  temporary  physiological  hyperasmia  which 
attends  digestion  passes  on  into  a  permanent  congestion  of  the  liver.  Thereby 
the  organ  is  enlarged,  there  are  painful  sensations  in  the  right  hypochon- 
drium,  digestive  disturbances,  and  occasional  slight  jaundice.  The  abnormal 
condition  just  described  is  certainly  often  met  with  in  practice,  but  it  would 
seem  hardly  possible  to  draw  a  clear  dividing  line  between  active  hypersemia 
of  the  liver  and  other  disturbances  which  give  rise  to  similar  symptoms.  Such 
are  chronic  gastric  and  intestinal  catarrhs,  cardiac  hypertrophy  and  func- 
tional cardiac  derangement,  with  passive  congestion  of  the  liver,  fatty  liver, 
and  incipient  cirrhosis. 

A  prominent  role  in  the  production  of  active  hyperasmia  of  the  liver  is  also 
ascribed  to  the  ingestion  of  such  matters  as  are  said  to  "  irritate  "  the  liver, 
like  the  various  spices,  coffee,  and,  above  all,  alcohol. 

It  should  also  be  noted  that  the  liver  may  be  much  engorged  in  many 
acute  infectious  diseases,  particularly  in  pernicious  malarial  diseases  and  in 
typhus  or  typhoid  fever. 

It  is  also  maintained  that  the  hyperasmia  may  result  from  the  cessation  of 
hemorrhages  elsewhere,  such  as  the  catamenia  or  bleeding  from  hemorrhoids. 
The  facts  that  have  been  brought  forward  to  sustain  this  view  are  none  of 
them  conclusive.  We  will  mention  that  the  "menstrual  jaundice"  which 
occasionally  appears  when  the  menses  are  scanty  or  absent  has  been  referred 
to  a  vicarious  hyperasmia  of  the  liver. 

It  is,  of  course,  impossible  to  make  general  statements  about  the  course  and 
duration  of  active  hyperasmia  of  the  liver.  The  treatment  of  the  first  variety 
mentioned — namely,  that  arising  from  an  improper  mode  of  life — demands 
careful  regulation  of  the  diet,  exclusion  of  all  alcoholic  beverages,  abundant 
exercise  in  the  open  air,  such  as  horseback  riding,  and  laxatives.  We  may 
order  rhubarb,  aloes,  or  a  course  of  the  waters  at  Carlsbad,  Marienbad,  Kissin- 
gen,  or  Homburg. 


ATROPHY,    HYPERTROPHY,   AND   DEGENERATIONS   OF   LIVER    713 

CHAPTEE    XII 
ATROPHY,    HYPERTROPHY,    AND    DEGENERATIONS    OF    THE    LIVER 

1.  Simple  Atrophy  of  the  Liver. — Simple  atrophy  is  not  of  rare  occurrence, 
being  seen  in  senile  marasmus  and  in  malnutrition  from  almost  any  cause. 
The  degree  of  atrophy  varies.  The  borders  of  the  organ  are  much  wrinkled. 
The  lobules  seem  decidedly  smaller  than  normal,  and  even  the  individual  cells 
that  still  remain  are  atrophied  and  also  usually  deeply  pigmented. 

The  condition  does  not  of  itself  give  rise  to  any  special  symptoms.  The 
diminution  in  the  perhaps  demonstrable  area  of  hepatic  dullness  is  a  sign  too 
ambiguous  ever  to  justify  us  in  making  from  it  a  positive  diagnosis  of  hepatic 
atrophy.  Perhaps  there  is  some  value  in  the  alleged  lighter  color  of  the  stools, 
as  indicating  a  diminished  secretion  of  bile. 

2.  Hypertrophy  of  the  Liver. — Even  under  normal  circumstances  the  liver 
undergoes  quite  marked  alterations  in  size.  The  exact  point,  therefore,  where 
an  abnormal  hypertrophy  begins  cannot  be  set.  Sometimes  the  autopsy  re- 
veals an  unusually  large  liver,  of  which  there  had  been  no  indications  during 
life,  and  for  which  no  cause  can  be  made  out. 

There  are  certain  diseases  in  which  enlargement  of  the  liver  is  found  with 
comparative  frequency:  diabetes  mellitus,  chronic  malarial  poisoning,  leu- 
kaemia, and  sometimes  rachitis.  Topers  quite  often  have  enlarged  livers, 
which,  as  a  rule,  present  simple  hypertrophic  changes.  Occasionally  a  liver 
has  been  reported  as  showing  spots  of  localized  hyperplasia,  which  may  form 
flattened  prominences  upon  the  surface  of  the  organ. 

Hypertrophy  is  to  be  diagnosticated  only  when  palpation  and  percussion 
give  proof  of  an  enlargement,  and  yet  amyloid,  hypertrophic  cirrhosis,  and 
other  diseases  which  cause  an  increase  in  the  size  of  the  liver,  can  be  excluded. 
The  aetiology  of  the  case  should  also  be  considered. 

3.  Fatty  Liver. — This  name  is  applied  to  excessive,  diffuse,  fatty  infiltra- 
tion of  the  hepatic  cells.  The  size  of  the  organ  is  increased.  It  is  firm, 
anaemic,  and  of  a  uniform  yellow  color,  both  externally  and  upon  section. 
The  microscope  shows  that  the  cells  of  the  parenchyma  are  filled  with  large 
and  small  globules  of  fat.  The  fat  is  most  abundant  toward  the  periphery 
of  the  lobules. 

The  causes  of  fatty  liver  are  by  no  means  clear.  Sometimes  it  is  found 
in  cases  of  general  obesity,  where  we  may  assume  that  the  amount  of  fat  which 
the  liver  receives  as  nourishment  is  abnormally  great;  but  often  we  find  a 
liver  that  contains  comparatively  little  fat  in  those  who  have  a  well-developed 
panniculus  adiposus  and  much  fat  in  other  organs.  Topers  may  have  a  de- 
cidedly fatty  liver.  The  occurrence  of  fatty  liver  in  the  cachectic,  and  par- 
ticularly in  the  consumptive,  is  remarkable;  and  individuals  suffering  from 
cancer,  marantic  children,  or  patients  with  severe  general  anaemia,  may  also 
exhibit  the  same  change.  We  have  no  intimate  knowledge  of  the  conditions 
that  prevent,  in  such  cases,  the  oxygenation  of  the  fat  which  comes  to  the  liver 
from  the  ingesta  or  from  other  organs. 

We  do  not  know  that  the  fatty  liver  is  in  any  way  functionally  impaired. 
The  only  clinical  indication,  therefore,  of  its  existence  is  the  increased  bulk 


714  DISEASES   OF   THE   DIGESTIVE   ORGANS 

of  the  organ.  In  phthisis  we  may  sometimes  feel  pretty  certain  that  the  liver 
is  fatty  if  an  increase  in  bulk  can  be  demonstrated,  and  if  other  causes  for 
this  enlargement,  such  as  amyloid  degeneration,  appear  improbable.  If  the 
anterior  edge  of  a  fatty  liver  can  be  felt,  it  is  usually  found  to  be  noticeably 
thick  and  blunt. 

The  treatment  of  fatty  liver  is  to  combat  the  original  disease. 

4.  Amyloid  Liver  (Waxy  Liver). — Amyloid  degeneration  of  the  liver  is  al- 
most invariably  a  part  of  extensive  amyloid  disease,  involving  also  the  spleen, 
kidneys,  intestine,  and  other  organs.  The  disease  occurs  chiefly  in  certain 
cachectic  conditions,  such  as  chronic  suppuration,  as  in  caries  and  persistent 
empyema,  and  also  in  chronic  pulmonary  tuberculosis  and  constitutional 
syphilis. 

The  amyloid  liver  is  usually  increased  in  bulk.  The  organ  may  even  be- 
come almost  double  its  normal  size.  It  feels  very  firm  and  hard,  its  surface  is 
perfectly  smooth,  and  its  edge  is  slightly  thickened.  The  cut  surface  presents 
a  characteristic  grayish-brown  "  waxy  "  appearance. 

The  microscope  shows  that  the  degenerative  process  attacks  chiefly  the  walls 
of  the  hepatic  capillaries,  the  hepatic  cells  proper  showing  infrequent  and 
slight  amyloid  changes.  Very  often  the  cells  of  the  parenchyma  are  atrophied 
and  somewhat  infiltrated  with  fat. 

The  diagnosis  of  amyloid  liver  requires  (1)  the  demonstration  by  palpa- 
tion and  percussion  of  hepatic  enlargement.  We  can  often  feel  a  large  part 
of  the  anterior  surface  and  the  margin  of  the  hard  and  firm  organ.  The  liver 
may  reach  as  low  as  the  level  of  the  umbilicus.  The  diagnosis  further  de- 
mands (2)  that  some  disease  which  predisposes  to  amyloid  be  present,  and 
(3)  that  there  be  evidence  of  the  degenerative  process  in  other  organs:  the 
spleen  should  be  enlarged,  and  the  kidneys  secrete  an  abundance  of  albu- 
minous urine. 

The  other  symptoms,  as  well  as  the  prognosis  and  treatment,  are  deter- 
mined mainly  by  the  nature  of  the  causative  affection.  The  use  of  iodid  of 
iron,  iodid  of  potassium,  the  alkaline  carbonates,  and  ammonic  chlorid,  re- 
spectively, has  been  recommended  as  particularly  efficient,  but  therapeutic 
claims  of  this  sort  do  not  withstand  a  rigorous  criticism.  The  chief  point 
is  the  general  improvement  of  nutrition  by  careful  diet  and  nursing.  Further 
particulars  about  amyloid  disease  in  general  will  be  found  in  the  chapter  on 
Amyloid  Degeneration  of  the  Kidney. 


CHAPTER    XIII 

ANOMALIES    IN    THE    SHAPE    AND    POSITION    OF    THE    LIVER 

1.  Corset  Liver. — The  constant  pressure  of  the  lower  ribs  against  the  liver, 
as  a  result  of  tight  lacing,  often  produces  an  atrophy  of  the  hepatic  parenchyma 
from  pressure,  as  shown  by  a  deep  furrow  crossing  transversely  the  anterior 
surface  of  the  organ.  This  "  corset  furrow  "  lies  chiefly  in  the  right  lobe.  Its 
usual  situation  corresponds  to  the  margin  of  the  ribs,  and  the  atrophy  may  be 
so  extreme  that  the  liver  is  divided  into  a  large  upper  part  and  a  small,  usually 
roundish,  lower  portion,  connected  by  a  narrow  isthmus  of  tissue.     At  the 


SUPPURATIVE   PYLEPHLEBITIS  715 

atrophic  place  the  connective-tissue  capsule  of  the  liver  is  almost  always  much 
thickened.  Often  the  lower  section  can  be  bent  upward  as  if  attached  by  a 
hinge. 

This  deformity  of  the  liver  is  found  quite  often  in  elderly  females,  and 
rarely  in  men,  as  in  soldiers.  Unless  extreme,  it  cannot  be  detected  during 
life,  and  it  causes  no  discomfort.  Even  the  bad  cases  do  not,  as  a  rule,  occasion 
any  special  symptoms;  but  they  can  be  clearly  made  out  if  the  abdominal  walls 
are  lax.  The  deep  transverse  furrow  can  be  felt,  and  also  the  lower  section, 
with  its  usually  blunt  edge.  Particularly  in  the  case  of  old  women  we  must 
bear  this  condition  in  mind,  else  we  might  easily  confound  it  with  some  en- 
largement of  the  liver,  such  as  amyloid  or  passive  congestion,  or  even  new 
growths. 

In  some  few  cases  a  well-marked  corset  liver  seems  to  cause  especial  symp- 
toms. It  occasions  a  constant  feeling  of  pressure  and  tugging  in  the  region 
of  the  liver.  Sometimes  there  are  attacks  of  violent  pain,  with  peritoneal  irri- 
tation and  vomiting,  and  a  mild  degree  of  collapse.  These  have  been  regarded 
as  the  result  of  temporary  congestion  and  swelling  in  the  portion  of  the  liver 
below  the  constriction,  but  we  should  view  this  explanation  with  reserve,  and 
should  bear  in  mind  that  in  corset  liver  gallstones  are  remarkably  frequent 
(vide  supra,  page  670),  and  that  consequently  the  symptoms  mentioned  may 
also  be  connected  with  cholelithiasis.  The  treatment  of  such  attacks,  even 
when  the  diagnosis  is  doubtful,  will  in  every  case  consist  chiefly  in  absolute 
rest  in  bed,  the  employment  of  poultices  or  perhaps  of  an  ice  bag,  and  a  re- 
stricted diet.    If  there  is  violent  pain,  we  must  resort  to  narcotics. 

2.  Movable  Liver. — This  name  has  been  applied  to  a  condition  exception- 
ally seen  in  women  with  very  lax  abdominal  walls,  in  which  the  liver  sinks 
deep  down  into  the  lower  portions  of  the  abdominal  cavity,  probably  as  a  result 
of  an  unnatural  length  of  the  suspensory  ligament.  The  organ  can  be  dis- 
tinctly felt  in  its  new  situation,  and  can  usually  be  brought  back  to  a  normal 
position  with  tolerable  ease  by  means  of  external  pressure.  It  is  invariably 
very  movable,  and  it  can  be  seen  to  change  its  place  when  the  patient  lies  upon 
the  side.  In  most  cases  there  are  at  the  same  time  the  indications  of  universal 
enteroptosis,  with  which  we  have  already  become  acquainted  (see  page  565). 
The  interpretation  of  the  symptoms  present,  such  as  pain  and  digestive  dis- 
turbance, is  consequently  difficult  in  most  cases,  especially  if  the  patient  is 
also  neurasthenic  and  hysterical,  which  is  not  infrequently  the  case.  The 
reader  may  compare  on  this  point  the  chapter  on  movable  kidney.  Treatment 
is  governed  by  the  same  principles  as  in  the  other  forms  of  enteroptosis.  Above 
all,  trial  should  be  made  of  a  suitably  applied  and  well-fitting  bandage. 


CHAPTEE   XIV 

SUPPURATIVE    PYLEPHLEBITIS 

(Purulent  Inflammation  of  the  Portal  Vein  and  its  Branches) 

etiology. — Purulent  pylephlebitis  is  seldom  a  primary,  idiopathic  disease. 
In  most  instances  it  is  due  to  the  propagation  of  a  suppurative  inflamma- 


716  DISEASES   OF   THE   DIGESTIVE   ORGANS 

tion  of  neighboring  tissues  to  the  walls  of  the  vein.  The  main  trunk  of  the 
portal  vein  is  rarely  directly  attacked.  Usually  the  process  originates  in  the 
hepatic  branches  of  the  vein  or  in  the  veins  of  the  portal  system,  and  thence 
extends  to  the  larger  vessel. 

Perityphlitic  abscess  is  the  most  frequent  source  of  suppurative  pyle- 
phlebitis. The  inflammation  involves  a  mesenteric  vein,  and  thence  extends 
upward.  Other  causes  are  gastric  ulcer,  intestinal  ulcers,  as  in  dysentery, 
splenic  abscess,  and  purulent  inflammation  at  the  porta  hepatis  or  within  the 
liver  itself,  as  in  abscess  due  to  gallstones.  The  mode  of  production  in  these 
cases  is  precisely  analogous  to  that  in  perityphlitic  abscess,  but  they  are  rare. 

A  special  form  of  pylephlebitis  is  observed  in  the  newborn.  Here  the 
inflammation  originates  in  the  umbilical  vein,  and  we  need  hardly  say  that 
the  cause  is  a  suppurative  infection  through  the  navel. 

In  rare  instances  it  has  been  found  that  pylephlebitis  has  resulted  from  the 
penetration  into  a  vein  of  some  foreign  body  that  had  been  swallowed,  such 
as  a  pin.  Here,  too,  the  true  factors  in  producing  the  inflammation  are,  of 
course,  the  bacteria  which  adhere  to  the  foreign  body. 

Pathology. — Where  the  inflammation  has  attacked  the  vascular  walls,  the 
vein  is  thickened,  and  often  the  surrounding  connective  tissue  is  infiltrated 
with  pus  cells  and  mottled  with  minute  ecchymoses.  If  the  vein  is  cut  open, 
the  intima  is  seen  to  be  opaque  and  often  superficially  ulcerated.  The  lumen 
of  the  vessel  is  filled  with  a  thrombus,  which  is  usually  to  a  great  extent  in  a 
state  of  purulent  softening,  so  that  offensive  purulent  fluid  flows  out.  The 
course  of  events  is  as  follows:  First,  the  wall  of  the  vein  becomes  inflamed. 
As  a  consequence  of  this,  a  thrombus  forms  at  the  same  place.  The  bacteria 
penetrate  this  thrombus  and  occasion  its  purulent  softening. 

The  extent  of  a  pylephlebitis  naturally  varies  in  different  cases.  As  a  rule, 
little  fragments  become  detached  from  the  thrombus  and  enter  the  liver,  pro- 
ducing metastatic  abscesses.  Secondary  suppuration  may  occur  also  in  the 
lungs,  kidneys,  brain,  and  joints,  so  that  we  have  all  the  anatomical  charac- 
teristics of  a  general  pyaemia. 

Clinical  History. — Inasmuch  as  the  primary,  causative  disease  may  be  very 
different  in  different  cases,  it  is  impossible  to  delineate  the  disease  compre- 
hensively. It  is,  however,  frequently  ushered  in  by  a  number  of  symptoms, 
which  render  a  diagnosis  possible,  at  least  in  some  cases,  if  the  original  disease 
has  been  recognized. 

The  symptoms  of  suppurative  pylephlebitis  are  in  part  due  directly  to  the 
local  disease  itself,  and  in  part  are  occasioned  by  the  general  pyaemia.  One  of 
the  local  symptoms  is  pain  in  the  epigastrium.  This  is  rare.  It  may  radiate 
downward  or  laterally,  according  to  the  starting  place  and  extent  of  the  in- 
flammation. An  inevitable  result  of  the  portal  thrombosis  is  portal  obstruc- 
tion. The  spleen  becomes  considerably  swollen,  and,  if  the  disease  be  not 
too  quickly  fatal,  there  is  an  evident  effusion  into  the  peritoneal  cavity.  The 
splenic  enlargement  Cannot  be  regarded  as  due  merely  to  venous  stasis,  but  is 
in  part  the  "  acute  splenic  tumor  "  of  constitutional  septic  conditions.  If  the 
inflammation  spreads  from  the  branches  of  the  portal  vein  to  the  neighboring 
bile  ducts,  jaundice  results.  Sometimes  it  is  due  also  to  the  hepatic  abscesses, 
or  to  a  gallstone  which. happens  to  cause  trouble  simultaneously.  Now  and 
then  there  is  no  jaundice  whatever. 


THROMBOSIS   OF   THE   PORTAL   VEIN  717 

Of  the  pyaemic  symptoms,  hepatic  abscesses  come  first.  They  are  due,  as 
we  have  said,  to  the  conveyance  of  infectious  matter  directly  into  the  liver  by 
emboli.  The  one  almost  constant  sign  of  their  occurrence  is  a  decided  enlarge- 
ment of  the  liver.  When  there  are  no  hepatic  abscesses,  the  organ  usually 
retains  its  normal  bulk. 

The  course  of  the  fever  is  very  characteristic.  As  in  other  pyaemic  condi- 
tions, there  are  almost  invariably  great  elevations,  to  106°  F.  (41°  C),  or 
higher,  accompanied  by  rigors,  and  followed  by  marked  remissions,  with  pro- 
fuse perspiration.  These  onsets  of  fever  occur  at  irregular  intervals,  either 
daily,  or  every  two  or  three  days. 

There  are  at  the  same  time  indications  of  constitutional  septic  infection, 
which  keep  increasing  in  severity.  The  pulse  grows  rapid  and  small.  Intelli- 
gence is  impaired.  Somnolence  and  delirium  come  on,  and  the  strength  rap- 
idly fails. 

There  are  other  symptoms.  Vomiting  is  frequently  seen.  The  bowels  are 
seldom  constipated,  but  usually  relaxed.  The  dejections  may  contain  blood, 
because  of  the  venous  stasis.  In  some  cases  the  inflammation  extends  so  as  to 
produce  a  fatal  general  peritonitis.  It  is  noticeable  that  the  urine  is  generally 
scanty,  and  the  amount  of  urea  is  strikingly  diminished. 

The  disease  usually  runs  a  rather  acute  course.  On  the  average,  it  lasts 
about  two  weeks,  but  it  may  occupy  three  or  four  weeks,  or  even  a  longer 
period.    It  is  invariably  fatal.    At  least,  no  cases  of  recovery  are  known. 

The  diagnosis  can  sometimes  be  made  with  considerable  positiveness.  In 
other  instances  it  is  impossible  to  exclude  other  pyaemic  conditions,  or  abscess 
due  to  gallstones,  etc.  Important  factors  are  the  origin  of  the  trouble — if  it 
can  be  made  out — the  pyasmic  rigors,  the  enlargement  of  the  spleen  and  liver, 
jaundice,  epigastric  pain,  and  the  evidences  of  general  sepsis. 

Treatment  is  unfortunately  almost  entirely  useless.  The  fever  is  not  af- 
fected even  by  large  doses  of  quinin.  All  we  can  aim  at  is  to  support  and 
relieve  the  sufferer  as  far  as  possible. 


CHAPTER   XV 

THROMBOSIS  OF  THE  PORTAL  VEIN 

(Chronic  Adhesive  Pylephlebitis.     Pylethrombosis) 

^Etiology  and  Pathology. — Like  suppurative  pylephlebitis,  chronic  portal 
thrombosis  is  not  an  independent  disease,  but  is  the  sequel  of  a  great  variety  of 
other  pathological  conditions.  Marantic  thrombosis  is  of  rare  occurrence,  and 
is  usually  formed  toward  the  close  of  life,  so  as  not  to  be  of  practical  interest. 
Apart  from  this,  almost  all  cases  of  thrombosis  of  the  portal  vein  are  due  to  a 
compression  and  constriction  of  the  trunk  of  that  vessel  or  one  of  its  main 
branches.  This  most  often  occurs  in  certain  chronic  hepatic  diseases  which 
involve  a  mechanical  stenosis,  either  of  the  smaller  branches  of  the  portal  vein 
within  the  liver  or  of  the  vein  itself,  with  resulting  coagulation  of  the  blood 
within  it.  Chief  among  these  diseases  are  cirrhosis  and  syphilis  of  the  liver, 
which  have  repeatedly  been  observed  to  entail  portal  thrombosis;  but  other 


718  DISEASES   OF  THE   DIGESTIVE   ORGANS 

diseases  in  the  neighborhood  of  the  vein  may  produce  a  similar  effect.  Portal 
thrombosis  may  also  arise  through  compression  of  the  vessel  by  a  chronic 
inflammatory  hyperplasia  of  the  connective  tissue  at  the  porta  hepatis.  This 
is  illustrated  in  chronic  peritonitis,  whether  circumscribed  or  diffuse,  an  ex- 
ample of  the  former  being  sometimes  seen  as  an  effect  of  duodenal  ulcer. 

It  was  formerly  held  that  many  forms  of  so-called  "  lobulated  liver  "  were 
due  to  a  primary  adhesive  pylephlebitis.  This  is  erroneous.  These  cases  are 
probably  all  due  to  some  primary  hepatic  disease,  usually  syphilitic.  The  size 
of  the  liver  is  little  influenced  by  obstruction  of  the  portal  vein,  even  if  long 
continued,  for  the  hepatic  artery  suffices  to  supply  all  the  blood  required  by 
the  organ. 

The  anatomical  changes  in  pylethrombosis  do  not  differ  essentially  from 
those  seen  in  thrombosis  of  any  other  vein.  If  fresh,  the  thrombus  is  still  red ; 
later  it  grows  harder,  paler,  and  more  friable.  If  the  thrombosis  has  existed 
a  long  while,  the  clot  becomes  completely  organized.  We  have  observed  this 
even  in  the  main  trunk  of  the  portal  vein. 

Clinical  History. — The  symptoms  of  portal  thrombosis  are  those  occasioned 
by  the  obstruction,  and  therefore  such  as  we  have  already  repeatedly  men- 
tioned, in  connection  with  various  hepatic  diseases.  The  intensity  and  extent 
of  these  results,  as  well  as  the  time  occupied  in  their  development,  depend,  of 
course,  upon  the  place  and  size  of  the  clot.  If  it  is  the  portal  vein  itself  which 
is  attacked,  and  if  the  thrombus  is  extensive  enough  to  obstruct  the  flow  of 
blood,  then  the  signs  of  venous  stasis  are  evident  throughout  the  portal  system. 
The  spleen  becomes  much  enlarged,  as  can  be  easily  demonstrated  by  percussion 
and  palpation.  Soon  ascites  appears  as  a  result  of  the  passive  congestion  of 
the  peritoneal  veins ;  and  from  a  (  similar  condition  of  the  gastrointestinal 
veins  arise  catarrhal  disorders,  such  as  diarrhea,  or,  not  so  very  exceptionally, 
there  is  repeated  gastric  and  intestinal  hemorrhage. 

As  we  have  seen,  a  collateral  circulation  may  be  developed  (vide  page  689), 
by  which  the  venous  blood  of  the  portal  system  is  enabled  to  reach  the  systemic 
veins.  This  explains  why  some  of  the  symptoms  of  venous  stasis  may  tem- 
porarily (perhaps  permanently)  vanish.  We  saw  one  case  of  portal  throm- 
bosis, the  sequel  to  what  was  apparently  a  syphilitic  disease  of  the  liver,  in 
which  quite  a  large  ascitic  effusion  appeared  some  six  or  seven  times  at  inter- 
vals of  three  to  six  months,  and  under  proper  nursing  and  treatment,  without 
aspiration,  as  often  disappeared.  The  patient  did  not  die  till  the  illness  had 
continued  six  years,  and  tapping  had  been  required  in  all  some  fifteen  times. 
At  the  autopsy  the  trunk  of  the  portal  vein  was  found  to  be  converted  into  a 
fibrous  cord  with  a  lumen  which  barely  admitted  a  knitting  needle. 

In  simple  pylethrombosis  there  are  no  local  symptoms  such  as  pain.  The 
condition  of  the  liver  depends  upon  the  primary  disease.  It  is  possible  that  a 
moderate  atrophy  of  the  entire  organ  might  at  length  ensue  if  the  portal  blood 
were  permanently  cut  off  from  it.  But,  as  we  have  said,  any  cirrhotic  changes, 
or  any  "lobulation,"  are  not  to  be  regarded  as  the  result,  but  as  the  cause 
of  the  thrombosis,  or  at  least  as  related  to  the  cause. 

The  course  and  duration  of  the  disease  are  according  to  the  nature  of  the 
original,  causative  trouble.     N/o  general  statements  can  be  made. 

The  diagnosis  of  thrombosis  of  the  portal  vein  is  usually  extremely  difficult, 
and  it  can  really  hardly  ever  be  made  with  absolute  certainty.     We  may,  in- 


DISEASES  OF  THE  PANCRE  719 

deed,  recognize  readily  that  there  is  some  decided  obstruction  to  the  portal 
circulation;  but  whether  this  be  due  to  a  thrombus,  or  to  compression  of  the 
portal  vein,  or  to  the  obliteration  of  a  large  number  of  the  smaller  branches 
of  that  vein  within  the  liver,  we  cannot  always  determine.  Pylethrombosis 
may  be  regarded  as  probable,  if  no  other  cause  of  the  portal  obstruction  seems 
likely,  and  if  certain  circumstances,  such  as  a  previous  syphilis,  point  to  the 
possibility  of  a  portal  thrombosis. 

The  prognosis  is  always  unfavorable,  although  there  may  be,  as  we  have 
said,  great  temporary  improvement.  Treatment  must  be  symptomatic,  and  it 
follows  in  the  main  the  principles  set  forth  under  cirrhosis  of  the  liver. 


APPENDIX 

DISEASES    OF    THE    PANCREAS 

Inasmuch  as  the  pancreas  is  almost  entirely  inaccessible  from  the  stand- 
point of  direct  clinical  examination,  attempts  have  been  frequently  made  of 
late  to  discover  methods  and  signs  that  point,  at  least  in  general,  to  a  disturbed 
function  of  that  organ  (functional  pancreatic  diagnosis).  On  account  of  the 
great  difficulty  of  this  problem,  the  results  are  mostly  very  indefinite.  Still,  the 
following  practical  and  important  facts  may  be  considered  at  the  present 
time : 

1.  Boldireff  has  found  that  upon  the  introduction  of  large  amounts  of  fat 
into  the  stomach,  a  regurgitation  of  bile,  intestinal  juice,  and  pancreatic  secre- 
tion into  the  stomach  occurs.  Volhard  has  attempted  to  utilize  this  fact  in  the 
diagnosis  of  pancreatic  disease.  Through  a  stomach  tube  he  introduces  into  the 
empty  stomach  of  the  patient  7  ounces  (gm.  200)  of  oil,  and  after  half  an  hour 
siphons  off  the  gastric  contents  and  examines  for  trypsin.  This  has  been 
demonstrated  repeatedly  and  proves,  at  least  if  positive,  that  the  pancreatic 
function  is  maintained. 

2.  The  attempt  has  been  frequently  made  to  draw  conclusions  as  to  the 
digestive  function  of  the  pancreas  from  the  condition  of  the  stools.  The  con- 
ditions are  quite  complicated  on  account  of  the  mixture  of  the  various  digestive 
juices  (bile,  intestinal  juice) .  Still,  we  may  say  that  very  fatty  stools — so  called 
steatorrhea — particularly  if  icterus  be  absent — are  always  suggestive  of  pan- 
creatic disease.  It  is  also  worthy  of  note  that  in  the  absence  of  the  pancreatic 
function  a  diminished  fat-splitting  occurs — i.  e.,  a  diminution  of  the  fatty 
acids  and  soaps  present  in  fatty  stools  to  below  seventy  per  cent  of  the  total 
amount  of  the  fat  present. 

3.  Worth  noting  is  the  not  infrequent  occurrence  of  glycosuria,  or,  at  least, 
of  "  alimentary  glycosuria,"  in  pancreatic  disease — i.  e.,  the  advent  of  glyco- 
suria after  the  administration  of  3.5  ounces  (gm.  100)  of  dissolved  dextrose. 

4.  The  attempts  made  by  E.  Miiller  and  Schlecht  in  my  Breslau  Clinic  to 
demonstrate  the  presence  of  pancreas  trypsin  in  the  stools  themselves  are  most 
definitive.  After  the  rectum  has  been  cleansed  by  an  enema,  the  patient  receives 
a  test  meal  of  5  ounces  (gm.  150)  of  meat  and  5  ounces  (gm.  150)  of  mashed 
potatoes,  and  about  half  an  hour  later  a  cathartic,  as,  for  instance,  calomel  and 


720  DISEASES   OF   THE   DIGESTIVE   ORGANS 

purgen,  aa  3  gr.  (gm.  0.2).  The  subsequent  stools  coming  from  the  small  intes- 
tine are  now  examined  for  their  trypsin  content,  with  the  aid  either  of  the  diges- 
tion test  on  the  so-called  Loffler  plate,  or,  what  is  simpler  in  practice,  of  Eum- 
pel's  gelodurat  capsules  filled  with  powdered  wood  charcoal.  Such  a  capsule  is 
placed  in  a  small  glass  with  about  0.5  ounce  (10  to  15  c.c.)  of  triturated  feces, 
and  allowed  to  stand  at  a  temperature  of  98.6°  F.  (37°  C).  If  the  stool  con- 
tains trypsin,  the  capsule  is  dissolved,  and  the  charcoal  which  is  discharged  col- 
ors the  entire  contents  of  the  glass  black.  If  trypsin  is  absent,  the  capsule  will 
not  be  dissolved. 

5.  An  interesting  and  peculiar  urine  reaction  is  the  so-called  Cammidge 
reaction.  Its  significance  is  still  not  entirely  clear,  but  a  positive  reaction  is 
supposed  to  speak  for  a  disease  of  the  pancreas.  We  cannot  enter  here  into  the 
details  of  this  rather  complicated  reaction  (boiling  of  the  urine  with  HCL, 
neutralizing  with  carbonate  of  lead,  addition  of  phenylhydrazin,  acetate  of 
sodium,  and  acetic  acid,  and  a  precipitation  after  twenty-four  hours  of  delicate 
crystalline  needles,  which  Cammidge  takes  to  be  osazone).  The  test  is  accepted 
as  a  proof  of  the  presence  of  decomposition  products  of  fat  (glycerin)  in  the 
urine.  In  general,  control  tests  of  this  reaction  which  have  been  made  up  to 
date  have  given  satisfactory  results,  so  that  it  seems  that  the  reaction  is  not 
without  practical  significance. 

The  most  important  anatomical  lesions  of  the  pancreas  which  are  known 
up  to  the  present  time  are  as  follows : 

1.  Atrophy  of  the  Pancreas. — The  organ  may  share  in  a  general  marasmus. 
There  is  sometimes  also  extreme  atrophy  of  the  pancreas  in  those  who  have  died 
of  diabetes  mellitus  (q.  v.). 

2.  Hemorrhages  Into  the  Pancreas. — Small  hemorrhages  occur  in  the  pan- 
creas in  cases  of  general  hemorrhagic  diathesis,  marked  passive  congestion,  severe 
acute  constitutional  infection,  and  trauma  of  the  abdomen.  These  do  not,  as  a 
rule,  cause  marked  clinical  symptoms.  On  the  other  hand,  Klebs,  Zenker,  and 
others  describe  cases  in  which  a  more  or  less  extensive  pancreatic  hemorrhage  has 
been  found  at  autopsy  as  the  only  demonstrable  cause  of  death.  The  patients 
were  previously  in  apparently  perfect  health  and  were  vigorous,  although  usu- 
ally corpulent  individuals,  and  they  died  suddenly.  Perhaps  it  was  the  influence 
of  the  hemorrhage  upon  the  semilunar  ganglia  or  the  solar  plexus  which  occa- 
sioned the  speedy  death.  At  any  rate,  we  find  in  such  cases  the  cavities  of  the 
heart  of  usual  size  and  empty,  while  the  abdominal  vessels  are  distended  with 
blood.  The  special  causes  which  lead  to  the  hemorrhage  are  not  always  clear. 
In  general,  we  probably  must  surmise  a  primary  disease  of  the  blood  vessels 
(syphilis,  atheroma).  It  is  noteworthy  that  a  comparatively  large  number  of 
cases  have  occurred  in  hard  drinkers.  Many  cases  also  seem  to  be  similar  to 
those  first  described  by  Balser.  These  have  an  uncertain  aetiology,  perhaps  in- 
fectious, and  exhibit  a  multiple  necrosis  of  fat  and  of  the  pancreatic  tissue — 
there  being  numerous  minute  necrotic  foci  in  the  pancreas  and  in  the  fat  tissue 
of  the  mesentery.  Extensive  disorder  of  this  kind  is  observed  particularly  in 
obese  persons,  but  is  not  confined  to  them.  Sometimes  in  cases  of  pancreatic 
hemorrhage  death  is  extremely  sudden  and  apoplectiform.  In  other  cases 
the  symptoms  last  from  twelve  to  twenty-four  hours  before  the  fatal  termina- 
tion. The  patient  suffers  from  violent  abdominal  pain,  vomiting,  abdominal 
distention,  and  general  collapse;  treatment  is  purely  symptomatic. 


DISEASES   OF  THE   PANCREAS  721 

3.  Pancreatitis. — In  rare  eases  primary  acute  pancreatitis,  usually  hemor- 
rhagic, has  been  observed.  It  begins  with  violent  colicky  pains  in  the  epig 
trium.  Vomiting  and  collapse  soon  follow.  The  pulse  grows  small,  the  ex- 
tremities become  cool,  and  death  is  speedy.  At  the  autopsy  the  pancreas  is 
found  to  be  much  enlarged,  and  mottled  with  ecchymoses,  or  it  even  presents 
scattered  foci  of  suppuration.  The  aetiology  is  unknown.  It  is  most  likely  tbat 
the  germs  which  excite  the  inflammation  originate  in  the  intestines.  There 
should  be  a  sharp  distinction  made  between  primary  pancreatic  hemorrhage  and 
acute  hemorrhagic  pancreatitis,  but  formerly  these  two  conditions  were  often 
confounded.    Secondary  abscesses  of  the  pancreas  are  not  infrequent  in  pyaemia. 

[Fitz,  in  the  Middleton-Goldsmith  lecture  for  1889,  threw  much  light  on  the 
aetiology  and  diagnosis  of  acute  pancreatitis,  which  he  subdivides  into  three  ana- 
tomical forms — the  hemorrhagic,  the  suppurative,  and  the  gangrenous.  He 
shows  that  the  affection  is  not  so  rare  as  has  been  supposed ;  that  its  victims  are 
usually  in  middle  life,  fat,  and  good  livers;  that  it  commonly  originates  by  the 
extension  of  a  gastroduodenal  inflammation  along  the  pancreatic  duct. 

"  If  the  case  does  not  end  fatally  in  the  course  of  a  few  days,  recovery  is  pos- 
sible, or  a  recurrence  of  the  symptoms  in  a  milder  form  takes  place,  and  the  char- 
acteristics of  a  subacute  peritonitis  are  developed." 

In  the  differential  diagnosis  irritant  poisoning,  perforation  of  the  digestive  or 
biliary  tracts,  and  acute  intestinal  obstruction  are  to  be  considered.  The  location 
of  peritonitic  symptoms,  their  suddenness  of  onset,  the  absence  of  apparently 
sufficient  cause,  and  the  age  and  habit  of  the  individual  are  important  points.] 

Chronic  interstitial  pancreatitis  sometimes  results  from  the  extension  of 
chronic  inflammatory  processes  affecting  neighboring  parts.  Friedreich  states 
that  it  sometimes  is  a  primary  disease  in  topers.  Syphilitic  lesions  of  the  pan- 
creas have  been  observed,  occasioning  contraction  and  induration. 

There  are  no  characteristic  clinical  symptoms  which  correspond  to  these 
various  changes.  The  symptoms  observed  in  the  cases  belonging  in  this  cate- 
gory are  digestive  disturbances,  indefinite  pain,  bodily  weakness,  emaciation, 
and  anaemia,  and  they  are  so  ambiguous  that  a  diagnosis  of  the  true  condition 
is  scarcely  ever  possible. 

We  find  a  peculiar  atrophy  and  induration  of  the  pancreas  associated  with 
hemosiderosis  (pigmentation  by  a  ferruginous  pigment)  in  the  so-called  bronze 
diabetes  (diabete  bronze).  This  deserves  brief  mention  here.  It  is  a  remark- 
able combination  of  diabetes  (marked  glycosuria)  with  dark  pigmentation  of 
the  skin,  dependent  upon  the  deposit  of  this  same  ferruginous  pigment  in  the 
skin.  Usually,  there  is  present  at  the  same  time  a  cirrhotic  induration  and 
enlargement  of  the  liver,  which  is  also  associated  with  hemosiderosis,  and  not 
infrequently,  too,  with  the  signs  of  portal  obstruction  (enlarged  spleen,  ascites). 
The  causes  of  this  remarkable  and  rare  disease  are  still  entirely  unknown. 

4.  Cysts  of  the  Pancreas. — After  closure  of  Wirsung's  duct  by  scars,  con- 
cretions, or  the  like,  cysts  of  the  pancreas  may  form,  as  a  result  of  the  damming 
up  of  the  secretion.  These  may  become  so  large  as  to  be  felt  as  great  tumors 
through  the  abdominal  walls.  In  other  cases  we  seem  to  be  dealing  with  cystic 
neoplasms.  The  cysts,  as  a  rule,  protrude  between  the  stomach  and  transverse 
colon,  although  the  greatest  variety  of  other  relations  between  the  cysts  and 
these  organs  may  occur.  A  cure  is  possible  only  by  operation.  Earely,  spaces 
are  found  in  the  neighborhood  of  the  pancreas  filled  with  a  thick,  slimy  fluid. 


722  DISEASES   OF   THE   DIGESTIVE   ORGANS 

These  seem  to  be  associated  with  the  above-mentioned  peculiar  multiple  necrosis 
of  fat  and  pancreatic  tissue,  but  with  regard  to  them  further  observations  are 
desirable. 

5.  Cancer  of  the  Pancreas. — Primary  cancer  is  the  most  frequent,  and 
therefore  clinicalty  the  most  important  disease  of  this  organ.  It  is  usually  of 
the  medullary  variety,  though  occasionally  colloid.  As-  a  rule,  the  new  growth  is 
situated  in  the  head  of  the  pancreas.  It  may  involve  neighboring  parts  by  direct 
extension,  and  a  great  many  organs  by  metastasis ;  for  example,  the  liver,  peri- 
toneum, and  lymph-glands. 

The  clinical  symptoms  of  cancer  of  the  pancreas  are  very  seldom  so  decided 
as  to  justify  a  positive  diagnosis.  Sometimes  the  secondary  nodules  can  be 
detected  in  the  liver,  peritoneum,  and  elsewhere.  Then  we  are  left  in  doubt 
about  the  seat  of  the  primary  growth.  Or  the  primary  tumor  may  be  plainly 
felt  through  the  abdominal  walls;  but  then  we  can  hardly  ever  exclude  cancer 
of  the  stomach  or  of  the  omentum  and  neighboring  parts. 

The  symptoms  of  pancreatic  cancer,  as  a  whole,  resemble  closely  those  occa- 
sioned by  most  cancers  of  abdominal  organs.  Usually  the  patient  is  elderly. 
The  first  symptoms  are  weakness,  emaciation,  and  indigestion,  or  they  are  the 
result  of  compression.  Often  there  is  complaint  of  a  persistent  dull  pain  in  the 
epigastrium.  If  the  portal  vein  is  pressed  upon  by  the  tumor,  ascites  appears. 
If  the  common  duct  is  compressed,  there  is  jaundice.  Icterus  is  an  especially 
frequent  symptom  of  pancreatic  carcinoma. 

The  diagnosis  is  difficult.  It  can  be  made  with  a  certain  degree  of  prob- 
ability when  there  is  a  slowly  growing  tumor  in  the  region  of  the  pancreas, 
without  enlargement  of  the  liver,  but  accompanied  by  jaundice,  deeply  seated 
epigastric  pain,  glycosuria,  and  the  above-mentioned  more  or  less  distinctly 
marked  pancreatic  symptoms — viz.,  fatty  stools,  imperfect  digestion  of  albumen 
and  starch  and  glycosuria.  Usually,  however,  the  clinical  picture  is  by  no  means 
so  characteristic,  and  it  is  often  impossible  to  avoid  confusing  cancer  of  the 
pancreas  with  cancer  of  the  stomach,  duodenum,  gall  bladder,  or  other  organs. 

The  prognosis  is  absolutely  bad.  With  increasing  marasmus,  the  patient 
usually  dies  at  the  end  of  six  months  or  a  year. 

The  treatment  is  merely  symptomatic,  with  the  aim  of  lessening  the 
patient's  suffering. 

6.  Pancreatic  Calculi. — In  the  excretory  ducts  of  the  pancreas  are  some- 
times found  calculi  of  small  or  moderate  size,  consisting  essentially  of  carbonate 
and  phosphate  of  lime.  The  cause  of  their  formation  is  as  little  settled  as  that 
of  gallstones  (which  see).  Because  of  the  obstruction  caused  by  these  calculi 
we  have  secondary  dilatation  of  the  ducts,  secondary  contraction  and  atrophy, 
and  in  some  cases  secondary  inflammation  and  suppuration;  these  probably 
result  from  processes  similar  to  those  with  which  we  have  become  acquainted 
while  considering  biliary  calculi.  There  may  be  no  symptoms.  Sometimes, 
however,  there  is  violent  pain,  either  continuous  or  paroxysmal,  also  digestive 
disturbances,  and  occasionally  the  above-mentioned  changes  in  the  dejecta,  and 
glycosuria,  In  only  a  very  few  cases  has  it  been  possible  to  find  pancreatic 
calculi  in  the  feces.  An  absolute  diagnosis  can  rarely  be  made.  As  a  thera- 
peutic measure  Eichhorst  has  recommended  the  stimulation  of  the  pancreatic 
secretion  by  means  of  injections  of  pilocarpin;  as  a  rule,  treatment  will  be 
purely  symptomatic. 


V.     DISEASES   OF  THE   URINARY   ORGANS 


SECTION   I 
Diseases  of  the  Kidneys 

CHAPTER   I 

GENERAL    PRELIMINARY    REMARKS    UPON   THE    PATHOLOGY 
OF    RENAL    DISEASE 

•Although  some  knowledge  of  the  occurrence  and  significance  of  renal 
affections  had  been  acquired  even  by  the  older  physicians,  still,  the  service  of 
having  pointed  out  the  frequency  of  these  diseases,  and  of  having  clearly  recog- 
nized their  most  important  anatomical  forms  and  their  chief  clinical  symptoms, 
belongs  undoubtedly  to  the  English  physician  Richard  Bright,  who  was  born  in 
1788  and  died  in  1858,  as  physician  in  ordinary  to  Queen  Victoria.  Bright's 
first  work  on  this  subject  appeared  in  the  year  1827.  In  this  he  brought  forward 
the  special  discovery  that,  in  many  cases  of  general  dropsy,  which  are  associated 
with  the  secretion  of  an  albuminous  urine,  a  primary  affection  of  the  kidneys 
must  be  regarded  as  the  true  cause  of  the  disease.  Since  then,  the  disease 
described  by  him  has  been  almost  universally  called  "  Bright's  disease '" 
("Morbus  Brightii"),  a  name  still  much  employed,  but  in  whose  stead  the 
anatomical  terms  would  be  more  proper,  since  many  forms  were  previously 
classed  under  it  which,  according  to  our  more  accurate  present  knowledge, 
must  be  separated. 

Bright's  statements  were  either  confirmed  or  expanded  in  subsequent  times 
by  many  other  observers.  Christison,  Osborne,  and  R.  Willis  in  England,  and 
Rayer  and  M.  Solon  in  France,  were  the  chief  students  in  renal  diseases. 
Frerichs  published  the  first  great  work  in  Germany  in  the  year  1851.  His  divi- 
sion of  Bright's  disease  into  three  different  "  stages,"  based  on  Reinhardt's  his- 
tological investigations,  was  for  a  long  time  quite  generally  accepted,  until 
gradually  further  clinical  experience  showed  that  it  was  untenable.  A  more 
accurate  division  of  renal  diseases  was  substituted  for  it  first  in  England  (John- 
son, S.  Wilks,  and  others),  and  then  in  Germany  (Traube,  Bartels).  However 
admirable  these  labors,  especially  the  work  of  Bartels  in  1871,  renal  pathology 
fell  into  subjection  to  theories,  with  which  the  facts  of  experience  could  be 
harmonized  only  by  force.  Only  of  late  years  has  a  natural  theory  of  renal  dis- 
eases, derived  from  general  pathological  observations,  become  accepted — a  the- 
ory which  is  based  chiefly  upon  the  anatomical  work  of  Weigert.     There  has 

723 


724  DISEASES   OF   THE   URINARY   ORGANS 

also  been  special  research  work  done  in  the  more  accurate  determination  of  the 
disturbed  function  of  the  diseased  organ  .(v.  Koranyi,  etc.). 

The  following  presentation  of  renal  pathology  is  intended  to  show  that, 
from  a  clinical  standpoint  as  well,  the  renal  diseases  may  be  viewed  compre- 
hensively as  a  unit,  and  this  not  in  a  schematic  way,  but  with  due  regard  to 
actual  conditions: 

The  chief  reason  why  the  kidneys  are  so  often  diseased,  either  alone  or  in 
conjunction  with  other  organs,  is  to  be  found  in  the  fact  that  the  body  must 
eliminate  all  forms  of  injurious  matter,  which  circulate  in  the  blood,  in  great 
part  by  the  kidneys.  Consequently  the  action  of  any  injurious  substance  is  often 
manifested  chiefly  in  the  kidneys,  and  they  must,  in  a  certain  measure,  suffer 
for  the  service  which  they  do  the  rest  of  the  body.  According  to  their  nature 
and  character,  the  injurious  substances,  which  are  here  to  be  considered,  are 
divided  chiefly  into  two  great  groups — the  chemico-toxic  and  the  organized 
infectious  substances.  At  the  same  time,  it  should  be  noted  that  in  case  of 
infection  it  is  comparatively  exceptional  for  the  germs  themselves  to  reach  the 
kidneys  and  there  fix  themselves.  Most  cases  are  referable  to  toxins,  which  are 
formed  in  the  body  as  the  result  of  the  infectious  process,  and,  being  excreted 
through  the  kidneys,  produce  a  nephritis.  In  this  way  the  kidneys  may  be 
involved  sympathetically  after  the  ingestion  of  many  poisons,  both  organic 
and  inorganic,  and  also  in  the  great  majority  of  all  the  infectious  diseases.  In 
these  cases,  of  course,  as  we  shall  see  later,  certain  chemical  and  infectious  poi- 
sons exert  their  action  in  a  particularly  frequent  and  in  a  particularly  severe 
or  definitely  characterized  fashion.  Besides  these  forms  of  origin  for  many 
renal  diseases  ("  hematogenous  nephritis  "),  which  are  the  chief  ones  to  be  con- 
sidered, we  must  consider  other  causes  of  disease  which  are  much  rarer.  One 
way  in  which  the  morbific  agents  may  also  enter  is  especially  important — 
namely,  from  the  lower  urinary  passages,  the  bladder,  and  pelvis  of  the  kidney, 
upward  into  the  kidney.  In  this  way  those  renal  diseases  arise  which  come  on 
secondarily  to  cystitis,  pyelitis,  etc.  Finally,  of  course,  disturbances  of  circula- 
tion and  mechanical  injuries  may  also  make  themselves  manifest  in  the  kidneys. 

The  clinical  symptoms  which  are  caused  by  the  different  forms  of  renal  dis- 
ease are  referable  only  in  very  small  part  directly  to  the  diseased  organ  itself. 
In  renal  diseases  characteristic  subjective  local  symptoms — such  as  local  pain 
— are  rare,  and  the  anatomical  position  and  the  physiological  conditions  of  the 
kidneys  make  it  almost  impossible  to  discover  any  changes  in  their  size,  their 
physical  consistence,  etc.,  by  a  direct  objective  examination.  In  the  diagnosis 
of  renal  diseases  we  are  therefore  confined  chiefly  to  the  investigation  of  two 
group  of  sympoms :  in  the  first  place  to  the  examination  of  the  secretion  from 
the  kidneys,  the  urine,  whose  character,  as  we  know  by  experience,  may  be 
materially  altered  when  there  is  renal  disease ;  and,  in  the  second  place,  to  the 
discovery  of  certain  phenomena  in  other  portions  of  the  body,  which  are  imme- 
diately dependent  upon  the  renal  affection.  Since  both  the  pathological 
changes  in  the  urine,  and  the  symptoms  in  other  organs  occurring  in  renal 
affections,  have  much  in  common  in  almost  all  the  forms  of  renal  disease,  it  is 
advisable  first  to  describe  the  main  features,  at  least,  of  the  general  symp- 
tomatology of  renal  disease.  We  shall  then  be  obliged,  in  the  following  chap- 
ters, to  mention  only  the  precise  circumstances  of  the  occurrence  and  onset  of 
each  symptom — the  general  significance  of  the  symptoms  being  already  known. 


REMARKS   UPON   THE   PATHOLOGY   OF   RENAL   DISEASE         725 

1.     ALBUMINURIA 

The  most  constant  symptom,  which  in  many  cases,  even  by  itself,  renders 
the  diagnosis  of  a  renal  affection  possible  with  complete  certainty,  is  albu- 
minuria— that  is,  the  appearance  of  albumen,  and  especially  of  serum  albumen 
and,  in  much  smaller  quantity,  serum  globulin,  in  the  urine.  Strictly  speaking, 
every  albuminuria  must  be  regarded  as  somewhat  pathological.  From  recent 
investigations  (Leube,  Furbringer,  Pavy,  Heubner,  and  others)  we  know  that 
in  some  cases  the  urine  may,  for  a  short  time,  contain  a  very  slight  amount  of 
albumen  even  in  healthy  persons,  especially  after  physical  exertion,  emotional 
disturbance,  a  cold  bath,  a  hearty  meal,  etc. 

As  we  may  assume  from  the  exciting  causes,  there  does  exist  a  slight  and 
rapidly  disappearing  disturbance  of  the  kidney,  which  produces  no  further 
sequela?.  In  such  cases  we  may  speak  of  a  temporary  and  insignificant,  but 
not  really  of  a  "  physiological "  albuminuria.  We  must  also  mention  here  the 
slight  albuminuria  which  is  not  infrequently  found  in  newborn  infants,  and 
which  disappears  after  eight  to  ten  days. 

Intermittent,  Orthostatic  Albuminuria. — The  conditions  are  similar  in  the 
rather  frequent  cases  of  so-called  intermittent  albuminuria.  Usually  by  acci- 
dent, a  slight  or  even  a  marked  albuminuria  may  be  found  in  individuals  who 
feel,  in  general,  entirely  well,  and  are,  as  a  rule,  still  of  youthful  age.  Not 
infrequently  the  patients  are  very  strong,  healthy-looking  children.  In  other 
cases  the  children  may  be  nervous  and  anaemic,  but  otherwise  they  do  not  give 
the  impression  of  really  being  sick.  Still,  they  frequently  complain  of  malaise, 
headache,  general  weakness  and  languor,  pains  in  the  limbs,  palpitation, 
anorexia,  etc.  No  cause  for  this  striking  symptom  can  be  found,  nor  are  there 
any  other  discoverable  objective  disturbances  of  the  body.  If  we  investigate 
closely,  we  find  that  the  urine  does  not  contain  albumen  constantly,  but  only 
at  certain  times  (cyclic  or  periodic  albuminuria).  This  remarkable  variation 
in  regard  to  the  absence  and  presence  of  albumen  can  almost  always  be  traced 
to  variations  in  bodily  rest  and  activity.  When  the  patient  is  at  rest  in  bed, 
or  sits  quiet,  the  urine  that  is  voided  thereafter  (hence  every  morning  urine 
also)  is  entirely  free  from  albumen.  If  the  children,  however,  are  out  of  bed, 
even  for  a  short  time,  move  about  more  actively,  or  perform  some  gymnastic  ex- 
ercises, a  distinct  albuminuria  develops.  This  by  no  means  rare  form  of  albu- 
minuria has  therefore  been  given  the  name  orthotic  or  orthostatic.  Sometimes 
the  albumen  content  of  the  urine  decreases  somewhat  toward  evening.  It  is 
worthy  of  mention  that  the  urine  even  shows  a  distinct  turbidity  on  the  addition 
of  acetic  acid  (nucleo-albumen?).  Casts  (vide  infra)  are  usually  not  present 
in  the  urine,  but  occasionally  in  a  centrifugalized  specimen  a  few  hyaline  casts 
are  found.  The  significance  of  this  practically  important  condition  is  not 
quite  certain.  It  is  clearly  not  due  to  permanent  organic  changes  in  the  kidney, 
hut  may  be  the  result  of  circulatory  disturbances.  Possibly,  in  the  children 
affected,  the  kidney  circulation  is  interfered  with  in  the  standing  position, 
as,  for  instance,  by  a  kinking  of  the  renal  vein.  It  is  claimed  that  sometimes 
the  unusual  mechanical  anatomical  conditions  are  indicated  by  a  lumbar  lordo- 
sis on  standing.  As  has  been  said,  however,  the  matter  has  not  been  entirely 
cleared  up.  It  is  of  practical  importance  to  know  that  in  time  the  condition 
entirely  disappears  of  its  own  accord.  After  the  twenty-fifth  to  the  thirtieth 
40 


726  DISEASES   OF   THE    URINARY   ORGANS 

year,  orthostatic  albuminuria  occurs  only  rarely.  The  condition  is,  therefore, 
as  a  rule,  to  be  looked  upon  as  not  serious,  although  it  must  always  be  regarded 
as  an  anomaly,  and  therefore  given  a  certain  amount  of  careful  consideration. 
Active  treatment  is  unnecessary.  Especially  is  prolonged  rest  in  bed  absolutely 
useless.  The  children  may,  in  general,  lead  their  customary  mode  of  life.  We 
think  that  only  a  certain  amount  of  dietetic  precaution  is  indicated. 

Diagnosis. — The  detection  of  albumen  in  the  urine  for  clinical  purposes, 
wherein  no  regard  need  be  paid  to  the  separation  of  serum  albumen  and  serum 
globulin,  is  performed  almost  exclusively  by  means  of  the  so-called  heat  test. 
If  the  urine  is  cloudy,  it  must  be  filtered  before  heating.  The  reaction  of  the 
urine  must  always  be  tested  first.  If  the  reaction  of  the  urine  is  acid,  as  it 
ordnarily  is,  it  is  heated  in  the  test-tube  without  any  further  addition.  If 
the  urine  is  neutral  or  alkaline,  then,  and  only  then,  we  acidify  it  slightly 
before  boiling,  by  means  of  a  few  drops  of  dilute  acetic  acid.  If  the  urine 
contains  albumen  there  will  appear,  upon  boiling,  a  distinct  flocculent  pre- 
cipitate of  coagulated  albumen.  The  possibility  of  an  error  lies  in  the  fact 
that  sometimes,  with  a  neutral  or  faintly  acid  urine,  upon  heating  there  ap- 
pears a  cloudiness  because  of  the  phosphates  and  carbonates  which  are  pre- 
cipitated. These  are  salts  of  lime  and  magnesia.  In  order  to  avoid 
confounding  such  phosphate  deposit  with  a  deposit  of  albumen,  we  must  in 
every  case  after  the  urine  has  boiled  for  a  short  time,  if  there  is  any  deposit 
formed,  add  a  few  drops  of  nitric  or  acetic  acid.  By  this  means  the  deposit 
of  phosphate  or  carbonate  is  immediately  dissolved,  while  a  deposit  of  albu- 
men is  not  affected.  The  change  in  the  color  of  the  urine,  which  is  sometimes 
caused  by  the  addition  of  nitric  acid,  is  due  to  the  action  of  the  acid  upon  the 
urinary  pigments.  We  can  measure  the  amount  of  albumen  contained  in  the 
urine  approximately  by  the  height  of  the  settled  precipitate  in  the  test-tube. 
We  often  speak  of  "  one  half  or  one  fourth  of  the  volume  being  albumen,"  but 
we  cannot  state  any  definite  relation  between  this  estimate  of  the  volume  and 
the  precise  amount  of  albumen.  Approximately,  however,  a  deposit  of  albu- 
men, which  upon  settling  occupies  about  half  the  volume  of  the  urine,  corre- 
sponds to  about  one  per  cent  by  weight  of  albumen,  a  deposit  of  about  one 
third  of  the  volume  to  about  one  half  per  cent  of  albumen,  and  so  on.  The 
quantitative  estimation  of  the  albumen  content  by  means  of  the  much-used 
Esbach's  apparatus  is  only  of  very  limited  value. 

Besides  the  test  by  boiling  there  is  a  very  distinct  test  which  can  be  highly 
recommended  to  practitioners,  in  which  acetic  acid  and  ferrocyanid  of  potas- 
sium are  employed.  A  rather  large  amount,  perhaps  one  tenth  of  the  volume,, 
of  acetic  acid  is  added  to  the  urine,  and  then  a  few  drops  of  a  ten-per-cent 
solution  of  ferrocyanid  of  potassium  are  added  to  the  mixture.  If  the  urine 
contains  albumen  there  is  formed  a  distinct  deposit.  This  reaction  usually 
takes  place  at  once,  but  if  the  amount  of  albumen  is  very  small  it  may  be  some- 
what delayed. 

The  so-called  Heller's  test  is  also  very  delicate,  but  less  used.  In  a  test- 
tube  a  layer  of  urine  is  carefully  floated  upon  concentrated  nitric  acid.  If 
albumen  is  present,  a  distinct  cloudy  ring  will  appear  at  the  point  of  contact 
of  the  two  liquids. 

If  we  have  found  out  that  the  urine  certainly  contains  albumen,  we  must 
then  decide  whether  we  have  really  a  true  renal  albuminuria — that  is,  whether 


REMARKS   UPON   THE   PATHOLOGY   OF   RENAL   DISEASE         727 

a  urine  already  albuminous  is  secreted  in  the  kidneys,  or  whether  the  albu- 
men is  not  mixed  with  a  perfectly  normal  or  at  least  nonalbuminous  urine 
later,  in  the  kidneys  themselves  or  in  the  urinary  passages,  the  pelvis  of  the 
kidney,  or  the  bladder  (spurious,  accidental  albuminuria).  Such  a  spurious 
albuminuria  occurs  when  the  urine  is  contaminated  with  blood  (as  in  hemor- 
rhages from  the  kidneys,  the  pelvis  of  the  kidney,  the  bladder,  or  the  urethra), 
or  with  pus  (in  pyelitis,  cystitis,  etc.).  In  these  cases,  of  course,  the  albumen 
contained  in  the  serum  of  the  blood  or  pus  is  found  in  the  urine.  Spurious 
albuminuria  is  usually  easily  recognized,  since  the  presence  of  pus  or  blood 
in  the  urine,  which  is  shown  by  the  appearance  of  the  urine  or  upon  micro- 
scopic examination  (red  blood  corpuscles,  pus  corpuscles),  points  with  im- 
mediate certainty  to  the  origin  of  the  albuminuria.  Moreover,  the  amount 
of  albumen  in  these  cases  is  usually  but  slight,  and  corresponds  to  the  amount 
of  pus  or  blood  in  the  urine.  A  disproportion  in  this  respect  must  excite 
the  suspicion  whether,  besides  the  spurious  albuminuria,  there  is  not  perhaps 
at  the  same  time  an  affection  of  the  kidneys  causing  a  true  renal  albuminuria. 
The  determination  of  this  point  is  not  always  perfectly  easy,  but  we  can 
usually  come  to  a  decision  by  finding  abnormal  morphological  constituents  in 
the  urine,  the  so-called  urinary  casts  (vide  infra),  which  give  indubitable 
evidence  of  the  existence  of  a  disease  of  the  kidneys. 

.ZEtiology  and  General  Pathology  of  Renal  Albuminuria. — What  general 
pathological  significance  has  the  true  renal  albuminuria,  and  what  are  the 
causes  of  its  origin?  According  to  our  present  theories,  the  answer  to  these 
questions  is  simply  this:  In  every  case  of  genuine  albuminuria  there  is  an 
abnormal  transudation  of  the  albumen  of  the  blood  into  the  urine.  Like 
every  glandular  organ,  the  kidney  has  not  only  the  ability  to  separate  certain 
substances  from  the  blood,  but  also  the  power  to  prevent  the  excretion  there- 
from of  certain  other  substances.  Among  the  latter  is  serum  albumen,  and 
the  passage  of  this  from  the  blood  into  the  urine  is  therefore  directly  indica- 
tive of  an  injury  to  the  kidney  parenchyma.  This  change  affects  both  the 
walls  of  the  blood  vessels  (analogous  to  all  inflammatory  vessel  changes)  and 
the  epithelium.  If  the  vessel  walls  become  abnormally  permeable,  and  if  the 
epithelium  covering  also  does  not  hold  back  the  albumen,  the  latter  will  enter 
the  secreted  urine  and  be  excreted  with  it.  Until  now  the  glomeruli  were 
regarded  as  the  main  site  of  albumen  excretion,  and  disease  of  the  glomerular 
epithelium  was  considered  the  main  cause  of  renal  albuminuria.  This  view, 
however,  is  certainly  too  one-sided.  To  be  sure,  we  know  from  experimental 
investigation  that  albumen  excretion '  can  occur  in  the  glomeruli,  but  it  is 
quite  as  certain  that  it  may  take  place  in  the  convoluted  and  straight  urinif- 
erous  tubules.  A  good  example  of  the  excretion  of  albumen  through  the 
glomeruli  is  furnished  by  the  experimentally  produced  albuminuria  which 
appears  whenever  the  supply  of  arterial  blood  to  the  kidney  is  checked  by  a 
temporary  constriction  of  the  renal  artery.  The  epithelium  of  the  glomeruli 
thereby  suffers  a  visible  microscopic  change.  If  the  kidneys  in  this  condi- 
tion are  removed  as  rapidly  as  possible  and  boiled,  according  to  Posner's  sug- 
gestion, we  can  discover  under  the  microscope  in  the  capsules  of  the  glomeruli 
the  albumen  that  is  thus  coagulated  (Eibbert) — a  most  certain  sign  that  the 
passage  of  the  albumen  from  the  blood  vessels  into  the  urinary  passages  has 
in  fact  taken  place  in  the  glomeruli.     On  the  other  hand,  we  know  from  the 


728  DISEASES  OF  THE  URINARY  ORGANS 

experiments  of  Senator  that,  in  artificial  venous  .hypersemia,  the  epithelium 
of  the  uriniferous  tubules  suffers  earlier  than  that  of  the  glomeruli.  Finally, 
we  have  the  toxic  nephritis  following  vinylamine  poisoning,  that  has  been 
studied  by  Ehrlich  and  A.  Heinecke,  in  which  the  cortex  of  the  kidney  re- 
mains almost  entirely  intact,  while  the  medullary  pyramids  become  intensely 
diseased.  Here,  also,  most  pronounced  albuminuria  develops.  It  follows  that 
in  the  various  pathological  processes  the  site  of  the  principal  albumen  ex- 
cretion is  probably  not  always  the  same.  We  must  still  believe,  however, 
that,  at  least  in  many  cases,  especially  in  the  many  milder  and  rapidly  dis- 
appearing albuminurias  the  glomerulus  is  the  chief  site  of  the  albumen 
excretion. 

Compared  to  the  changes  in  the  kidney  tissue,  including  its  blood  vessels, 
all  other  factors  no  doubt  play  only  a  secondary  role  in  the  causation  of  albu- 
minuria, although  they  may,  of  course,  have  an  influence  upon  the  quantity 
of  albumen  excreted. 

The  changes  in  the  composition  of  the  blood,  on  which  formerly,  and 
again  by  some  investigators  recently,  great  stress  has  been  laid,  especially 
the  hydrasmia  and  hypalbuminosis  (the  diminished  amount  of  albumen)  of  the 
blood,  have  probably  only  an  indirect  significance,  since  the  nutrition  of  the 
walls  of  the  glomeruli  suffers  from  such  a  faulty  condition  of  the  blood,  and 
this  circumstance  again  influences  the  true  cause  of  elimination  of  the  albu- 
men. The  significance  of  the  blood  pressure  with  regard  to  the  occurrence 
of  albuminuria  was  also  formerly  very  much  overrated.  According  to  the 
older  hypothesis,  it  was  believed  that,  in  an  increase  of  the  blood  pressure,  the 
molecules  of  albumen  in  the  blood  could  be  pressed  through  the  filter  formed 
by  the  membrane  of  the  glomeruli.  This  hypothesis  has  been  disproved,  es- 
pecially by  the  experiments  of  Euneberg;  these  experiments  showed  that,  in 
the  nitration  of  solutions  of  albumen  through  animal  membranes,  a  rise 
in  the  filtration  pressure  was  followed  by  a  decrease,  and  a  fall  in  the  pressure 
by  an  increase  of  percentage  of  albumen  in  the  filtrate.  The  extent  of  the 
albumen  excretion  is  frequently  and  distinctly  affected  by  circulatory  dis- 
turbances. If  the  condition  of  the  kidney  epithelium  suffers  from  the  circu- 
latory disturbances,  albuminuria  frequently  develops  or  is  increased  (vide 
infra,  chapter  on  Congested  Kidney). 

2.    CASTS   AND    OTHER   ABNORMAL   MORPHOLOGICAL   CON- 
STITUENTS   OF   THE   URINE   IN   RENAL   DISEASE 

Besides  albuminuria,  certain  peculiar  morphological  constituents  of  the 
urine,  visible  under  the  microscope,  are  of  especial  importance  for  the  diag- 
nosis of  renal  affections,  namely,  the  urinary  casts,  whose  significance  was  first 
correctly  recognized  by  Henle  in  1842.  These  are  cylindrical  bodies,  whose 
breadth  corresponds  to  the  width  of  the  uriniferous  tubule,  and  whose  length 
only  exceptionally  reaches  a  millimeter,  which  must  be  regarded  in  their 
chemical  nature  as  consisting  mainly  of  a  coagulated  albuminous  substance. 
To  the  latter  circumstance  we  owe  their  old  name  of  "  fibrin  casts,"  or  "  fibrous 
casts,"  a  name  which  is  obsolete,  and  properly  so,  since  the  coagulated  albu- 
minous substance  of  casts  is  certainly  not  identical  with  fibrin. 

Since  the  precise  conditions  of  the  occurrence  and  the  character  of  the 


REMARKS   UPON    THE   PATHOLOGY    OP    RENAL    DISEASE 


729 


Fig.  95. — Different  forms  of  casts,  a.  Hyaline 
cast  with  occasional  granules,  b.  Hyaline  cast 
with  fat  drops  and  granular  cells,  c.  Hyaline 
cast  with  red  blood  corpuscles  attached,  d. 
Hyaline  cast  with  white  blood  corpuscles  at- 
tached, e.  Cast  with  a  large  number  of  fat 
drops. 


renal  casts,  in  the  different  diseases  of  the  kidneys,  will  be  spoken  of  Later, 
we  need  discuss  here  only  the  general  properties,  the  origin  and  the  signifi- 
cance of  casts  (see  Fig.  95). 

1.  Hyaline  Casts. — The  hyaline  casts  are  the  commonest  ami  mosi  im- 
portant form  of  casts,  and,  to  a  certain  extent,  are  the  ground  form  for  dif- 
ferent varieties.  They  are  perfectly 
homogeneous,  clear  as  glass,  color- 
less, soft,  and  flexible.  We  find 
them  either  wide  or  narrow,  some- 
times broken  off  short,  sometimes 
quite  long,  usually  straight,  but  in 
many  cases  partly  curved.  They 
are  easily  stained  with  carmine  or 
gentian  violet.  On  heating  the 
urine  they  are  dissolved,  but  they 
are  quite  resistant  to  acids. 

The  hyaline  casts  are  very  often 
covered  to  a  greater  or  less  extent 
with  all  sorts  of  deposits,  which  are 
usually  affixed  to  the  soft  substance 
of  the  cast  in  the  kidney  itself,  but 
which  may  often  be  attached  to  it 
later.  These  deposits  are  as  fol- 
lows :  First,  red  blood  corpuscles. 
This  condition  is  important,  be- 
cause it  points  with  certainty  to  the  existence  of  hemorrhages  in  the  kid- 
neys themselves.  Second,  of  white  blood  corpuscles.  These  are  often  consid- 
erably swollen,  so  that  we  must  guard  against  mistaking  them  for  epithelium. 
Third,  of  renal  epithelium,  which  may  be  recognized  by  its  size,  its  more 
angular  shape,  and  its  nuclei.  Of  course  we  often  find  the  epithelium  cloudy 
and  granular,  or  shriveled  and  atrophied.  Fourth,  of  fatty  granular  globules 
— that  is,  both  fatty-degenerated  epithelium  and  also  white  blood  corpuscles 
which  are  filled  with  fat  drops  from  the  fatty-degenerated  cells.  Fifth,  of 
little  granular  masses  whose  nature  cannot  always  be  easily  recognized.  They 
are  either  coagulated  granules  of  albumen,  or  fat  drops,  or  urates,  or  bac- 
teria, or,  finally,  granules  of  hematoidin,  which  have  come  from  the  destruc- 
tion of  red  blood  corpuscles,  and  are  usually  easily  recognized  by  their  dark, 
brownish-yellow  color.  Sixth,  we  rarely  find  in  the  casts  drops  like  myelin, 
as  to  whose  precise  significance  nothing  is  known. 

As  to  the  origin  of  hyaline  casts,  despite  many  investigations  the  question 
has  not  been  fully  answered.  Probably  they  are  due  to  the  coagulation  of  the 
excreted  albumen  occasioned  by  the  dying  epithelial  cells  and  the  escaped 
leucocytes. 

Two  factors  are,  therefore,  always  necessary  for  the  formation  of  casts,  viz., 
the  excretion  of  coagulable  albumen  and  the  presence  of  substances  to  pro- 
duce coagulation.  In  this  way  the  fact  is  explained  that  we  sometimes  have 
a  marked  albuminuria  with  only  very  slight  cast  formation.  When,  on  the 
other  hand,  we  observe  casts  in  the  urine  without  albuminuria,  the  casts  are 
usually  not  of  the  ordinary  hyaline  variety,  but  are  some  other  formation  in 


730 


DISEASES   OF   THE    URINARY   ORGANS 


; 


the  uriniferous  tubules.  Besides,  the  number  of  casts  found  in  the  urine  does 
not  always  correspond  to  the  extent  of  their  formation.  In  the  severest  forms 
of  acute  nephritis  almost  all  the  tubules  can  be  plugged  with  casts  which  may- 
be washed  out  into  the  urine  to  only  a  very  slight  degree. 

2.  Epithelial  Casts. — The  epithelial  casts  are  composed  exclusively  of  renal 
epithelium,  although  probably  hyaline  casts  not  infrequently  form  a  basis  to 
which  the  epithelial  cells  adhere.  Epithelial  casts  are  usually  easily 
recognized,  and  always  indicate  an  excessive  desquamation  of  epi- 
thelium in  the  diseased  kidneys.  One  must  be  on  one's  guard,  as 
already  mentioned,  not  to  confound  renal  epithelium  with  swollen 
white  blood  corpuscles.  The  separate  epithelial  cells  and  the  epi- 
thelial casts  may  present  various  changes,  such  as  granular  opacity, 
fatty  degeneration,  and  atrophy. 

3.  Waxy  Casts. — The  so-called  waxy  casts 
are  almost  always  rather  broad  and  usually 
yellowish  colored,  opaque 
casts,  of  evidently  a  much 
tougher  consistence  than 
hyaline  casts.  We  have 
found  them  most  frequent- 
ly in  severe  acute  nephri- 
tis, either  primary  or  sec- 
ondary to  scarlet  fever,  but 
they  also  appear  in  the 
severer  forms  of  chronic 
diffuse  nephritis.  As  to 
their  origin,  we  are  con- 
vinced that  they  certainly  Fig.  97. — Epithelial 
in  many  cases  are  formed  cast.grai  h 
out  of  epithelial  casts. 
The  closely  apposed  renal 
epithelial  cells  degenerate  into  waxy  flakes,  and  gradually  coalesce.  One 
can,  in  fact,  observe  all  stages  of  transition  between  the  epithelial  casts  and 
the  almost  completely  homogeneous  waxy  casts.  Fiirbringer,  therefore,  terms 
waxy  casts  "  metamorphosed,"  and  he  insists,  correctly,  that  they  always 
indicate  severe  disease  of  the  kidnejr. 

4.  Granular  Casts. — A  kind  of  cast  which  is  composed  of  coarse,  yellowish, 
flaky  granules  represents  the  just-mentioned  transition  of  epithelial  casts  into 
waxy  casts.  In  other  cases  the  waxy  casts  are  nothing  but  hyaline  casts  com- 
pletely covered  with  the  above-mentioned  granules  of  various  kinds.  Some- 
times, also,  coagulated  masses  of  albumen  or  granules  of  hematoidin  may 
themselves  be  formed  into  cylindrical  shapes. 

Genuine  blood  casts  are  not  very  frequent.  They  consist  of  coagulated 
blood  and  represent  casts  of  the  renal  canals  into  which  hemorrhage  has  taken 
place. 

Casts  in  Diagnosis. — The  clinical  diagnostic  significance  of  renal  casts  is 
very  great.  They  are,  in  the  first  place,  always  a  sure  sign  of  the  existence 
of  some  renal  disease,  since  in  normal  urine  casts  are  not  found  at  all,  or,  at 
most,  they  are  exceptional  and  are  present  in  small  numbers.     The  consider- 


Fig.  96. — a.  Waxy  cast.  b.  Waxy  cast 
bearing  crystals  of  calcic  oxalate. 
c.  Fragments  of  waxy  casts.  (From 
von  Jaksch.) 


lower  half.    (From 
von  Jaksch.) 


REMARKS   UPON   THE   PATHOLOGY  OF  RENAL   DISEASE         731 

ation  of  the  special  forms  of  casts,  and  of  the  deposit  upon  them,  is  also  of 
great  diagnostic  importance,  although  from  it  we  can  never  decide  imme- 
diately upon  the  general  form  of  the  renal  disease,  hut  we  can  recognize  with 
certainty  the  type  of  special  pathological  processes  in  the  kidneys.  Frerichs 
has  well  named  casts  "  messengers  from  the  kidneys."  The  hlood  casts  and 
the  red  blood  corpuscles  sticking  to  the  cylinders  point  to  the  occurrence  of 
renal  hemorrhages;  the  epithelial  casts  to  a  desquamation  of  the  epithelium 
in  the  kidneys;  the  white  blood  corpuscles  to  an  emigration  of  the  colorless 
cells  from  the  vessels ;  the  fatty  granular  cells  to  processes  of  fatty  degeneration 
in  the  kidneys. 

We  have  already  learned  to  recognize  in  a  great  measure  in  the  preceding, 
as  occasional  deposits  on  the  casts,  the  other  morphological  constituents  found, 
besides  the  casts,  in  the  sediment  of  the  urine  in  renal  disease.  Briefly  reca- 
pitulated, they  are  as  follows : 

1.  Red  blood  corpuscles.  The  presence  of  a  large  amount  of  blood  in  the 
urine  (hematuria)  is  almost  always  to  be  recognized  by  its  blood-red  color. 
The  blood  may  be  made  out  with  certainty  by  the  microscope,  or  by  Heller's 
blood  test.  The  latter  is  performed  by  heating  the  urine  in  a  test-tube  with 
sodic  or  potassic  hydrate.  The  blood  corpuscles  are  thus  dissolved,  and  the 
hematin  formed  from  the  blood  pigment  is  precipitated  with  the  phosphates, 
giving  to  the  precipitate  of  the  latter  a  very  characeristic  blood-red  color. 
Van  Deen's  test  is  very  distinct  and  easily  performed.  It  requires  a  freshly 
prepared  mixture  of  equal  parts  of  old  oil  of  turpentine  and  newly  made 
tincture  of  guaiac.  This  mixture  is  poured  upon  the  urine  to  be  examined, 
and  slightly  shaken.  At  the  place  of  contact  of  the  two  fluids  there  will  im- 
mediately form  a  beautiful  blue  ring,  if  there  is  the  slightest  trace  of  blood 
in  the  urine.  It  is  important  to  know,  however,  that  urine  containing  pus 
also  reacts  positively  with  the  guaiac  test.  Finally,  of  course,  the  spectro- 
scope may  serve  for  the  detection  of  hematuria.  Hemoglobinuria  will  be  de- 
scribed in  a  special  chapter  later. 

2.  White  blood  corpuscles.  Only  when  they  are  also  attached  to  the  casts 
can  we  assume  with  certainty  that  these  come  from  the  kidneys,  and  not  from 
the  lower  portions  of  the  urinary  tract. 

3.  Renal  epithelium. 

4.  Fat  drops  and  fatty  granular  cells. 

5.  Uric-acid  crystals,  urates  and  calcic  oxalate,  bacteria,  etc. 

For  microscopic  examination  of  the  urinary  sediment,  we  let  the  urine  set- 
tle in  a  tall  beaker ;  it  is  more  convenient,  and,  if  the  urine  contains  few  mor- 
phological constituents,  far  more  reliable  to  employ  a  centrifugal  machine. 

3.     THE   DROPSY   OF   RENAL   DISEASE 

Although  the  changes  in  the  urine  must  be  alone  decisive  in  the  diagnosis 
of  any  renal  disease,  there  are  yet  certain  other  symptoms  which  are  also  due 
immediately  to  the  renal  affection,  and  which  may  first  direct  our  suspicions  to 
the  existence  of  a  disease  of  the  kidneys,  and  consequently  lead  to  a  careful 
examination  of  the  urine.  Among  these  symptoms  the  dropsy  of  renal  disease 
is  one  of  the  commonest  and  most  important.  Every  trace  of  oedema  may, 
indeed,  quite  frequently  be  entirely  absent,  both  in  acute  and  chronic  nephritis, 


732  DISEASES   OF   THE   URINARY   ORGANS 

and  in  other  diseases  of  the  kidneys ;  but  in  many  cases  the  dropsy  is  decidedly 
prominent  in  the  whole  clinical  picture. 

iEtiology  and  Pathology. — If  we  ask  what  is  the  reason  of  the  frequent 
occurrence  of  dropsy  in  renal  disease,  the  answer  at  first  does  not  seem  dif- 
ficult. Since  the  main  function  of  the  kidneys  is  to  excrete  water  from  the 
body,  and  since,  as  we  shall  see  later,  in  many  cases  the  diseased  kidney  can 
no  longer  fulfill  this  task,  or  can  fulfill  it  only  to  a  slight  degree,  we  are  not, 
in  fact,  very  much  out  of  the  way  in  considering  the  retention  of  water  in  the 
body  as  the  main  cause  of  the  consequent  cedema.  Clinical  observation  seems 
in  general  to  agree  completely  with  this  assumption.  The  cedema  in  renal 
disease  seldom  appears  until  the  daily  amount  of  urine  has  been  below  the 
normal  for  some  time,  while,  on  the  other  hand,  in  those  cases  where  the 
amount  of  urine  passed  is  normal,  or  even  abnormally  great,  in  spite  of  the 
existing  renal  disease,  cedema  is  wholly  absent.  In  individual  cases,  too,  we 
very  often  see  a  decrease  of  the  cedema  associated  with  an  increase  in  the 
amount  of  urine,  and  an  increase  of  the  cedema  associated  with  a  correspond- 
ing diminution  in  the  excretion  of  urine.  The  pathological  process  accord- 
ingly seems  to  consist  of  an  accumulation  in  the  body  of  the  water  which 
cannot  be  excreted  from  it,  and  which  transudes  from  the  vessels  and  thus, 
gives  rise  to  the  development  of  cedema. 

On  more  careful  consideration,  however,  there  are  some  objections  to  this 
theory,  which  is  apparently  so  simple.  In  the  first  place,  it  might  be  supposed 
that,  when  there  is  retention  of  water,  the  body  must  get  rid  of  the  surplus 
water  by  employing  to  a  greater  degree  the  other  channels  of  elimination 
which  are  at  its  service — the  skin  and  the  intestines.  Since  we  can  never 
determine  accurately  the  time  when  the  water  first  begins  to  be  retained  in 
the  body,  the  clinical  experience  just  mentioned  may  also  be  thus  interpreted,, 
that  the  lessened  excretion  of  urine  is  not  the  cause  of  the  cedema,  but  that, 
on  the  contrary,  the  appearance  of  cedema  is  rather  the  cause  of  the  diminished 
elimination  of  water  by  the  kidneys.  The  other  clinical  facts,  also,  are  incon- 
sistent with  the  view  that  the  oedema  depends  upon  the  simple  accumulation 
of  water  in  the  blood.  In  many  forms  of  nephritis,  and  particularly  in  the 
nephritis  of  scarlet  fever,  we  very  often  see  extreme  cedema  appear  suddenly, 
while,  on  the  other  hand,  many  severe  varieties  of  nephritis — e.  g.,  those  asso- 
ciated with  diphtheria,  septic  diseases,  and  pneumonia,  run  their  course  with 
little  or  no  cedema,  although  they  are  characterized  by  a  marked  diminution 
in  the  amount  of  urine.  Moreover,  cases  have  been  repeatedly  observed  in 
which,  as  a  result  of  obstruction  of  the  ureters,  or  from  pressure  on  these 
canals,  there  has  been  complete  anuria  for  several  days  without  a  trace  of 
cedema  developing;  and  experimental  investigations  have  given  corresponding 
results.  The  bilateral  ligation  of  the  ureters  in  animals  does  not  lead  to  the 
development  of  cedema  even  after  several  days.  Cohnheim  and  Lichtheim 
introduced  large  amounts  of  a  one-half  to  one-per-cent  solution  of  common 
salt  into  the  vascular  system  of  an  animal,  and  despite  this  great  artificial 
"  hydremic  plethora,"  observed  no  cedema,  even  when  the  renal  arteries  were 
tied.  Nor  can  cedema  be  provoked  by  slow  and  continuous  infusion  (Gartner,, 
Francotte). 

Consequently,  we  must  seek  some  other  cause  to  explain  the  cedema  of 
nephritis,  and  this  is  in  all  probability  the  peculiar  change  in  the  vascular 


REMARKS   UPON   THE   PATHOLOGY   OF   RENAL   DISEASE         733 

walls,  which  renders  them  more  permeable  and  permits  the  water  accumulated 
in  the  blood  to  transude  into  the  tissues.  Just  what  this  change  in  the  vas- 
cular walls  may  be  and  what  produces  it  we  do  not  yet  know;  probably  there 
are  chemical  agents  which  change  the  vascular  walls,  either  the  same  sub- 
stances which  excite  the  nephritis,  or  matters  secondarily  formed,  or  certain 
products  of  tissue  metabolism  retained  in  the  blood  because  of  the  inefficiency 
of  the  kidneys.  This  explains  why  certain  forms  of  nephritis  produce  pro- 
nounced cedema  and  others  do  not.  In  experimental  nephritis,  the  occurrence 
of  cedema  is  also  dependent  upon  special  circumstances.  Certain  kidney  poi- 
sons (chromium  salts,  cantharides,  etc.)  always  produce  a  nephritis  without 
cedema,  while,  on  the  other  hand,  the  nephritis  produced  by  uranium  salts 
is  almost  always  associated  with  pronounced  cedema.  In  the  blood  serum  of 
animals  poisoned  with  uranium  a  substance  is  present  that  causes  cedema. 
If  a  chromium  nephritis  is  produced  in  an  animal,  and  this  animal  is  injected 
with  blood  serum,  or  cedematous  fluid  of  an  animal  suffering  from  an  uranium 
nephritis,  an  cedema  will  follow  (A.  Heineke).  The  role  played  by  changes 
in  the  osmotic  tension  of  the  blood  and  tissues  in  the  development  of  cedema 
is  not  yet  perfectly  clear.  Especial  weight  has  been  laid  on  the  not  infre- 
quently observed  diminution  of  the  sodium  chlorid  excretion  (H.  Strauss)  in 
nephritics.  The  consequent  increase  of  the  sodium  chlorid  in  the  blood  serum 
may  lead  to  an  increased  passage  of  that  salt  into  the  tissues,  with  a  corre- 
sponding exudation  of  water. 

That  dropsy  develops  because  of  direct  damage  to  the  blood  vessels  is  ren- 
dered probable  from  the  cases  of  so-called ""  acute  essential  dropsy,"  in  which 
there  develops  a  considerable  general  dropsy,  just  as  in  acute  nephritis,  often 
preceded  by  mild  gastrointestinal  symptoms,  and  yet  without  a  trace  of  al- 
bumen in  the  urine  or  any  other  demonstrable  cause  for  this  dropsy,  which 
usually  soon  abates. 

Many  clinical  peculiarities  of  nephritic  oedema  harmonize  with  this  con- 
ception of  its  origin.  In  general,  we  may  say  that  the  cedema  of  nephritic 
patients  appears  first  in  the  skin  ("anasarca"),  and  has  a  striking  tendency 
to  show  first  in  the  face,  in  contrast  with  the  cedema  due  to  the  passive  con- 
gestion of  heart  disease,  which  usually  begins  in  the  ankles.  The  puffy  and 
noticeably  pale  countenance  of  the  patient  will  often  suggest  the  existence  of 
kidney  trouble  at  the  first  glance.  In  severe  cases  the  dropsy  often  develops 
over  the  whole  body  in  an  extreme  degree,  involving  the  skin  of  the  trunk, 
and  particularly  the  dependent  parts,  the  extremities  and  scrotum,  so  that 
the  patient  is  a  pitiable  object.  In  such  cases  there  are  also  apt  to  be  dropsical 
transudations  into  the  internal  cavities  of  the  body,  causing  hydrothorax, 
ascites,  and  hydropericardium ;  and  these  aggravate  the  patient's  distress.  It 
is,  however,  a  striking  fact  that  often  there  will  be  marked  dropsical  effusions 
(ascites,  hydrothorax),  and  yet  no  marked  cedema  of  the  skin;  and  hydro- 
thorax  is  sometime^  much  greater  on  one  side  than  on  the  other.  All  these 
facts  indicate  special  local  conditions — viz.,  the  changes  in  the  blood  vessels, 
which  we  have  surmised.  Still  more  is  this  the  case  with  regard  to  the  cedema 
of  mucous  membranes  which  sometimes  occurs.  There  may  be  cedema  of 
the  conjunctiva,  of  the  soft  palate,  of  the  aryepiglottic  ligaments  (cedema  of 
the  glottis),  and  other  parts.  (Edema  of  this  sort  is  apt  to  resemble  a  mild 
local  inflammation,  and  in  general  it  is  impossible  to  deny  a  certain  relation- 


734  DISEASES   OF  THE   URINARY  ORGANS 

ship  between  "  inflammatory  "  oedema  and  nephritic  oedema.  The  nephritic 
oedema  of  the  skin  may  in  places  have  suggestions  of  an  inflammatory  nature, 
such  as  slight  redness  and  tenderness.  (Edema  may  affect  the  internal  organs, 
and  nephritic  pulmonary  oedema  is  of  great  practical  importance.  The  ques- 
tion of  the  existence  of  cerebral  oedema  and  of  its  possible  importance  will  be 
discussed  below  (see  uraemia). 

The  preceding  remarks  relate  only  to  genuine  nephritic  oedema.  We  shall 
see  later  that  oedema  may  have  an  entirely  different  origin,  particularly  in 
cases  of  chronic  nephritis — that  is,  if  there  is  a  cardiac  hypertrophy  and  the 
powers  of  the  heart  become  impaired,  dropsy  may  at  last  develop.  This  oedema 
is,  of  course,  a  genuine  congestive  oedema,  and  exactly  similar  to  that  seen  in 
failing  compensation  in  heart  disease. 

In  its  chemical  composition,  the  dropsical  fluid  corresponds  to  a  very  thin 
blood  serum.  The  amount  of  water  is  usually  ninety-seven  to  ninety-eight  per 
cent.  The  amount  of  albumen  is  usually  very  slight,  while  the  percentage  of 
sodium  chlorid  (one  to  one  and  a  half  per  cent)  is  always  somewhat  higher 
than  in  the  blood  serum.  This  fact  indicates  an  active  participation  of  the  ves- 
sel walls  in  the  formation  of  the  oedema.  The  high  sodium-chlorid  percentage 
of  the  oedema  fluid  is  connected  with  the  disability  of  the  diseased  kidney  to 
excrete  all  of  that  salt  which  is  brought  to  it  (vide  infra).  In  this  way  the 
body  maintains  the  necessary  normal  sodium-chlorid  content  of  its  blood. 
An  increased  intake  can  therefore  under  certain  conditions  lead  to  an  increase 
of  the  oedema. 

4.    URiEMIA 

If  the  diseased  kidneys  can  no  longer  perform  their  secretory  functions  in 
a  satisfactory  way,  not  only  does  the  elimination  of  water  from  the  body  thereby 
suffer,  but  the  soluble  constituents  of  the  urine,  the  salts,  the  urea,  and  the 
other  final  products  of  tissue  metamorphosis  may  also  be  retained  in  the  blood 
and  accumulate  there.  Hence  we  often  find  the  blood,  in  patients  with  renal 
disease,  not  only  more  watery  than  under  normal  conditions,  so  that  the  specific 
gravity  of  the  serum  may  fall  from  1.030  to  1.020,  or  even  lower,  but,  in  almost 
all  cases  where  there  is  a  diminished  excretion  of  urine,  it  is  also  richer  in 
urea,  as  many  experiments  have  shown,  and  under  corresponding  conditions 
it  is  probably  also  frequently  richer  in  the  other  constituents  of  the  urine,  or 
in  substances  corresponding  to  them,  but  not  completely  metamorphosed. 

This  accumulation  of  the  urinary  constituents  in  the  blood  and,  further, 
perhaps  in  the  tissues  themselves,  is  the  cause  of  a  class  of  symptoms  which 
are  often  seen  in  diseases  of  the  kidneys,  and  which  are  termed  uraemic  symp- 
toms or  uraemia. 

iEtiology  and  Pathology. — Probably  no  one  to-day  doubts  that  uraemia 
must  be  regarded  as  essentially  an  intoxication  of  the  body  by  the  retained 
products  of  tissue  metamorphosis.  Numerous  experimental  investigations 
have  proved  that  in  animals  extirpation  of  the  kidneys,  or  ligation  of  the 
nreters,  will  produce  a  symptom-complex,  characterized  by  vomiting,  convul- 
sions, and  coma,  completely  analogous  to  the  uraemia  of  Bright's  disease; 
but  if  we  inquire  what  constituents  of  the  urine  are  the  particular  occasion 
of  the  uraemic  phenomena,  we  cannot  as  yet  obtain  any  definite  answer.  For 
a  long  time  it  was  believed  that  urea  played  a  chief  part  in  the  development 


REMARKS   UPON   THE   PATHOLOGY  OF   RENAL   DISEASE         735 

of  uraemia,  but  the  result  of  experiments  upon  animals  does  not  support  this 
view.  It  is  possible  to  inject  enormous  amounts  of  urea  into  the  circulation 
or  into  the  peritoneal  cavity  of  animals  without  any  symptoms  of  poisoning. 
Voit  did,  indeed,  show  that  the  healthy  kidneys  remove  from  the  blood  the 
excessive  amount  of  urea  with  extreme  rapidity,  and  that  accordingly  uraemic 
symptoms  do  really  appear  if,  while  we  are  feeding  an  animal  with  large 
amounts  of  urea,  we  impede  the  .excretion  of  the  urea  by  a  simultaneous  with- 
holding of  water.  Yet  the  amount  of  urea  necessary  for  the  success  of  this 
experiment  is  greater  than  can  possibly  exist  in  the  ordinary  uraemia  of 
Bright's  disease,  and,  moreover,  the  withholding  of  water  might  also  prevent 
the  excretion  of  other  matters.  The  hypothesis  of  Frerichs,  accepted  in  many 
quarters  for  a  time,  has  also  been  universally  discarded.  He  assumed  that 
through  fermentation  the  urea  in  the  blood  of  nephritics  was  converted  into 
carbonate  of  ammonia.  Hence  we  must  seek  for  other  poisonous  substances 
as  factors  in  the  production  of  uraemia.  Many  experiments  seem  to  indicate 
that  the  potassium  salts  are  poisonous,  while  some  authors  have  laid  the  blame 
mainly  on  the  extractive  matters,  such  as  creatinin.  Bouchard  has  sought  to 
prove  that  certain  alkaloid  substances  (urotoxins),  which  are  presumably  de- 
veloped during  the  digestion  of  albumens  and  are  always  demonstrable  in 
normal  urine,  occasion  the  phenomena  of  uraemia,  while  other  authors  (Ascoli 
and  others)  speak  of  special  poisons,  the  product  of  disintegration  of  the  tis- 
sues ( "  nephrolysin,"  "nephrotoxin").  At  any  rate  the  fact  is  worthy  of 
note  that  the  suppression  of  the  urinary  excretion  in  kidneys  that  are  other- 
wise healthy — for  instance,  in  obstruction  of  the  ureter  by  an  impacted  cal- 
culus— may  be  tolerated  many  days  without  the  occurrence  of  uraemia.  It 
would  thus  seem  that  there  are  still  certain  factors  in  the  kidney  disease,  as 
such,  which  must  be  considered  in  the  development  of  the  uraemic  phenomena. 
In  accordance  with  certain  modern  views  regarding  the  significance  of  the 
so-called  internal  secretions,  some  investigators  also  assume  an  "  internal  se- 
cretion "  from  the  kidneys  into  the  blood,  and  believe  that  the  uraemia  can 
be  traced  to  a  disturbance  of  this  function  somewhat  analogous  to  similar  oc- 
currences iu  diseases  of  the  liver,  the  thyroid  gland,  and  the  suprarenal  s.  But 
against  all  of  these  hypotheses  objections  may  be  offered,  so  that  the  question 
of  the  more  exact  nature  of  the  products  which  occasion  uraemic  intoxication 
must  still  be  regarded  as  unsolved.  The  newer  physico-chemical  examinations 
of  the  blood  have  likewise  given  no  certain  solution.  The  molecular  concen- 
tration of  the  blood  is  naturally  usually  increased  without,  however,  the  exist- 
ence of  a  regular  parallelism  between  the  severity  of  the  uraemic  symptoms 
and  the  degree  of  the  retention.  The  electric  conductivity  of  the  blood  is  not 
increased  in  uraemia,  which  would  indicate  that  the  inorganic  blood  salts  do 
not  play  any  causative  role.  From  the  chemical  standpoint,  an  increase  in 
the  so-called  residual  nitrogen  (i.  e.,  the  nitrogen  remaining  in  the  blood  after 
the  complete  precipitation  of  albumen)  is  of  significance,  as  from  this  we 
might  suspect  that  it  is  the  nitrogenous  decomposition  products  of  albumen 
which  produce  the  uraemic  poisoning.  It  is  not  impossible  that,  after  all,  a 
number  of  substances  come  into  play. 

The  mode  of  action  of  the  toxic  material  is  as  unsettled  as  is  its  chemical 
nature.  This  much  only  is  certain,  that  in  uraemia  the  disturbances  are  almost 
exclusively  cerebral,  and  in  the  main  located  in  the  cortex  of  the  brain;  but 


736  DISEASES   OF   THE   URINARY  ORGANS 

whether  there  is  actually  a  direct  injury  of  the  nervous  elements,  or  whether 
the  immediate  action  is  upon  the  blood  vessels  (spasm),  is  uncertain.  The 
occurrence  of  ursemic  focal  symptoms,  to  which  we  shall  refer  below,  renders 
the  former  supposition  the  more  likely. 

Clinical  experience  agrees  perfectly  with  the  theory  that  ursemia  is  caused 
by  a  retention  of  urinary  constituents  in  the  body.  In  most  cases  the  ursemic 
symptoms  appear  only  when  the  daily  amount  of  urine  has  fallen  to  a  very  low 
figure,  or  when  the  secretion  of  urine  has  wholly  ceased  for  several  days.  That 
in  these  cases  not  only  the  elimination  of  water,  but  also  the  elimination  of 
the  other  urinary  constituents,  is  very  much  diminished,  is  shown  by  experi- 
ments made  in  regard  to  this  point. 

Of  course  there  can  be  no  question  that  some  clinical  facts  cannot  be' 
brought  into  exact  harmony  with  what  has  been  previously  said.  If  cases  are' 
repeatedly  reported  in  which  no  ursemic  symptoms  have  appeared  in  spite  of 
anuria  lasting  several  days,  it  does  not  prove  very  much,  since  we  can  never 
make  an  exact  estimate  of  the  matter  accumulated  in  the  blood  which  ought 
to  have  been  eliminated;  for  the  organism  can  certainly  get  rid  of  the  final 
products  of  tissue  metamorphosis  in  other  ways  than  through  the  kidneys — 
for  instance,  through  the  skin,  the  intestines,  or  the  fluid  of  oedema — and  we 
must  also  bear  in  mind  that  different  individuals  show  a  great  diversity  in 
tolerating  the  action  of  any  poison  in  the  body,  particularly  as  regards  the 
nervous  system.  It  is  harder  to  explain  those  cases  which  are  sometimes  seen,, 
in  which  ursemic  symptoms  suddenly  appear  in  patients  with  renal  disease, 
although  these  symptoms  are  not  preceded  by  any  noticeable  diminution  of 
the  secretion  of  urine.  We  may,  however,  assume  that,  despite  the  abundant 
excretion  of  water  and  the  normal  amount  of  urine,  there  has  been  a  slight 
retention  of  solid  matters.  Analogy  with  other  kinds  of  poisoning  makes  the' 
supposition  very  plausible  that  the  long-persistent  retention  of  even  extremely 
small  portions  of  toxic  matter  may  occasion  an  absolutely  sudden  explosion 
of  the  severest  symptoms.  In  chronic  lead  and  mercurial  poisoning  the  symp- 
toms often  appear  with  great  abruptness,  although  the  poisoning  has  taken 
place  very  slowly  and  gradually.  In  the  same  way  we  explain  to  ourselves  the 
not  very  infrequent  cases  of  the  sudden  development  of  severe  urasmic  symp- 
toms, as  seen  particularly  in  patients  with  contracted  kidney  (vide  infra),  in 
whom  it  may  seem  as  if  no  single  prodromal  symptoms  had  indicated  the 
impending  outburst  of  intoxication.  Often,  also,  peculiar  circumstances  may 
favor  the  occurrence  of  ursemia;  for  example,  the  development  of  cardiac 
weakness,  so  that  the  blood  tension  is  diminished  and  the  excretion  of  urine 
impeded.  In  some  cases  again  it  is  observed  that  the  development  of  ursemia 
coincides  with  the  absorption  of  previously  existing  oedema.  This  is  explained 
by  the  supposition  that  the  rapid  absorption  of  the  oedema  introduces  into  the 
blood  a  comparatively  large  amount  of  the  poisonous  products  of  metabolism, 
which  had  not  been  excreted,  but  had  been  contained  in  the  oedematous  fluid. 

While  we  are  firmly  of  the  opinion  that  urasmia  is  to  be  regarded  as  a 
poisoning  of  the  body  by  the  retained  constituents  of  the  urine,  yet  we  should 
not  fail  to  mention  that  attempts  have  been  made  to  explain  in  other  ways 
the  ursemic  phenomena.  In  particular,  Traube  has  propounded  the  theory 
that  the  so-called  ursemic  symptoms  are  dependent  upon  an  acutely  developing 
cerebral  oedema,  and  consequent  cerebral  ansemia.    This  theory  can  be  regarded 


REMARKS   UPON   THE   PATHOLOGY   OF   RENAL   DISEASE         737 

as,  on  the  whole,  untenable.  Still,  it  may  contain  a  certain  amount  of  truth, 
for  we  cannot  wholly  deny  that  sometimes  there  may  be  actual  anatomical 
lesions,  such  as  inflammatory  oedema  of  the  brain,  in  the  course  of  a  nephri 
sufficient  to  occasion  severe  cerebral  symptoms.  During  nephritis  secondary 
inflammation  may  appear  in  almost  all  the  internal  organs,  and  often  sud- 
denly; and  this  sort  of  nephritic  inflammation  is  especially  frequent  in  the 
retina,  a  structure  composed  of  nervous  elements,  so  that  the  possibility  of 
similar  disease  in  the  brain  is  very  great.  If  we  consider  that  cases  of  uraemic 
hemiplegia  and  monoplegia  have  been  repeatedly  observed,  and  that  likewise 
cases  have  been  described  of  urgemic  Jacksonian  epilepsy,  hemianopsia,  and 
aphasia,  it  will  be  seen  that  the  supposition  of  an  actual  local  lesion  as  the 
explanation  of  such  well-marked  focal  symptoms  is  very  plausible.  Yet  we 
must  also  consider  that  in  the  last  analysis  the  cause  of  such  limited  cedem- 
atous — or  inflammatory-cedematous — changes  in  the  brain  is  to  be  sought  in 
the  action  of  some  retained  products  of  metamorphosis. 

Symptoms. — In  regard  to  the  clinical  symptoms  of  uraemia  in  the  indi- 
vidual case,  they  show  all  possible  transitions,  from  the  mildest  symptoms, 
which  are  only  intimated,  up  to  the  severest  nervous  symptoms,  which  may 
be  the  immediate  cause  of  death.  The  severe  forms  of  uraemia  may  sometimes 
come  on  quite  suddenly,  while  in  other  cases  they  may  be  preceded  for  a  long 
time  by  milder  uraemic  symptoms,  which  are  then  termed  prodromata.  The 
severest  symptoms  may  not  appear  at  all,  and  the  milder  sjnnptoms  may  exist 
alone  for  a  longer  or  shorter  time.  This  latter  condition  is  called  chronic 
uraemia. 

The  milder  ursemic  symptoms,  which  are  observed  either  alone  or  as  pre- 
cursors or  as  sequela?  of  severe  uraamia,  consist  of  headache,  somnolence,  and 
mental  stupor;  of  a  peculiar  uneasiness,  or  of  a  feeling  of  anxiety  and  con- 
straint (sometimes  associated  with  hurried  respiration),  and  very  often  of 
nausea,  spasmodic  eructations,  and  repeated  vomiting  (vide  infra).  Very 
characteristic  of  uraemic  intoxication  are  signs  of  motor  irritation,  especially 
isolated,  brief  twitchings,  or  even  persistent  tonic  rigidity  of  the  extremities 
or  face.  Signs  of  sensory  irritation,  formication  and  numbness  of  the  fingers, 
and  also  particularly  an  annoying,  persistent  itching  of  the  skin  (vide  infra) 
are  not  uncommon.  Among  the  symptoms  of  this  milder  form  of  uraemia, 
besides  the  vomiting,  we  would  place  the  peculiar  restlessness  and  praecordial 
distress  of  patients  as  especially  important.  Not  infrequently  observers  use 
the  term  uraemic  asthma  (vide  infra). 

The  most  characteristic  symptom  of  severe  uraemia  is  the  uraemic  convul- 
sion. It  corresponds  almost  exactly  in  its  details  to  an  epileptic  attack;  it 
usually  begins  with  a  short  tonic  stage,  in  which  the  whole  body  is  generally 
in  a  position  of  extension  in  opisthotonos,  and  then  follow  vigorous  clonic  con- 
tractions in  the  face  and  extremities.  The  face  becomes  cyanotic,  a  bloody 
froth  comes  from  the  mouth,  the  pupils  are  usually  dilated  and  almost  without 
reaction,  the  respiration  is  accelerated  (but  at  times  it  is  intermittent  from 
spasm  of  the  respiratory  muscles),  the  pulse  is  small  and  accelerated,  and  it 
can  scarcely  be  felt  in  the  radial  artery,  and  the  temperature  is  sometimes 
raised.  In  other  cases  the  spasm  begins  with  short,  jerky  contractions  in  one 
extremity,  as  in  the  arm,  and  then  invades  the  trunk  muscles,  the  face,  and 
the  legs.     One  half  the  body  is  often  more  affected  in  the  attacks  than  the 


738  DISEASES   OF   THE   URINARY   ORGANS 

other.  The  spasms  usually  cease  in  a  few  minutes,  and  are  followed  by  deep 
coma  and  stertor,  or  even  Cheyne-Stokes'  breathing,  which  last  for  several 
hours  or  more.  There  is  only  rarely  a  single  attack.  The  attacks  are  much 
oftener  repeated  after  longer  or  shorter  intervals,  so  that  there  may  even  be 
twenty  or  more  in  the  twenty-four  hours,  during  the  whole  of  which  time  a 
complete  loss  of  consciousness  persists.  Severe  and  fully  developed  epilepti- 
form attacks  often  alternate  with  slighter  convulsions. 

Some  other  uraemic  symptoms,  besides  the  convulsions,  which  have  already 
been  briefly  mentioned,  merit  a  somewhat  fuller  description. 

The  uraemic  amaurosis  occasionally  seen  is  especially  interesting.  It  is 
usually  left  after  recovery  from  the  convulsions.  Only  rarely  does  it  precede 
them  or  appear  without  them.  It  always  develops  quite  rapidly,  so  that  the 
first  disturbance  of  vision  soon  passes  into  complete  blindness.  The  reaction 
of  the  pupils  to  light  is  almost  always  retained,  and  the  ophthalmoscope  shows 
a  perfectly  normal  retinal  image.  At  what  spot  in  the  visual  apparatus  the 
lesion  is  situated  is  not  yet  known.  Many  investigators  assume  that  there  is 
an  oedema  of  the  sheath  of  the  optic  nerve ;  while  others,  including  the  author, 
think  it  more  probable  that  there  is  disturbance  of  the  cerebral  visual  centers, 
and  particularly  of  the  occipital  cortex. 

Its  prognosis  is,  on  the  whole,  favorable,  since  the  disturbance  of  vision 
usually  disappears  completely  in  a  day  or  two,  though  sometimes  not  until 
after  a  longer  time.  Anomalies  are  only  rarely  seen  in  the  domain  of  the 
other  nerves  of  special  sense,  the  most  frequent,  comparatively,  being  a  diffi- 
culty in  hearing,  or  even  complete  deafness. 

Other  motor  disturbances,  except  twitchings  and  convulsions,  are  rare. 
Only  in  a  few  cases  have  hemiplegic  or  monoplegic  paralyses,  contractures,, 
trembling,  etc.,  been  observed.  Mental  symptoms  are  more  common.  De- 
lirium, and  maniacal  or  sometimes  melancholic  states,  occasionally  follow 
uraemic  coma. 

Those  ursemic  symptoms  also  have  a  great  interest  which  are  to  be  re- 
garded as  a  sort  of  self-help  on  the  part  of  the  organism,  since  they  often  lead 
to  a  vicarious  elimination  of  urea  and  presumably  of  the  other  products  of 
tissue  metamorphosis.  The  first  of  these  is  uraemic  vomiting,  which  is  a  fre- 
quent and  often  an  extremely  obstinate  symptom  both  in  acute  and  chronic 
uraemia.  In  many  cases  it  is  of  central  origin,  and  is  to  be  regarded  as  anal- 
ogous to  the  vomiting  so  frequent  in  different  forms  of  cerebral  disease;  but 
it  is  often  produced  by  the  irritation  which  the  gastric  mucous  membrane 
suffers  from  the  urea  eliminated,  or  rather  from  the  carbonate  of  ammonium 
arising  from  it.  The  latter  is  always  first  formed  from  the  urea  in  the  stomach 
itself,  and  we  find  in  the  vomitus  of  uraemic  patients  either  the  still  unde- 
composed  urea  or  the  carbonate  of  ammonium  in  considerable  quantities. 
Sometimes  there  is  quite  a  violent  hiccough  besides  the  vomiting. 

Uraemic  diarrhea  has  the  same  significance  as  uraemic  vomiting.  It  is  usu- 
ally provoked  by  the  carbonate  of  ammonium  arising  from  the  urea  in  the 
intestines.  The  former  often  causes  quite  a  severe  catarrhal,  and  even  at  times 
a  diphtheritic,  inflammation  of  the  intestinal  mucous  membrane. 

Another  way  in  which  the  organism  sometimes  tries  to  get  rid  of  the 
large  amount  of  urea  accumulated  in  it  is  by  the  sweat  glands.  Schottin  first 
described  the  remarkable  discovery  of  a  coating  of  urea  on  the  skin  in  the 


REMARKS   UPON   THE   PATHOLOGY   OF   RENAL   DISEASE         739 

uraemia  of  cholera,  an  observation  which  since  then  has  been  repeatedly  con- 
firmed in  other  cases  of  uraemia.  This  coating  is  most  frequently  seen  on  the 
face,  especially  on  the  sides  of  the  nose,  to  which  little  faintly  lustrous  scales 
are  seen  sticking  after  the  evaporation  of  a  clammy  sweat.  Chemical  exam- 
ination shows  that  these  scales  are  urea.  The  excretion  of  urea  is  much  more 
rare  in  other  parts  of  the  skin,  but  perhaps  the  occasional  severe  uraemic  itch- 
ing of  the  skin  is  due  to  an  irritation  of  the  cutaneous  nerves  by  some  of  the 
constituents  of  the  urine  that  are  excreted. 

Other  organs  besides  the  skin  and  the  digestive  tract  are  but  rarely  to  be 
considered  as  a  means  of  the  vicarious  elimination  of  urea,  but  Fleischer  was 
once  able  to  discover  considerable  amounts  of  urea  in  the  saliva  and  sputum 
of  a  uraemic  patient. 

In  conclusion,  we  must  describe  the  condition  of  the  pulse,  of  the  tem- 
perature, and  of  the  respiration  in  uraemia.  The  pulse  is  often  very  slow 
before  the  appearance  of  severe  symptoms,  sometimes  48  or  40,  but  it  is 
almost  always  tense  and  hard.  In  chronic  uraemia,  also,  a  moderate  slowness 
of  the  pulse  is  not  infrequent.  When  uraemic  convulsions  appear,  however, 
the  pulse  usually  becomes  small  and  very  frequent,  especially  in  cases  that 
terminate  unfavorably.  The  temperature  but  rarely  remains  unchanged  in 
severe  uraemia.  If  there  are  convulsions,  it  usually  rises  several  degrees,  in 
severe  cases  even  to  106°  or  108°  F.  (41°  to  42°  C).  We  have  seen  these 
high  temperatures,  especially,  as  a  terminal  rise  with  an  unfavorable  issue, 
although  there  may  sometimes  be  an  improvement  even  in  such  cases.  On 
the  other  hand,  there  are  also  great  declines  in  temperature,  down  to  93°  or 
91°  F.  (34°  to  33°  C),  most  frequently  again  as  a  terminal  temperature  of 
collapse,  in  cases  which  end  in  deep  coma  without  marked  symptoms  of  motor 
irritation.  We  might  also  mention  the  "  uraemic  chills  "  which  we  have  seen 
several  times — that  is,  a  chill  coming  on  suddenly  along  with  other  uraemic 
symptoms,  with  a  great  increase  of  temperature,  and  followed  by  a  rapid  fall 
in  the  temperature.  The  respiration  in  uraemic  patients  is  sometimes  very 
much  accelerated,  and  is  especially  deep — a  symptom  which  recalls  the  pecul- 
iar breathing  in  diabetic  coma  (vide  infra).  Certain  severe  attacks  of  dysp- 
noea in  patients  with  renal  disease  have  been  described  as  "  uraemic  dyspnoea  " 
or  "  uraemic  asthma,"  but  it  is  not  always  easy  to  decide  whether  this  is  really 
a  uraemic  nervous  symptom  in  these  cases,  since  similar  conditions  of  sudden 
dyspnoea  may  depend  upon  coincident  heart  disease  and  insufficiency  of  the 
left  ventricle,  or  upon  inflammatory  affections  of  the  lungs.  The  occurrence 
of  Cheyne- Stokes'  breathing  in  uraemia  has  already  been  referred  to  above. 

In  regard  to  the  duration  of  uraemic  symptoms  and  to  the  different  forms 
and  ways  in  which  the  various  uraemic  symptoms  may  be  combined  in  the 
clinical  picture,  we  can  give  only  a  few  general  statements.  The  division  of 
uraemia  into  an  acute  and  a  chronic  form,  already  mentioned,  is  generally 
very  useful  practically.  In  the  acute  form  we  usually  have  the  severe  uraemic 
symptoms,  especially  uraemic  convulsions  and  uraemic  coma.  This  condition 
usually  lasts  some  days,  while  chronic  uraemia,  in  which  the  milder  cerebral 
symptoms — uraemic  vomiting,  difficulty  in  breathing,  etc. — are  most  promi- 
nent, may  last  as  many  weeks.  The  severe  acute  form  of  uraemia  may,  as  has 
been  already  stated,  begin  with  almost  absolute  abruptness.  Quite  often, 
however,  there  are  first  mild  uraemic  symptoms,  such  as  headache,  vomiting, 


740  DISEASES   OF   THE   URINARY  ORGANS 

general  restlessness,  and  an  occasional  slight  twitching  of  the  muscles,  and 
then  suddenly  ursemic  convulsions  or  other  ursemic  symptoms. 

Prognosis. — The  termination  of  urgemia  is  always  doubtful  in  every  severe 
case,  but  it  is  by  no  means  always  unfavorable.  Even  after  coma  lasting  for 
several  days,  with  very  severe  and  often  repeated  convulsions,  the  ursemic 
symptoms  may  wholly  disappear,  while  on  the  other  hand,  of  course,  uraemia 
is  by  no  means  a  rare  cause  of  death  in  the  most  diverse  forms  of  acute  and 
chronic  renal  disease.  In  judging  of  the  individual  case,  the  most  stress  is 
to  be  laid  on  the  condition  of  the  pulse,  the  respiration,  and  the  temperature; 
we  must  also  consider,  of  course,  the  character  of  the  urinary  secretion,  and 
especially  the  other  morbid  symptoms  dependent  upon  the  primary  disease. 

5.     THE  CHANGES  IN  THE  CIRCULATORY  APPARATUS  IN  RENAL 

DISEASE 

Although  it  had  not  escaped  Bright' s  observation  that  changes  in  the  heart 
■are  also  present  in  diseases  of  the  kidney,  this  condition  was  first  generally 
known  when  Traube,  in  1856,  in  a  treatise  which  has  become  famous,  ex- 
plained that  a  change  in  the  heart  was  very  common  in  certain  renal  affec- 
tions, and  thus  gave  the  chief  impulse  to  the  numerous  clinical  and  experi- 
mental investigations  that  have  been  made  since  then  as  to  the  connection 
between  cardiac  and  renal  disease. 

This  connection,  generally  considered,  may  be  accounted  for  in  three  ways : 

First,  the  heart  disease  may  without  doubt  be  the  primary  disease,  and 
only  secondarily  lead  to  a  disease  of  the  kidneys.  In  this  way  develop  the 
kidney  of  passive  congestion  (vide  infra,  and  page  433),  acute  nephritis  sec- 
ondary to  acute  primary  or  recurrent  endocarditis,  and  the  embolic  processes 
in  the  kidney  (vide  infra). 

Secondly,  heart  disease  and  renal  affections  may  also  develop  independently 
■of  each  other,  as  a  result  of  an  injurious  influence  that  affects  both  organs 
at  the  same  time.  Thus,  for  example,  a  general  arteriosclerosis  leads  to  car- 
diac hypertrophy  or  to  myocarditis,  and  also  to  a  granular  kidney  (vide  infra), 
as  a  result  of  an  implication  of  the  renal  vessels.  Certain  other  injurious 
influences,  such  as  toxic  and  constitutional  influences,  alcohol,  syphilis,  or 
improper  living,  may  also  cause  a  disease  of  the  heart  and  the  kidneys  at  the 
same  time.  Later  on,  if  both  affections  have  developed,  their  influence  upon 
each  other  is  often,  of  course,  considerable — a  circumstance  which  may  render 
our  judgment  as  to  the  condition  decidedly  difficult. 

In  the  third  place — and  this  is  the  point  with  which  we  are  here  chiefly 
concerned — the  renal  affection  may  be  the  primary  disease,  and  of  itself  the 
cause  of  a  change  in  the  heart.  This  is  usually  a  secondary  hypertrophy  of 
the  heart,  particularly  of  the  left  ventricle,  but  also  of  the  other  parts  of  the 
heart.  There  can  be  no  doubt  of  the  fact  of  this  dependence.  We  also  know 
that  the  secondary  development  of  cardiac  hypertrophy  is  not  confined  to 
-one  form  of  chronic  nephritis,  the  so-called  contracted  kidney,  as  was  at 
first  believed,  but  that  it  is  just  as  constant  in  all  other  forms  of  chronic, 
and  also  even  in  prolonged  acute,  nephritis.  Opinions  are  at  present  still 
much  divided  as  to  the  precise  nature  of  this  connection,  and  as  to  the  causal 
factors. 


REMARKS   UPON   THE   PATHOLOGY   OF   RENAL   DISEASE         741 

The  theory  which  Traube  himself  advanced  for  the  explanation  of  the 
cardiac  hypertrophy  in  nephritis  rested  on  the  assumptions  that,  in  the  first 
place,  less  water  is  withdrawn  from  the  blood  in  nephritis  for  the  formation 
of  the  renal  secretion,  and  that,  in  the  second  place,  the  flow  of  arterial  blood 
into  the  venous  system  is  hindered  by  the  changes  in  the  kidneys,  particularly 
by  the  destruction  of  many  of  the  smaller  blood  vessels.  Both  circumstances 
must  raise  the  pressure  in  the  arterial  system,  and  therefore  gradually  lead 
to  cardiac  hypertrophy.  Traube's  theory  cannot  be  maintained.  The  first 
claim  especially  is  untenable,  because  in  many  cases  of  chronic  contraction  of 
the  kidneys  with  coexisting  cardiac  hypertrophy  there  is  never  a  diminution 
of  the  elimination  of  water  by  the  kidneys,  and,  besides,  this  can  never  of  it- 
self cause  an  increase  of  the  arterial  pressure.  The  second  supposition,  that 
the  destruction  or  the  narrowing  of  a  large  number  of  the  small  blood  vessels 
of  the  kidneys  must  produce  a  general  rise  in  arterial  tension,  is  disproved 
by  the  fact  that  even  the  complete  ligation  of  both  renal  arteries  does  not 
raise  the  tension  in  the  arterial  system,  because  the  blood  at  once  passes  off 
into  other  vessels  which  dilate. 

In  place  of  the  "  mechanical  theory,"  therefore,  there  have  been  of  late 
many  supporters  of  the  "  chemical  theory  "  of  cardiac  hypertrophy,  which  was 
in  a  certain  sense  propounded  by  Bright  himself,  and  later  by  Johnson  and 
others.  According  to  this  view  which,  with  some  modifications,  is  held  by  the 
author,  the  retention  of  urinary  constituents,  or  other  abnormal  material,  in 
the  blood  is  the  cause  of  the  cardiac  hypertrophy  because  the  retained  material 
occasions  a  rise  in  arterial  tension,  and  this  increased  tension,  if  it  persists 
for  a  sufficiently  long  time,  must  occasion  an  hypertrophy  of  the  left  ventricle. 
Clinical  experience  shows  beyond  a  doubt  that  any  severe  case  of  acute 
nephritis  occasions  in  a  few  days  an  increase  in  the  arterial  tension,  which 
can  usually  be  easily  perceived  in  the  pulse.  This  increased  tension,  which 
certainly  precedes  the  cardiac  hypertrophy,  is  best  explained  by  the  supposi- 
tion that  the  matters  which  ought  to  be  but  are  not  excreted  occasion  a  con- 
traction of  the  smaller  arteries.  It  is  also  possible  to  conceive  that  there  may 
be  a  direct  irritation  of  the  cardiac  muscle.  At  any  rate,  the  occurrence  of 
a  rise  in  arterial  tension  is  of  decided  benefit  to  the  body,  as  it  promotes  the 
excretion  of  urine.  If,  in  the  course  of  a  nephritis,  the  normal  conditions 
return  after  a  few  days  or  weeks,  the  increased  tension  is  relaxed  and  the 
heart  suffers  no  noticeable  change;  but  if  the  nephritis  and  consequent  im- 
pairment in  urinary  secretion  and  increased  arterial  pressure  persist  for  a 
considerable  time,  we  often  see,  even  after  six  or  eight  weeks,  a  hypertrophy 
of  the  left  ventricle  develop,  under  our  own  eyes,  in  a  way  that  can  be  demon- 
strated most  distinctly  at  the  bedside.  This  is  the  necessary  consequence  of 
the  increased  effort  which  the  heart  is  obliged  to  make  in  order  to  overcome 
the  abnormal  resistance  in  the  systemic  arteries. 

We  have  precisely  the  same  conditions  in  the  chronic  forms  of  nephritis, 
except  that  they  develop  more  slowly  and  insidiously.  In  these,  also,  the  first 
factor  is  the  insufficiency  of  the  kidneys,  occasioned  by  the  disease — that  is, 
failure  to  excrete  all  the  products  of  metabolism.  To  this  the  body  responds 
immediately  by  a  rise  in  arterial  tension,  which  is  intended  to  serve,  and  does 
actually  serve,  as  a  compensation  of  the  impairment;  then,  thirdly,  hyper- 
trophy of  the  left  ventricle  develops,  and  enables  the  heart  for  a  long  while 
47 


742  DISEASES   OF   THE   URINARY   ORGANS 

to  supply  the  demands  put  upon  it.  This  hypertrophy  is  consequently  the 
most  important  compensatory  arrangement  by  means  of  which  the  body  is. 
protected  from  the  onset  of  urgemic  intoxication.  Just  as  any  patient  with 
valvular  heart  disease  would  invariably  fail  much  earlier  if  his  heart  did  not 
become  hypertrophied  in  portions  corresponding  to  the  lesion,  so,  also,  in 
chronic  nephritis,  the  unfavorable  termination  would  occur  much  earlier  if 
the  body  were  not  in  a  position  to  effect  and  maintain  an  increase  in  the  arterial 
tension,  and  thus  for  a  time,  at  least,  ward  off  the  threatening  enemy.  Viewed 
in  this  light,  the  chemical  theory  of  cardiac  hypertrophy  not  only  gives  us  an 
insight  into  the  clinical  phenomenon  as  such,  but  also  enables  us  to  perceive 
its  true  significance. 

The  question  naturally  arises  here,  just  as  when  we  were  considering  the 
theory  of  uraemia,  what  substances  are  the  chief  occasion  of  the  rise  in  arterial 
tension.  This  question,  however,  cannot  at  present  be  answered.  We  can 
merely  say  that  the  results  of  experiment  indicate  that  urea  probably  does 
not  play  the  most  essential,  and  certainly  not  the  sole,  part  in  the  matter. 
As  regards  the  form  of  the  cardiac  hypertrophy  developing  in  nephritis,  it  is. 
primarily  a  so-called  concentric  hypertrophy,  as  no  reason  exists  for  an  in- 
creased filling  of  the  chambers  of  the  heart.  We  therefore  notice  an  increased 
force  of  the  apex  beat  before  we  observe  an  increase  in  the  cardiac  dullness. 
Only  later,  when  the  heart  muscle  begins  to  fail,  is  a  dilatation  of  its  cavities 
added  to  the  hypertrophy.  It  should  furthermore  be  noted  that  while  the 
hypertrophy  always  affects  the  left  ventricle  chiefly,  yet,  as  a  rule,  the  right 
ventricle,  even  if  later,  is  also  found  to  be  hypertrophied.  If  we  assume 
that  there  is  a  direct  irritation  of  the  myocardium  (vide  supra),  this 
condition  will  not  seem  remarkable.  On  the  other  hand,  Passler  has 
emphasized  the  fact  that  the  right  heart  in  nephritis  then  becomes  hyper- 
trophic only  when  the  signs  of  muscular  insufficiency  of  the  left  heart  be- 
come evident. 

The  relation  between  certain  diseases  of  the  vessels  and  diseases  of  the 
kidneys,  which  must  likewise  be  considered  in  connection  with  the  question 
of  the  development  of  nephritic  cardiac  hypertrophy,  will  be  spoken  of  in  the 
chapter  on  Contracted  Kidney. 

6.     FUNCTIONAL  KIDNEY  DIAGNOSIS 

As  in  diseases  of  other  organs,  an  attempt  has  been  made  in  diseases  of  the 
kidney  to  elaborate  a  functional  diagnosis,  aside  from  an  anatomical  one,  or 
the  recognition  of  any  anatomical  changes  in  the  organ.  This  concerns  itself 
with  a  determination  of  the  more  exact  nature  and  the  degree  of  the  disturb- 
ances in  the  physiological  functions  of  the  kidney.  A  vast  amount  of  painstak- 
ing work  has  been  devoted  to  this  object,  and  many  valuable  points  have 
thereby  been  brought  to  light.  The  conditions,  however,  are  so  complicated 
that  it  is  difficult  to  deduce  useful  definite  rules  for  practice.  In  what  follows, 
therefore,  we  are  only  able  to  give  a  brief  review  of  the  experiments  made  in 
this  direction  for  the  purpose  of  a  temporary  orientation.  In  practice,  we 
must,  in  general,  be  satisfied  as  heretofore  with  the  determination  of  the  total 
amount  of  urine  excreted,  and  its  specific  weight,  and  with  the  examination  of 
the  abnormal  constituents  excreted. 


REMARKS   UPON   THE   PATHOLOGY   OF   RENAL   DISEASE         743 

1.  Cryoscopy. — The  freezing  point  and  likewise  the  boiling  point  of  a 
solution  is  dependent  upon  the  number  of  molecules  presenl  in  it.  The  fewer 
solid  constituents  the  kidney  excretes,  the  less  will  the  freezing  point  of  the 
urine  be  below  the  freezing  point  of  distilled  water.  Under  normal  conditions 
this  lowering  (usually  indicated  by  a)  is  about  1°  to  2.3°  C.  below  0°.  If  it 
is  less  than  1°  C,  an  insufficiency  of  the  kidney  is  probable.  Still,  the  findings 
are  rarely  definite,  and  cryoscopy,  in  general,  especially  in  urine  free  from 
albumen,  is  not  of  much  more  value  than  the  determination  of  the  specific 
weight.  If,  however,  the  urine  contains  albumen,  then,  on  account  of  the 
heavy  albuminous  molecules,  the  specific  weight  rises  more  than  the  molecu- 
lar concentration  would  warrant,  and  cryoscopy  will  give  a  more  correct  idea 
of  the  excretion  of  solid  substances  than  the  determination  of  the  specific 
gravity.  Great  hopes  were  built  upon  the  separate  examination  of  the  urine 
secreted  by  each  kidney,  and  obtained  by  means  of  ureter  catheterization  or 
other  methods.  These  hopes,  however,  have  not  been  entirely  realized,  since  the 
two  kidneys,  even  under  normal  conditions,  do  not  functionate  alike.  The 
cryoscopy  of  the  blood  has  also  been  considerably  utilized  to  determine  the 
activity  of  the  kidneys.  Under  normal  conditions,  the  molecular  concentration 
of  the  blood  shows  only  very  slight  variations,  so  that  the  freezing  point  of 
blood  (usually  indicated  by  8)  varies  very  slightly,  and  is  generally  more  or 
less  exactly  0.56°  C.  below  that  of  water.  In  disease  of  the  kidney,  if  the  excre- 
tion of  the  solid  urinary  constituents  is  interfered  with,  the  molecular  concen- 
tration of  the  blood  is  increased,  and  8  sinks  noticeably.  In  uraemia  it  has 
been  found  as  low  as  0.70°  to  0.75°  C.  On  the  other  hand,  in  nephritis  and 
even  in  uraemia,  normal  values  have  also  been  found.  This  is  obviously  due 
to  the  fact  that  the  body,  despite  the  existing  difficulties,  always  attempts  to 
keep  the  molecular  concentration  of  the  blood  as  near  normal  as  possible  by 
dilution  of  the  blood  with  water,  by  excretion  into  dropsical  exudate,  and  by 
the  retention  of  residual  products  of  metabolism  in  the  tissues.  Variations  of 
8   are  therefore  of  more  significance  than  normal  readings. 

2.  Resistance  to  Electric  Conductivity. — The  resistance  to  electric  con- 
ductivity of  a  fluid  depends  upon  the  amount  of  electrolytes — i.  e.,  dissociated 
ions  of  the  inorganic  salts — contained  therein.  Increased  concentration  of  the 
salts  adds  to  the  electric  conductivity.  In  nephritic  urine  the  conductivity  is 
therefore  often  diminished.  Analogous  conditions  apply  to  the  blood.  The 
results  of  numerous  determinations  are  not  without  interest,  especially  in 
combination  with  the  cryoscopic  examinations.  No  important  new  points  of 
view  have,  however,  developed  from  this. 

3.  The  excretion  of  water  and  the  solid  urinary  constituents  suffer  to  a 
great  extent  in  the  various  forms  of  nephritis,  and  efforts  have  not  been  lack- 
ing to  find  a  firm  basis  in  this  connection  for  the  determination  of  the  kidney 
function.  The  complexity  of  the  existing  conditions  renders  it  difficult,  how- 
ever, to  establish  any  general  rules.  The  excretion  of  water  is  relatively  easiest 
to  observe.  In  many  cases  of  acute  and  chronic  nephritis  the  excretion  of 
water  is  decidedly  lowered,  and  even  an  increased  intake  of  water  does  not 
increase  the  total  quantity  of  urine.  The  water  taken  is  only  slowly  excreted, 
or  it  accumulates  in  the  tissues  and  increases  the  oedema.  In  other  cases  of 
kidney  disease,  however  (vide  infra,  contracted  kidney),  an  increased  excretion 
of  water  takes  place.    The  excretion  of  the  nitrogenous  substances  in  the  urine 


744  DISEASES   OF   THE   URINARY   ORGANS 

is  likewise  frequently,  but  by  no  means  always,  disturbed.  In  individual 
cases,  the  N  excretion  also  frequently  shows  great  variations.  With  an  increased 
ingestion  of  nitrogen,  the  increase  in  the  N  excretion  in  kidney  disease  occurs, 
in  general,  more  slowly  than  in  the  healthy  organ.  In  severe  cases  there  is 
certainly  a  retention  of  nitrogen  in  the  body.  Special  mention  should  be  made 
of  the  findings  of  H.  Strauss  relative  to  the  increase  in  the  residual  nitrogen 
(i.  e.,  the  nitrogen  of  the  blood  not  in  albuminous  combination)  in  cases  of 
severe  nephritis  in  which  uraemia  can  readily  develop. 

The  excretion  of  uric  acid  is  often  comparatively  least  disturbed.  Of  the 
inorganic  constituents  of  the  urine,  the  greatest  attention  has  been  paid  to 
chlorid  of  sodium.  Here,  also,  greatly  varying  conditions  are  found;  still, 
as  a  rule,  it  is  precisely  the  NaCI  excretion,  which  is  often  much  diminished. 
Since,  however,  the  blood  and  the  fluid  of  the  various  organs  are  restricted  to 
a  NaCI  percentage,  which  fluctuates  within  very  narrow  limits  ("  physiological 
salt  solution  "),  in  continued  and  even  increased  NaCI  ingestion  and  insufficient 
NaCI  excretion  through  the  kidneys,  the  body  must  find  other  means  of  elimina- 
tion. This  explains  the  relation,  often  emphasized,  of  the  NaCI  excretion  to 
the  development  of  oedema  (vide  supra).  We  can  then  make  the  general  state- 
ment that  the  NaCl  excretion  is  little  disturbed  in  cases  of  nephritis  without 
oedema,  and  that  it  is  markedly  disturbed  in  such  as  are  accompanied  by  oedema. 
In  the  latter  case  a  voluntary  increase  in  the  NaCl  ingestion  may  therefore 
lead  to  an  increase  of  the  oedema,  and  a  diminution  in  the  NaCI  intake  to  its 
decrease.  To  deduce  from  this  that  the  decreased  NaCl  excretion  is  the  main 
cause  of  the  oedema  is  not  correct.  On  the  contrary,  frequently  the  oedema 
formation,  owing  to  the  abnormal  permeability  of  the  vessels  (vide  supra),  is 
certainly  one  of  the  causes  of  the  diminished  quantity  of  sodium  chlorid  in 
the  urine. 

4.  The  elimination  of  foreign  substances  through  the  kidneys  may  also  be 
used  to  test  the  functional  activity  of  these  organs.  Indigo-carmin  and  methyl- 
ene blue  have  frequently  been  used  for  this  purpose.  After  an  injection  of  a 
Pravaz  syringeful  [about  TTLxiij]  of  a  five-per-cent  solution  of  methylene  blue, 
the  urine,  under  normal  circumstances,  will  be  colored  blue  in  about  an  hour. 
In  a  day  and  a  half  to  two  days  the  dye  is  completely  eliminated.  In  nephritis 
the  excretion  begins  later,  and  lasts  a  much  longer  time  (several  days).  Simi- 
lar results  are  observed  with  iodid  of  potassium.  After  the  administration  of 
7.5  gr.  (gm.  0.5)  of  KI,  the  excretion  of  iodin  in  the  urine  lasts  about  one  to 
one  day  and  a  half  in  healthy  persons,  while  in  nephritics  it  may  be  extended 
to  four  or  five  days  (F.  Miiller) . 

5.  Phloridzin  Test. — As  the  occurrence  of  glycosuria  after  a  phloridzin  in- 
jection, TV  gr.  (gm.  0.005) — i.  e.,  a  syringeful  of  a  solution  of  4  gr.  (gm.  0.25) 
of  phloridzin,  3  gr.  (gm.  0.2)  of  sodium  carbonate,  and  2  ounces  (gm.  50)  of 
water — is  dependent  upon  the  function  of  the  kidney  epithelium,  the  action 
of  phloridzin  in  nephritics  has  been  often  studied.  In  many  cases  a  diminu- 
tion, or  even  a  complete  absence,  of  phloridzin  glycosuria,  has  been  found.  The 
test  has  as  yet  been  of  no  great  practical  importance,  aside  from  the  surgical 
question  as  to  the  justification  of  a  unilateral  nephrectomy. 


ACUTE    NEPHRITIS  745 


CHAPTER    II 

ACUTE    NEPHRITIS 

(Acute  Bright'a  Disease) 


etiology. — Acute  nephritis,  like  most  of  the  other  forms  of  nephritis,  is 
not  a  disease  whose  aetiology  is  uniform.  The  same  anatomical  change,  which 
we  term  "nephritis,"  and  which  is  attended  by  about  the  same  morbid  phe- 
nomena, may  be  excited  by  influences  of  very  different  kinds.  Almost  all  these 
influences  have  one  thing  in  common — namely,  that,  as  we  have  stated  in  the 
preceding  chapter,  they  reach  the  kidneys  by  way  of  the  circulation  and  are 
here  in  part  eliminated,  and  thus  exert  their  specific  injurious  action  upon  the 
parenchyma  of  the  kidneys ;  but  they  differ  considerably  from  one  another  in 
their  precise  chemical  nature.  Since  the  pathological  change  in  the  kidneys 
depends  upon  the  amount  of  the  noxious  material,  upon  the  intensity  of  its 
action  and  the  duration  of  its  influence,  we  see  that  the  cases  of  nephritis  that 
arise  in  this  way  must  present  a  perfectly  continuous  series  from  the  mildest 
to  the  severest,  from  those  that  pass  off  rapidly  to  those  that  last  perhaps  for 
years  and  years.  The  history  of  renal  pathology  teaches  us  in  the  plainest  way 
that  all  attempts  to  divide  the  forms  of  nephritis  into  different  clinical  and 
pathological  "varieties"  cannot  be  strictly  carried  out.  The  more  scientific 
experience  increases,  the  more  numerous  must  be  the  forms  established,  and 
still  we  only  too  frequently  have  to  assume  all  sorts  of  "  transitional  forms  " 
merely  to  bring  the  reality  into  harmony  with  the  scheme.  It  therefore  corre- 
sponds merely  to  our  practical  needs  if  we  take  certain  types  from  this  whole 
list  and  divide  nephritis  into  various  groups ;  for,  from  the  nature  of  the  case, 
there  can  be  no  question  of  a  sharp  separation  of  the  various  forms. 

We  accordingly  call  those  inflammatory  renal  affections  acute  nephritis 
which  arise  comparatively  rapidly  from  any  of  the  injurious  influences  soon  to 
be  enumerated,  and  which  terminate,  after  a  few  days  or  a  few  weeks,  either 
fatally  or  with  recovery ;  or  occasionally,  after  a  rapid  onset  of  this  sort,  pass 
gradually  into  a  chronic  form.  Acute  nephritis,  on  the  one  hand,  follows 
immediately,  without  any  fixed  boundary,  the  mildest  morbid  changes  in  the 
kidney,  which  are  usually  not  termed  actual  nephritis,  but  simple  "  parenchym- 
atous degeneration";  while  on  the  other  hand  it  shows  a  continuous  transi- 
tion to  those  forms  which  last  for  several  weeks  or  months,  or  longer,  and  hence 
are  called  subacute  or  subchronic  nephritis. 

Let  us  now  consider  more  minutely  the  conditions  under  which  acute 
nephritis  develops.  In  the  first  place,  it  occurs  with  very  great  frequency  as 
a  sequel  or  complication  of  all  sorts  of  infectious  diseases.  We  may  assert  that 
there  is  really  no  acute  infectious  disease  in  which  a  secondary  acute  nephritis 
may  not  occasionally  appear.  There  are,  however,  many  diseases  in  which  this 
complication  is  peculiarly  frequent  and  characteristic.  The  exact  causes  of  its 
development  are  as  yet  imperfectly  known.  Formerly,  authorities  were  inclined 
to  assume  that  the  original  germs  had  directly  invaded  the  kidney  itself,  but 
probably  this  is  true  in  only  a  few  cases,  if  we  except  genuine  metastatic  pyo- 
nephritis.  According  to  the  views  of  the  present  day,  it  is  much  more  likely 
that  abnormal  chemical  substances,  toxins,  which  develop  in  the  body  under 


746  DISEASES   OF   THE   URINARY  ORGANS 

the  influence  of  the  infection,  reach  the  kidneys  and  excite  disease  in  them. 
The  amount  and  character  of  these  substances  determine,  of  course,  the  severity 
of  the  renal  disease.  Since  we  have  already  dwelt  upon  the  occurrence,  the 
frequency,  and  certain  peculiarities  of  secondary  nephritis  in  the  description  of 
the  different  infectious  diseases,  a  brief  recapitulation  of  the  facts,  which  have 
already  been  for  the  most  part  discussed,  will  suffice  here. 

The  infectious  disease  which  most  frequently  gives  rise  to  an  acute  nephritis 
is  scarlet  fever.  As  has  been  shown  previously,  the  renal  affection  appears 
but  rarely  at  the  beginning  of  the  disease,  and  then  in  a  very  mild  form, 
while  the  special  severe  scarlatinous  nephritis  usually  attains  its  development 
only  toward  the  end  of  the  third  week  of  the  disease.  In  measles,  secondary 
nephritis  is  very  much  rarer  than  in  scarlet  fever ;  in  rotheln  it  is  only  of  very 
exceptional  occurrence.  It  is  commoner  again  in  smallpox,  especially  in  the 
severe  hemorrhagic  forms.  In  varicella,  renal  affections  are  very  rare,  but  they 
have  been  occasionally  observed.  They  are  always  of  but  slight  intensity.  In 
typhoid  fever  a  slight  albuminuria  is  very  common,  but  genuine  acute  nephritis 
is  quite  rare.  There  are  some  cases,  however,  where  a  nephritis  appears  very 
early,  and  where  the  other  typhoid  symptoms  are  so  crowded  into  the  background 
by  it  that  we  have  decided  difficulty  in  making  the  diagnosis  of  typhoid ;  this  is 
called  the  "  renal  form  of  typhoid  fever."  In  typhus  and  recurrent  fevers 
severe  cases  of  nephritis  are  not  especially  common,  but  they  are  seen  more 
frequently  than  in  typhoid  fever. 

The  nephritis  that  often  comes  on  in  cholera  is  of  great  practical  importance. 
This  is  seen  in  the  earlier  stages,  and  is  especially  one  of  the  most  frequent 
causes  of  the  so-called  cholera  typhoid  (see  page  103).  Of  course  it  may  appear 
questionable  whether  the  renal  affection  here  is  always  of  a  genuine  inflamma- 
tory nature,  or  develops  only  in  consequence  of  the  disturbance  of  circulation, 

Nephritis  develops  quite  frequently  in  the  course  of  diphtheria,  especially  in 
severe  cases  of  this  disease;  but  the  renal  affection  only  rarely  reaches  a  high 
degree.  We  sometimes  see,  however,  very  severe  forms  of  nephritis  in  all  the 
so-called  septic  diseases  (septic  nephritis,  see  page  138),  in  acute  ulcerative  en- 
docarditis and  endocarditis  verrucosa,  and  allied  affections,  such  as  puerperal 
fever,  septic  wounds,  etc.  Erysipelas  also  is  very  often  associated  with  nephritis, 
and  likewise  croupous  pneumonia;  while,  on  the  other  hand,  acute  articular 
rheumatism  is  seldom  accompanied  by  albuminuria.  It  is  not  very  exceptional 
for  sore  throat,  particularly  follicular  tonsillitis,  to  occasion  acute  nephritis. 
It  is  of  great  practical  importance  to  know  that  a  severe  secondary  nephritis 
may  follow  primary  diseases  of  this  sort,  even  if  the  latter  seem  to  be  very  mild. 
In  every  seemingly  primary  acute  nephritis  we  should  therefore  look  for  a 
possible  previous  tonsillitis.  Following  tonsillitis,  acute  infectious  inflamma- 
tions of  the  nasopharynx  may  occur,  particularly  in  children.  These,  as  I 
have  repeatedly  observed,  sometimes  lead  to  severe  acute  hemorrhagic  nephritis, 
usually  associated  with  pronounced  acute  swelling  of  the  lymph-glands  of  the 
neck.  Much  more  rarely  than  the  diseases  of  the  pharynx  do  the  acute  infec- 
tious and  toxic  gastric  and  intestinal  diseases  lead  to  a  secondary  nephritis. 

We  ought  also  to  speak  of  the  acute  nephritis  sometimes  seen  in  patients 
with  pustular  eruptions,  such  as  impetigo,  pustular  eczema,  severe  scabies,  etc. 
Probably  we  have  to  do  in  most  of  these  cases  with  a  mild  septic  infection,  which 
has  found  ingress  through  one  of  the  many  minute  scratches  or  other  lesions  of 


ACUTE   NEPHRITIS  747 

the  skin.  We  must  also  bear  in  mind  the  possibility  (vide  infra)  of  damage 
done  by  external  applications  which  are  absorbed  by  the  skin. 

There  are  many  chronic  infectious  diseases  besides  these  acute  ones,  in  the 
course  of  which  acute  nephritis  may  appear.  We  see  this  complication  most 
frequently  in  the  case  of  primary  tuberculosis,  but  it  seems  to  us  highly  probable 
that  the  nephritis  in  this  instance  is  not  directly  connected  with  the  tubercu- 
losis, but  is  the  result  of  absorption  of  septic  matters  from  the  pulmonary  cav- 
ities and  similar  places.  Syphilis  should  also  be  mentioned  in  this  connection. 
We  have  ourselves  repeatedly  seen  mild  and  even  severe  acute  nephritis  develop 
in  the  secondary  stage  of  syphilis.  Finally,  malaria  might  be  mentioned,  al- 
though the  nephritis  which  occurs  in  this  connection  usually  takes  a  chronic 
form. 

Besides  the  infectious  forms  of  nephritis  just  described,  there  is  a  second 
great  group,  which  may  be  classed  under  the  general  heading  of  toxic  nephritis. 
In  these  cases  we  are  dealing  with  the  deleterious  action  of  definite  chemical 
substances  which  enter  the  body  from  without  and  are  excreted  from  it  by  the 
kidneys.  It  is  wholly  impossible  to  enumerate  all  the  substances  which  have  this 
injurious  effect ;  we  will  therefore  confine  ourselves  to  mentioning  those  of  the 
greatest  practical  importance.  Among  the  poisons  proper  we  may  mention  the 
mineral  acids,  sulphuric,  hydrochloric,  and  nitric  acids,  oxalic  acid,  phosphorus, 
arsenic,  lead,  mercury  (corrosive  sublimate),  and  chromate  of  potassium. 
Among  remedies  used  internally,  which  may  excite  nephritis  when  given  in  too 
great  doses,  we  may  mention  cantharides,  squills,  balsam  of  copaiba,  turpentine, 
salicylic  acid,  and  chlorate  of  potassium.  This  last  causes  hemoglobinuria  as 
well  as  nephritis.  It  is  also  very  important  to  know  that  many  remedies  applied 
externally  are  absorbed  by  the  skin,  and  that  in  this  way  they  may  reach  the 
kidneys  and  excite  severe  changes  there.  Among  these  are  cantharidal  plaster, 
preparations  of  tar,  petroleum,  styrax,  naphthol,  and  pyrogallic  acid.  We  would 
like  to  call  attention  here  to  what,  in  our  opinion,  is  no  insignificant  danger — 
namely,  the  effect  of  too  active  and  long-continued  mercurial  treatment  upon 
the  kidneys.  We  must  mention,  in  addition  to  these,  the  nephritis  which  may 
arise  from  the  too  abundant  use  of  carbolic  acid  or  iodoform  on  the  surface  of 
open  wounds.  This  has  been  repeatedly  observed,  and  it  might  be  stated  as  a 
general  fact,  that  acute  nephritis  is  by  no  means  uncommon  as  a  result  of  the 
careless  use  of  drugs,  such  as  arsenic,  bichlorid  of  mercury,  carbolic  acid,  etc. 
At  any  rate,  every  conscientious  physician  must  keep  this  danger  constantly 
in  mind !  Under  some  circumstances  renal  affections  may  even  arise  in  indi- 
vidual cases  from  taking  excessive  amounts  of  certain  foods  and  drinks,  such 
as  spices,  alcohol,  horse  radish,  or  very  acid  foods. 

Aside  from  the  forms  of  acute  nephritis  thus  far  discussed,  there  is  also 
a  type  where  the  acute  nephritis  appears  as  an  apparently  primary  disease  in 
persons  previously  healthy.  In  many  such  cases  we  are  absolutely  unable  to 
make  out  any  causative  factor,  while  in  others,  again,  we  do  find  certain  unfa- 
vorable influences  affecting  the  patient,  such  as  hard  drinking  or  severe  labor 
in  the  open  air.  It  cannot  be  doubted  that  exposure  to  severe  cold  and  thor- 
ough wetting  promote  the  development  of  acute  nephritis.  The  author's  experi- 
ence has  convinced  him  of  this  fact.  Thus,  the  disease  may  occur  when  a  man 
works  in  the  snow  or  in  cold  water.  We  possess  as  yet,  however,  scarcely  any 
knowledge  of  the  conditions  which  bring  about  this  result.    Many  investigators 


748  DISEASES   OF   THE   URINARY   ORGANS 

assume  that  cold  interferes  with  the  excretory  function  of  the  skin;  others 
imagine  that  the  hlood  is  damaged  as  it  circulates  in  the  cutaneous  vessels. 
We  have  repeatedly  seen  cases  of  apparently  primary  acute  nephritis  in  great 
beer  drinkers.  We  suppose  that  in  such  cases  the  effect  of  the  long-continued 
chronic  intoxication  with  alcohol  is  cumulative,  and  finally  leads  to  the  appar- 
ently spontaneous  acute  development  of  nephritis  (acute  alcoholic  nephritis). 
Sometimes,  however,  even  in  such  cases  there  seems  to  be  some  other  factor,  such 
as  catching  cold,  or  an  infection  which  gives  the  final  impulse  to  the  develop- 
ment of  the  disease. 

A  considerable  number  of  cases  of  apparently  primary  acute  nephritis  must,, 
however,  be  regarded  in  the  last  analysis  as  the  results  of  a  septic  infection  of 
some  sort.  If  we  question  the  patient  closely,  we  learn  in  such  cases  that  the 
appearance  of  the  nephritic  phenomena  has  often  been  preceded  by  symptoms 
of  a  mild  sore  throat  which  scarcely  attracted  the  patient's  attention,  or  an 
insignificant  gastrointestinal  disturbance,  etc.  Such  statements  are  indicative 
of  the  possible  place  of  infection.  Again,  slight  purulent  affections  of  the  skin, 
such  as  furunculosis,  phlegmon  of  a  finger  or  toe,  and  eczema  may  sometimes 
furnish  a  gate  of  entrance  for  infection.  In  considering  all  cases  of  apparently 
primary  idiopathic  and  acute  nephritis,  it  is  very  important  to  remember  that 
not  infrequently  a  chronic  nephritis  may  exist  for  a  long  while,  perhaps  without 
any  symptoms  whatever,  and  suddenly  flame  up  into  an  acute  disease  (acute 
recurrent  nephritis  of  Wagner),  and  thus  simulate  a  primary  acute  nephritis. 
We  cannot  get  at  the  correct  interpretation  of  such  cases  without  careful  inquiry 
into  the  previous  history,  and  sometimes  only  after  observing  the  subsequent 
course  of  the  disease. 

In  conclusion,  we  have  an  especial  form  of  acute  renal  disease  to  mention  in 
this  connection — viz.,  the  nephritis  of  pregnancy  (nephritis  gravidarum) .  This 
does  not  usually  appear  until  the  last  months  of  pregnancy.  It  may  attack 
women  whose  health  was  previously  perfect,  and  it  is  much  more  frequent  in 
primiparse  than  in  multipara.  The  precise  causes  of  the  nephritis  of  pregnancy 
are  very  obscure.  The  earlier  explanations,  according  to  which  the  renal  dis- 
turbance was  occasioned  by  pressure  of  the  pregnant  uterus  upon  the  renal 
arteries,  the  renal  veins,  or  the  ureters,  are  entirely  unsatisfactory.  It  is  prob- 
ably due  to  the  action  of  toxins,  the  formation  of  which  is  dependent  upon 
specific  processes  of  pregnancy,  such  as  placental  metabolism. 

Pathological  Anatomy. — The  anatomical  changes  of  acute  nephritis  show 
a  continuous  series  from  the  mildest  to  the  severest  degrees,  according  to  the 
intensity  of  the  injurious  action.  The  mildest  changes,  which,  as  we  have  said, 
are  not  called  actual  "  inflammation,"  but  usually  simple  parenchymatous  de- 
generation, affect  exclusively  the  parenchyma  of  the  kidney — that  is,  the  epi- 
thelium— while  the  interstitial  tissue,  the  connective  tissue,  and  the  vessels 
remain  perfectly  normal.  This  fact  is  of  prime  importance,  since  it  implies 
that,  in  almost  all  the  injurious  influences  acting  on  the  kidneys,  the  specific 
renal  parenchyma  itself  is  diseased  first  and  before  any  other.  On  macroscopic 
examination,  the  kidneys  of  "  parenchymatous  degeneration "  may  show 
scarcely  any  plainly  perceptible  changes,  but  it  sometimes  strikes  the  practiced 
eye  that  the  kidneys  are  a  little  enlarged,  that  the  cortex  on  section  shows  either 
a  more  reddish-gray,  dimmed  coloring  (cloudy  swelling),  or  a  more  grayish- 
white,  yellowish  hue  (fatty  degeneration).    The  microscopic  examination  gives 


ACUTE   NEPHRITIS  749 

more  accurate  information  as  to  the  degree  and  the  extent  of  the  disease.  We 
distinguish  different  conditions  according  to  the  form  of  change  in  the  epithe- 
lium, of  which  the  three  following  are  most  important:  1.  Cloudy  swelling:  Jt 
is  most  easily  made  out  in  the  epithelium  of  the  cortical  tubules,  but  it  may 
also  be  seen  in  the  epithelium  of  the  glomeruli.  The  cells  swell,  their  content- 
become  uniformly  granular  and  cloudy,  the  nuclei  swell,  and  finally  disappear. 
Such  changes  are  often  found  in  acute  infectious  disease,  such  as  typhoid,  -mall- 
pox,  and  diphtheria.  2.  Fatty  degeneration:  This  may  proceed  from  the 
cloudy  swelling,  or  may  develop  independently.  Many  fat  drops  appear  both  in 
the  cells  of  the  uriniferous  tubules  and  also  in  the  epithelium  of  the  glomeruli, 
and  they  may  finally  lead  to  the  disintegration  of  the  cells.  Simple  fatty 
degeneration  of  the  kidneys  is  sometimes  found  in  acute  infectious  diseases, 
after  certain  poisons,  such  as  phosphorus,  and  finally  in  anaemic  conditions.  3. 
Necrosis  of  the  Renal  Epithelium:  The  nuclei  of  the  cells  disappear,  and  the 
cells  are  changed  to  clear  homogeneous  flakes,  while  in  some  cases  they  are 
greatly  swollen  ("dropsical  degeneration"  of  Nauwerck-Ziegler).  Genuine 
epithelial  necrosis  is  found  in  the  kidneys,  chiefly  after  the  action  of  toxic 
substances — cantharides,  the  chromic  and  chloric  salts,  etc. — but  sometimes 
also  in  infectious  diseases.  Combinations  of  simple  necrosis  with  granular 
cloudiness  and  fatty  degeneration  are  not  infrecpient.  Both  the  last-named 
states  may  undergo  resolution  if  the}^  have  not  reached  a  high  degree.  Other- 
wise all  the  degenerations  mentioned  lead  to  the  destruction  and  disintegration 
of  the  cells ;  nevertheless,  a  complete  restoration  is  possible,  from  the  regenera- 
tion of  new  epithelial  cells  from  epithelium  that  is  still  present. 

We  term  those  changes  in  the  kidneys  genuine  acute  nephritis,  in  which  not 
only  the  renal  parenchyma  proper,  the  epithelium,  but  also  the  interstitial  tis- 
sue, especially  the  vessels,  is  affected;  so  that  we  can  make  out  the  exudative 
changes  characteristic  of  all  inflammatory  processes — the  escape  of  fluid  and 
cells  from  the  vessels.  In  these  cases  the  different  histological  processes  may 
be  combined  in  the  most  varied  ways,  so  that  the  anatomical  picture  presents 
quite  great  variations,  although  it  is  almost  always  seen  on  analysis  to  display 
the  same  processes. 

If  we  begin  with  the  histological  lesions  in  acute  nephritis,  in  order  to  learn 
to  recognize  at  once  the  essential  changes,  we  have  first  precisely  the  same  proc- 
esses of  degeneration  in  the  epithelium  which  have  been  already  described,  but 
they  are  usually  present  here  in  a  more  marked  degree.  In  some  cases  the  sim- 
ple necrotic  processes  predominate ;  in  others,  the  fatty  degeneration.  We  often 
find  degenerated  cells,  and  not  infrequently  a  more  or  less  marked  desquamation 
of  epithelium.  We  see  also  the  special  inflammatory  changes.  We  find  a  fluid 
inflammatory  exudation,  rich  in  fibrin,  and  therefore  soon  coagulating  in  the 
interstitial  connective  tissue,  which  is  dilated  and  swollen  by  it — inflammatory 
oedema.  The  same  exudation  is  also  found  in  the  uriniferous  tubules,  and,  by 
the  proper  methods,  by  alcohol  or  by  boiling  the  fresh  kidney,  the  albuminous 
effusion  can  be  made  out  both  in  the  capsules  of  the  glomeruli  and  in  the 
uriniferous  tubules.  The  interpretation  of  the  exudation  is,  of  course,  made 
very  difficult,  or  often  wholly  impossible,  by  the  presence  of  albuminous  urine 
in  the  uriniferous  tubules.  The  second  characteristic  of  inflammation,  the 
"  cellular  exudation  " — that  is,  the  emigration  of  white  blood  corpuscles — is  also 
present.    In  the  interstitial  tissue  we  find  accumulations  of  round  cells,  usually 


750  DISEASES  OF   THE    URINARY  ORGANS 

distributed  in  foci,  and  white  blood  corpuscles  in  greater  or  less  numbers  also 
enter  the  interior  of  the  uriniferous-tubules.  We  often  find  many  hyaline  casts 
in  the  lumen  of  the  straight  tubules  or  of  Henle's  loops,  whose  origin  is,  in  all 
probability,  connected  with  the  albuminous  exudation  and  the  emigrated  white 
blood  corpuscles  (see  page  729).  The  vessels  themselves  are  often  hyperasmic 
.and  dilated,  but  in  some  cases  they  are  compressed  by  the  interstitial  inflamma- 
tory oedema.  It  is  of  special  significance  that  in  very  many  cases  there  are 
hemorrhages,  either  into  the  interstitial  tissue  or  into  the  interior  of  the 
uriniferous  tubules,  or  even  into  Malpighi's  capsules: 

Special  care  has  been  recently  devoted  to  the  study  of  the  minute  changes 
in  the  glomeruli,  although  at  present  there  is  a  conflict  in  the  views  regarding 
them.  Klebs  called  attention  to  the  fact  that  in  scarlatinal  nephritis  the 
lesions  may  be  almost  exclusively  confined  to  the  glomeruli  (glomerulo- 
nephritis) .  Sometimes  kidneys  of  this  sort  seem  almost  normal  to  the  naked 
«ye,  although  during  the  life  of  the  patient  there  have  been  the  severest  symp- 
toms, such  as  anuria  and  uraemia.  Priedlander,  Kibbert,  Langhans,  and 
others  have  pursued  the  study  of  the  histological  changes  in  the  glomeruli. 
In  part  there  are  degeneration,  hyperplasia,  and  desquamation  of  the 
glomerular  epithelium ;  in  part  changes  in  the  walls  of  the  blood  vessels  them- 
selves. With  regard  to  the  secretion  of  urine,  and,  in  particular,  the  develop- 
ment of  albuminuria,  these  changes  in  the  glomeruli  are  certainly  of  the 
greatest  importance,  and  it  is  not  improbable  that  in  many  cases  of  acute 
nephritis  the  disease  begins  chiefly  in  the  glomeruli;  but,  on  the  other  hand, 
it  is  not  proper  to  suppress  too  completely  the  other  changes  in  the  renal 
parenchyma  as  compared  with  the  glomeruli-nephritis. 

In  regard  to  the  extent  of  all  these  changes  which  have  been  described, 
it  should  be  noted  that  not  infrequently  certain  portions  of  the  kidney  are 
more  severely  diseased  than  others,  so  that  sometimes  the  nephritis  tends  to 
develop  in  separate  foci.    In  general,  however,  acute  nephritis  is  diffuse. 

If  the  histological  processes  have  been  made  clear,  the  understanding  of 
the  microscopic  appearance  of  the  inflamed  kidney  is  very  simple.  We  can 
understand  that  either  this  or  that  "  form  "  of  acute  nephritis  must  be  present 
according  to  the  predominance  of  this  or  that  histological  process.  If  an 
abundant  interstitial  exudation  is  present,  the  kidney  is  much  enlarged;  if 
this  exudation  is  slight,  the  kidney  varies  but  little,  or  not  at  all,  from  its 
normal  size,  notwithstanding  any  other  severe  changes.  In  the  first  case  it 
usually  feels  soft,  from  inflammatory  oedema;  in  the  second  case,  it  is  com- 
paratively firm.  If  there  is  a  marked  hypergemia  of  the  kidney,  it  appears  much 
reddened;  if  the  kidney  is  ansemic,  it  is  paler;  and  if  an  extensive  fatty  de- 
generation is  also  present,  it  is  yellowish  white  or  yellow.  If  hemorrhages  are 
present,  they  can  easily  be  .recognized  with  the  naked  eye  on  the  outer  surface 
beneath  the  capsule  as  dark  red  points  that  cannot  be  wiped  away.  We  speak 
then  of  an  "  acute  hemorrhagic  nephritis."  On  section,  the  medullary  sub- 
stance is  more  or  less  swollen,  often  projecting  somewhat  above  the  general 
level  of  the  cut  surface,  its  normal  striated  appearance  is  almost  always  oblit- 
erated, and  its  color  shows  the  same  variations  as  the  outer  surface  of  the 
kidney.  Not  infrequently  the  diseased  Malpighian  corpuscles  can  be  recog- 
nized by  the  naked  eye  as  grayish-red  or  whitish  points.  Since,  as  we  have 
said,   the   nephritic   changes   often   show  not  a  uniform   and  diffuse,   but  a 


ACUTE   NEPHRITIS  751 

nodular  arrangement,  we  can  understand  that  the  kidneys  sometimes  have 
quite  a  mottled  appearance,  since  hypersemic  or  hemorrhagic  red  Bpota  alter- 
nate with  the  lighter  anamiic  and  the  yellow  fatty-degenerated  parts. 

There  are,  accordingly,  cases  of  nephritis  which  show  almost  nothing  ab- 
normal to  the  naked  eye,  while,  on  the  other  hand,  there  are  hemorrhagic  and 
nonhemorrhagic  forms,  appearing  pale  yellow,  red,  or  variegated,  none  of 
which  can  in  the  essential  features  he  separated  from  one  another,  but  which 
are  combined  with  one  another  in  all  conceivable  ways.  The  forms  of  ne- 
phritis that  differ  in  astiology  have,  to  a  certain  degree,  definite  and  charac- 
teristic anatomical  types,  but  strict  rules  cannot  he  laid  down  in  regard  to  this. 

Clinical  History. — The  most  essential  symptom  of  acute  nephritis  is  the 
abnormal  character  of  the  urine.  In  most  of  the  milder,  and  even  in  many 
of  the  severer  cases  of  nephritis,  the  change  in  the  urine  is  the  sole  objective 
clinical  symptom  which  renders  the  diagnosis  possible.  The  physician  must, 
therefore,  make  it  his  practice  to  submit  the  urine  to  repeated  examinations 
in  every  case  of  disease  where  there  is  any  possibility  of  the  presence  of  a 
nephritis. 

The  simple  parenchymatous  degeneration  of  the  kidneys,  cloudy  swelling, 
fatty  degeneration,  etc.,  may  probably  sometimes  exist  without  being  followed 
by  any  discoverable  change  in  the  urine;  but  they  often  lead  to  a  slight  albu- 
minuria, dependent  upon  the  change  in  the  epithelium  of  the  glomeruli.  If, 
then,  the  urine  contains  a  slight  amount  of  albumen  (which  usually  soon 
passes  off)  in  the  course  of  any  febrile  infectious  disease  or  other  affection 
(the  so-called  febrile  albuminuria,  etc.),  we  are  justified  in  assuming  some 
of  these  mild  conditions  of  degeneration  in  the  kidneys.  Sometimes  we  find 
in  the  sediment  of  the  urine  a  few  hyaline  casts,  a  few  white  blood  corpuscles, 
etc.  As  we  have  repeatedly  stated,  these  conditions  pass  into  nephritis  proper 
without  any  sharp  limitations. 

Character  of  the  Urine  in  Acute  Nephritis. — In  almost  every  case  of 
severe  nephritis  the  amount  of  urine  for  the  twenty-four  hours  is  more  or  less 
diminished.  This  is  caused  directly  either  by  the  lessened  elimination  of 
water  by  the  kidneys,  or  by  the  plugging  of  many  uriniferous  tubules  by  casts, 
desquamated  epithelium,  etc.  The  amount  evacuated  daily  is  often  only  15 
or  20  ounces  (400  to  700  c.c),  but  it  sometimes  falls  to  a  much  lower  figure, 
2  or  3  ounces  (100  to  50  c.c),  and  there  may  finally  be  even  complete  anuria. 
In  general,  though  not  without  exceptions,  the  diminution  of  the  amount  of 
urine  runs  parallel  to  the  severity  of  the  anatomical  changes  in  the  kidney. 
Improvement  in  the  disease  is  very  often  first  seen  in  an  increase  of  the 
amount  of  urine.  If  there  was  a  previous  oedema,  and  this  is  absorbed,  the 
daily  amount  of  urine  often  rises  during  convalescence  to  a  very  considerable 
quantity,  80  to  100  ounces  (2,500  to  3,000  c.c).  Even  in  cases  in  which 
there  had  been  no  decided  oedema,  we  have  often  seen  during  recovery  from 
acute  nephritis  very  abundant  diuresis.  In  so  far  as  this  symptom  did  not 
relate  to  the  excretion  of  water  that  had  been  retained  in  the  system,  it  might 
perhaps  be  referable  to  an  abnormal  permeability  of  the  glomeruli,  similar 
to  the  condition  sometimes  seen  after  a  severe  attack  of  typhoid  fever. 

The  specific  gravity  of  the  urine  is  at  first  usually  increased,  since  the 
urine  is  poor  in  water,  but  comparatively  rich  in  solid  constituents,  especially 
in  albumen   (vide  infra).     Of  course  there  are  great  differences  here,  and  a 


752  DISEASES   OF   THE   URINARY   ORGANS 

urine  secreted  in  an  abnormally  small  amount  may  show  a  specific  gravity  of 
only  1.010  or  1.015,  while,  on  the  other  hand,  urines  with  a  specific  gravity 
of  1.020  to  1.030,  or  even  more,  have  been  observed.  If  during  convalescence 
a  very  abundant,  watery  urine  is  passed,  it  of  course  usually  has  a  low  specific 
gravity,  about  1.005  to  1.008. 

In  many  cases,  but  of  course  not  in  all,  we  may  suspect  the  abnormal  char- 
acter of  the  urine  from  its  appearance.  This  depends  chiefly  upon  an  ad- 
mixture of  abnormal  morphological  constituents.  If  these  are  present  in 
large  numbers,  as  is  usually  the  case,  the  freshly  passed  urine  is  cloudy,  and 
deposits  a  more  or  less  abundant  floccular  sediment.  The  appearance  of  the 
urine  is  most  altered  if  blood  be  mixed  with  it  (hemorrhagic  urine).  Ac- 
cording to  the  amount  of  blood,  the  urine  is  a  light  or  dark  reel,  or  even  a 
dark  black-red,  and  often  has  a  greenish  reflection  when  the  light  falls  on  it. 

The  microscopic  examination  of  the  sediment  gives  more  accurate  informa- 
tion upon  the  different  morphological  constituents.  In  general,  it  may  be^ 
said  that  in  most  of  the  severe  cases  of  acute  nephritis  the  urine  contains 
numerous  casts  of  the  hyaline  and  other  varieties.  As  has  been  already  men- 
tioned, the  epithelial  casts  and  the  firm,  waxy  casts  are  especially  common. in 
the  severer  forms  of  acute  nephritis.  The  hyaline  casts  have  usually  adherent 
to  them  red  and  white  blood  corpuscles,  as  well  as  epithelium,  fat  drops,  and 
detritus.  These  morphological  constituents  are  also  found  free  in  greater  or 
less  amount.  The  sediment  is  apt  to  contain  also  numerous  beautiful  crystals 
of  uric  acid. 

Individual  cases  are  often  characterized  by  a  striking  predominance  of 
some  one  constituent — epithelium,  white  blood  corpuscles,  or  red  blood  cor- 
puscles— but  no  special  rules  in  regard  to  this  can  be  given.  We  have  spoken 
previously  (page  731)  of  the  special  conclusions  we  can  draw  from  the  dif- 
ferent objects  found  in  the  sediment.  We  can  accordingly  distinguish  an 
acute  hemorrhagic,  or  nonhemorrhagic,  an  acute  desquamative,  and  a  fatty 
degenerative  nephritis,  but  we  must  always  bear  in  mind  that  all  these  forms 
pass  into  one  another  without  sharp  boundaries. 

The  chemical  examination  of  the  urine  gives,  as  the  most  important  and 
constant  result,  usually  a  considerable  amount  of  albumen.  Since  the  reac- 
tion of  the  urine  is  almost  invariably  acid,  the  albumen  is  immediately  pre- 
cipitated on  heating  the  urine,  and  sinks  to  the  bottom  of  the  test-tube,  where 
it  usually  takes  up  about  one  half  or  three  fourths  of  the  volume  of  urine 
used  for  the  heat  test.  More  accurate  quantitative  determinations  of  albumen 
give  most  frequently  in  acute  nephritis  an  amount  of  albumen  of  from  three 
tenths  to  one  per  cent;  higher  percentages  are  rare.  The  daily  total  amount 
of  albumen  eliminated  amounts  to  about  1  or  2  drachms  (gm.  5  to  8),  or  some- 
times more,  but  the  daily  loss  of  albumen  from  the  body  hardly  ever  exceeds 
the  amount  of  5  drachms  (gm.  20).  The  variation  in  the  amount  of  albumen 
eliminated  in  different  cases  is  quite  noticeable. 

The  examination  of  the  other  solid  constituents,  which  is  not  generally 
employed  in  practice,  usually  gives  a  diminished  secretion  of  urea,  sodium 
chlorid,  phosphoric  acid,  etc.,  corresponding  to  the  diminution  in  the  whole 
amount  of  urine   (vide  supra,  page  743). 

The  Other  Symptoms  of  Acute  Nephritis. — Local  symptoms  in  the- 
kidneys  appear  only  exceptionally  to  any  extent.     There  is,  of  course,  a  cer- 


ACUTE   NEPHRITIS  753 

tain  tenderness  in  the  region  of  the  kidneys,  which,  however,  i-  boo  ambigu- 
ous to  have  very  great  symptomatic  importance.     It  is  more  often  the  - 
that  the  abnormally  concentrated  urine  causes  frequent  micturition,  associated 
with  a  disagreeable  burning  sensation — a  sort  of  vesical  tenesmus. 

The  subsequent  symptoms  of  acute  nephritis,  which  appear  in  the  resl  of 
the  body,  and  among  which  dropsy  takes  the  first  place,  are  far  more  important 
than  the  local  symptoms.  (Edema  may  be  entirely  wanting  in  acute  nephritis, 
particularly  in  cases  of  secondary  nephritis  after  pneumonia,  erysipelas,  diph- 
theria, and  usually  in  cases  of  septic  nephritis.  On  the  other  hand,  oedema 
is  especially  characteristic  of  many  cases  of  acute  nephritis,  including. cases 
due  to  scarlet  fever,  to  catching  cold,  to  alcoholic  excess,  and  to  pregnancy, 
as  well  as  the  so-called  primary  nephritis  and  the  nephritis  which  follows 
cutaneous  diseases,  such  as  scabies  or  pustulous  eczema.  This  oedema  is  not 
infrequently  the  most  prominent  clinical  symptom.  We  must  always  be  pre- 
pared for  its  appearance,  especially  when  the  amount  of  urine  shows  a  con- 
siderable and  persistent  diminution. 

The  oedema  is  usually  discovered  first  in  the  face,  which  has  a  bloated 
and  often  a  pale  and  somewhat  shiny  appearance.  The  eyelids  are  usually 
most  swollen  at  first.  Besides  the  face,  the  ankles,  the  legs,  the  scrotum,  and 
the  dependent  parts  of  the  trunk  may  be  the  chief  seat  of  the  oedema,  the 
severity  and  extent  of  which  may,  of  course,  vary  greatly  in  different  cases. 
If  a  high  degree  of  general  dropsy  develops,  this  is  a  source  of  great  distress 
to  the  patient.  The  movements  of  the  body  are  much  restrained,  and  all 
changes  of  position  are  difficult,  associated  with  great  exertion,  and  painful. 
In  the  severest  degrees  of  dropsy  small  fissures  may  form  here  and  there  in 
the  excessively  tense  skin,  from  which  the  dropsical  fluid  oozes.  Such  little 
wounds  are  sometimes  the  starting  point  for  disagreeable  erysipelatous  inflam- 
mations, etc. 

If  great  oedema  of  the  skin  is  present,  we  usually  find  at  the  same  time  a 
more  or  less  marked  dropsy  of  the  serous  cavities.  It  is  often  hard,  however, 
to  make  out  ascites  or  hydrothorax  on  physical  examination,  owing  to  the 
oedema  of  the  skin  that  is  present.  The  symptoms  mentioned  acquire  their 
chief  clinical  significance  from  the  difficulty  of  respiration  necessarily  associ- 
ated with  them,  since  the  diaphragm  is  pressed  upward  by  ascites,  and  the 
lungs  are  compressed  by  hydrothorax.  If  a  hydrothorax  is  more  marked  on 
the  left,  or  especially  if  hydropericardium  sets  in,  the  activity  of  the  heart 
is  materially  impaired. 

A  marked  oedema  of  the  mucous  membranes  develops  but  rarely;  in  a  few 
cases  we  have  seen  oedema  of  the  conjunctivae,  oedema  of  the  soft  palate,  and 
oedema  of  the  glottis.  Of  the  oedemas  of  internal  organs,  oedema  of  the  brain 
has  already  been  mentioned  as  a  possible  cause  of  severe  nervous  urgemic  symp- 
toms. (Edema  of  the  lungs,  which  often  comes  on  toward  the  end  of  the 
disease,  when  it  terminates  unfavorably,  is  usually  not  to  be  regarded  as  a 
part  of  the  general  oedema,  but  as  a  result  of  the  final  cardiac  weakness. 

In  regard  to  the  other  symptoms  in  the  different  organs,  the  symptoms  on 
the  part  of  the  circulatory  apparatus  must  first  be  mentioned.  The  pulse  is 
often  abnormally  tense,  hard,  and  full  (see  page  741).  In  the  beginning  of 
the  disease  it  is  often  somewhat  slow;  later  it  is  usually  accelerated.  A  be- 
ginning cardiac  hypertrophy  can  often  be  made  out  postmortem,  and  some- 


754  DISEASES   OF   THE   URINARY   ORGANS 

times  clinically,  in  cases  which  have  lasted  a  rather  long  time — four  to  six 
weeks.  It  seems  to  develop  most  rapidly  in  children  who  were  previously 
well  and  strong.  We  pay  especial  regard  to  the  character  of  the  apex  beat  and 
to  the  accentuation  of  the  aortic  second  sound.  The  occasional  nosebleeds  are 
probably  connected  with  the  increased  arterial  tension.  Pericarditis  is  seen 
as  a  rare  complication — a  complication  which  is  connected  with  the  general 
fact  that  in  all  forms  of  nephritis  the  different  internal  organs,  especially  the 
serous  membranes,  have  a  tendency  to  inflammation.     • 

Of  the  symptoms  in  the  respiratory  apparatus,  we  have  mentioned  above 
the  dyspnoea  consequent  upon  the  dropsical  symptoms.  In  severe  cases  the 
lungs  themselves  are  often  drawn  into  sympathy,  as  shown  by  the  development 
of  a  diffuse  bronchitis  or  a  peculiar  form  of  pneumonia.  The  latter  stands 
midway  between  a  catarrhal  and  a  croupous  inflammation.  It  exhibits,  to 
a  certain  degree,  a  form  of  stiff  inflammatory  (edema,  and  occurs  in  just  the 
same  way  in  the  chronic  forms  of  nephritis  as  in  acute  nephritis.  When  it 
involves  both  lungs  to  a  great  extent,  it  may  be  the  immediate  cause  of  death. 
The  development  of  general  pulmonary  oedema  is  •  usually  a  sign  of  begin- 
ning weakness  of  the  left  ventricle,  as  we  have  said  above,  although  here,  too, 
inflammatory  factors  may  have  some  influence. 

Vomiting  is  the  most  important  symptom  in  the  digestive  apparatus. 
If  it  appears  in  a  marked  degree,  it  may  almost  always  be  considered  as  a 
ursemic  symptom,  and  then  is  often  the  precursor  of  severe  nervous  symp- 
toms. The  appetite  is  almost  always  diminished  in  acute  nephritis;  the 
bowels  are  usually  constipated,  but  there  may  be  quite  severe  diarrhea.  We 
may  mention  peritonitis,  which  is  sometimes  purulent,  as  a  very  rare  com- 
plication (vide  supra). 

The  temperature  is  markedly  influenced  by  acute  nephritis  only  in  those 
cases  where  the  disease  develops  in  previously  healthy  persons,  or  at  least 
in  those  free  from  fever.  Then  we  see  quite  frequently  a  moderate  fever,  with 
an  irregular  rise  of  temperature  to  about  100°  to  102°  F.  (38°  to  39°  C).  It 
is  quite  rare  that  an  apparently  primary  acute  nephritis  begins  suddenly  with 
a  chill  and  high  fever,  104°  F.  (40°  C).  The  behavior  of  the  temperature 
on  the  onset  of  ursemic  symptoms  has  already  been  described  (page  739). 

The  state  of  the  general  nutrition  suffers  in  quite  a  noticeable  degree  in 
most  of  the  severe  cases  of  acute  nephritis.  The  emaciation  is  often  concealed 
by  the  oedema ;  but  the  ansemia  is  the  more  prominent,  and  often  lends  to  the 
bloated  face  a  peculiar  aspect. 

Ursemic  symptoms  may  come  on  at  any  time  in  the  course  of  acute  ne- 
phritis. We  are  often  prepared  for  the  onset  of  ursemia  by  a  previous  marked 
decrease  in  the  secretion  of  urine,  or  by  the  well-known  prodromal  symptoms, 
but  in  other  cases  it  begins  very  suddenly  with  severe  symptoms  of  eclampsia. 
In  regard  to  all  further  details  we  may  refer  to  what  was  said  on  page  734 
et  seq. 

The  Course  and  Different  Forms  of  Acute  Nephritis. — The  whole 
clinical  picture  of  acute  nephritis  depends  very  materially  upon  the  form  of 
its  development.  If  an  acute  nephritis  comes  on  in  the  course  of  a  severe  in- 
fectious general  disease,  as  in  the  course  of  a  septic  affection,  of  ulcerative 
endocarditis,  or  of  severe  typhoid,  the  changes  in  the  urine  are  often  the  sole 
indication  of  the  occurrence  of  the  complication.     The  type  of  the  severe 


ACUTE   NEPHRITIS  755 

febrile  general  disease  is  in  no  way  materially  modified  by  the  added  renal 
affection;  oedema  and  uraemic  symptoms  do  not  usually  appear,  often  because 
the  primary  disease  soon  ends  in  death. 

Also  when  nephritis  comes  on  in  previously  healthy  persons  or  in  chronic 
invalids,  the  tuberculous,  etc.,  in  many  cases  the  changes  in  the  urine  are  the 
chief  symptom,  while  the  other  general  and  secondary  symptoms  are  scarcely 
evident  at  all,  or  at  least  only  in  a  very  slight  degree.  Such  mild  cases  are 
associated  only  with  more  or  less  general  dullness  and  loss  of  appetite. 
(Edema  is  entirely  absent,  or  present  only  to  a  very  slight  degree.  Of  course 
such  cases  demand  great  caution,  since  even  in  them  we  may  have  a  sudden 
outbreak  of  severe  urasmic  symptoms. 

The  fully  developed  type  of  severe  acute  nephritis  is  seen  especially  in 
scarlatinal  nephritis  (q.  v.)  ;  it  is  also  seen  in  many  cases  of  apparently  idio- 
pathic nephritis  (vide  supra),  or  nephritis  coming  on  after  exposure  to  cold, 
etc.  In  these  cases  there  is  often  the  development  of  a  general  dropsy,  sec- 
ondary pulmonary  affections,  urasmic  symptoms,  the  symptoms  mentioned  in 
the  circulatory  apparatus,  etc.  In  these  cases,  too,  the  examination  of  the 
urine  affords  the  only  certain  means  of  judging  accurately  of  the  condition, 
but  the  other  morbid  symptoms  which  appear  early — oedema,  anaemia,  and 
vomiting — may  direct  our  suspicions  to  the  developing  renal  affection. 

Scarcely  any  general  statements  can  be  made  as  to  the  course  and  the 
duration  of  acute  nephritis,  since  the  variations  in  this  respect  are  too  great. 
We  will  refer  to  the  description  of  the  different  primary  diseases,  in  which 
the  characteristic  marks  of  any  renal  complication  are  always  stated.  A  few 
remarks  must  be  added  about  some  of  the  simple  forms  of  acute  nephritis. 

The  so-called  primary  idiopathic  nephritis  usually  appears  rather  sud- 
denly without  any  demonstrable  cause,  or  it  may  follow  a  marked  chill  ("  ne- 
phritis due  to  catching  cold").  The  first  symptoms  of  the  disease  are  some- 
times insignificant,  but  at  other  times  they  are  quite  severe — chills,  fever, 
renal  pain,  etc.  Sometimes  other  "  rheumatic  symptoms,"  such  as  angina  or 
articular  pains,  are  also  present.  Often  the  first  thing  which  attracts  the 
attention  of  the  patient  is  the  occurrence  of  oedema,  the  puffiness  of  the  face, 
or  slight  shortness  of  breath  due  to  hydrothorax.  Sometimes  the  first  symp- 
tom is  vomiting.  The  further  course  of  the  illness  may  be  mild  or  severe. 
In  the  former  case  the  oedema  that  has  appeared  is  but  slight,  the  changes  in 
the  urine  (albuminuria,  hematuria,  etc.),  do  not  attain  a  very  high  degree, 
and  after  a  few  weeks  complete  recovery  ensues.  In  other  cases,  however,  the 
type  of  a  severe,  acute,  and  very  often  hemorrhagic  nephritis  develops,  with 
great  general  dropsy,  uraemia,  etc.,  which  in  three  or  four  weeks,  or  sooner,, 
may  lead  to  death ;  but  improvement  may  follow  in  spite  of  the  severest  symp- 
toms. Then  the  amount  of  urine  gradually  increases,  and  the  abnormal  con- 
stituents of  the  urine,  the  oedema,  and  the  other  morbid  symptoms,  gradually 
disappear.  Of  course,  it  is  often  a  long  time  before  complete  recovery  ensues,, 
since,  even  when  the  patient  feels  perfectly  well  subjectively,  the  urine  may 
still  sometimes  contain  some  albumen,  a  few  casts,  or  a  few  red  blood  corpus- 
cles. In  such  cases  one  must  think  of  the  possibility  of  a  transition  of  acute 
into  chronic  nephritis.  Not  infrequently  there  is  apparently  complete  recov- 
ery, but  several  weeks  or  months  later  there  appears  suddenly,  perhaps  after 
some  special  cause,  such  as  catching  cold,  or  overexertion,  or  some  febrile  dis- 


756  DISEASES   OF   THE    URINARY  ORGANS 

ease,  a  fresh  attack  of  acute  nephritis  ("  acute  recurrent  nephritis/'  vide 
supra) . 

The  nephritis  of  pregnancy  usually  begins  gradually.  Frequent  micturi- 
tion and  cedema  of  the  lower  extremities  make  their  appearance,  and  besides 
these  there  are  often  nausea  and  even  vomiting.  Frequently  these  symptoms 
are  so  slight  that  the  changes  in  the  kidneys  are  easily  overlooked.  If  we 
examine  the  urine,  however,  we  usually  find  it  quite  rich  in  albumen,  but 
comparatively  poor  in  morphological  elements.  The  slight  sediment  consists 
of  hyaline  casts,  a  few  white  blood  corpuscles,  and  some  epithelium.  Only 
rarely  does  the  urine  assume  a  hemorrhagic  character.  If  such  is  the  case, 
we  find  in  the  sediment  red  blood  cells  in  more  or  less  profusion,  and  some- 
times a  considerable  amount  of  hematoidin  crystals  also.  Albuminuric  retini- 
tis, with  the  corresponding  disturbances  of  vision,  is  not  infrequently  observed. 

The  condition  described  almost  always  lasts  to  the  end  of  pregnancy.  In 
the  cases  that  proceed  favorably  a  very  rapid  recovery  often  follows  after  the 
birth  of  the  child;  but  the  onset  of  eclampsia  gravidarum  is  to  be  dreaded  as 
a  not  infrequent  and  dangerous  complication.  It  begins  usually  shortly  before 
or  during  labor,  and,  very  rarely,  only  a  short  time  after  delivery.  After 
mild  prodromal  symptoms,  or  even  quite  suddenly,  violent  general  convul- 
sions develop,  during  which  the  child  is  usually  born.  A  more  or  less  per- 
sistent coma  follows  the  convulsions.  The  convulsions  may  be  very  frequently 
repeated.  Death  ensues  in  about  one  third  of  the  cases;  the  other  cases  usu- 
ally recover,  only  rarely  passing  into  chronic  nephritis.  The  prognosis  is  still 
more  unfavorable  for  the  child  than  for  the  mother,  inasmuch  as  the  child 
dies  in  nearly  one  half  of  the  cases. 

The  causes  of  eclampsia  have  not  been  entirely  cleared  up.  Some  authors 
look  upon  it  as  a  real  ursemia.  Against  this  view  is  the  fact  that  sometimes 
eclampsia  develops  without  a  previously  existing  albuminuria.  It  may,  how- 
ever, in  itself  lead  to  a  mild  albuminuria.  It  is  probable  that  specific  toxic 
influences  play  a  causative  role  in  eclampsia. 

The  prognosis  of  the  nephritis  of  pregnancy,  aside  from  eclampsia,  is  in 
general  favorable.  Only  rarely  does  a  mild  albuminuria  persist  for  any  length 
<of  time  after  confinement.  Then  we  must  think  of  the  possibility  of  the 
development  of  a  chronic  nephritis.  The  possibility  of  recurrences  in  the 
•event  of  subsequent  pregnancy  must  be  borne  in  mind.  The  treatment  should 
be  according  to  the  general  principles  in  vogue  for  nephritis  (vide  infra). 
The  artificial  interruption  of  pregnancy  is  indicated  only  in  the  severer  cases. 
More  definite  information  may  be  found  in  the  text-books  on  obstetrics. 

The  anatomical  changes  in  the  nephritis  of  pregnancy  are  hardly  ever  very 
striking  to  the  eye.  The  kidneys  are  usually  pale  and  but  little  enlarged. 
Under  the  microscope  we  usually  find  a  slight  interstitial  oedema  and  degen- 
erative changes  in  the  epithelium.  Only  rarely  are  more  marked  nephritic 
appearances  present. 

Acute  alcoholic  nephritis  is  a  term  which  we  apply  to  that  form  of  the 
disease  which  we  have  repeatedly  observed  in  excessive  beer  drinkers — for  in- 
stance, in  brewers.  The  appearance  of  the  disease  seems  to  be  favored  by  coin- 
cident exciting  causes,  such  as  catching  cold,  but  beyond  this  it  is  to  be  re- 
garded as  the  sudden  development  of  a  renal  disease  resulting  from  the  toxic 
influences  of  alcohol  habitually  ingested.    There  is  a  rapid  and  great  develop- 


ACUTE   NEPHRITIS  757 

ment  of  general  dropsy.    The  amount  of  mine  is  moderately  diminished. 
urine  contains  much  albumen,  bul  usually  remains  rather  clear  and  contains 
no  blood.    As  a  rule,  the  patients  are  obese,  and  their  discomforl  is  great.    A 
favorable  termination  is  possible  under  suitable  treatment,   but  yet  there  i- 
always  danger  of  a  transition  into  chronic  nephritis. 

Diagnosis. — Acute  nephritis  can  be  overlooked  only  when  the  examination 
of  the  urine  is  neglected,  or  when  it  is  impracticable.  The  latter  sometimes 
happens,  for  example,  when  the  patient  does  not  come  under  observation  until 
after  the  onset  of  severe  ursemic  symptoms.  Otherwise,  however,  the  changes 
in  the  urine  always  furnish  evidence  enough  to  recognize  the  existence  of.  the 
affection  of  the  kidneys.  We  can,  of  course,  decide  that  the  nephritis  is  acute 
only  by  consideration  of  the  history,  the  serological  conditions,  and  the  whole 
course  of  the  disease.  We  must  also  bear  in  mind  the  possibility  that  there 
may  be  an  acute  exacerbation  in  a  chronic  nephritis  that  has  already  existed 
for  a  long  time,  and  has  been  perhaps  without  symptoms — acute  recurrent 
nephritis,  usually  hemorrhagic. 

Prognosis. — The  prognosis  of  acute  nephritis  depends  in  many  cases  not 
only  upon  the  renal  affection,  but  also  upon  the  underlying  primary  disease. 
Many  cases  of  primary  nephritis  from  toxic  action,  or  exposure  to  cold,  and  also 
many  cases  of  secondary  nephritis  after  scarlet  fever,  in  pneumonia,  typhoid 
fever,  or  syphilis,  during  pregnancy,  etc.,  recover  perfectly  in  a  short  time  or 
after  several  weeks,  according  to  the  severity  of  the  individual  case.  On  the 
other  hand,  however,  it  must  be  said  that  every  case  of  nephritis  must  be  judged 
with  great  caution,  partly  because  it  may  be  the  starting-point  of  a  subsequent 
chronic  renal  disease,  and  partly  because  dangerous  sequelae  may  sometimes  de- 
velop in  eases  that  at  first  are  apparently  mild.  The  dangers  of  acute  nephritis 
are  chiefly:  First,  the  appearance  of  severe  general  dropsy,  especially  in  the 
internal  cavities  of  the  body.  Of  the  forms  of  dropsy  hydrothorax  is  the  most 
dangerous,  as  it  may  produce  suffocation  by  compression  of  the  lungs.  Second, 
uraemia,  especially  in  its  severe  convulsive  forms,  with  high  temperature  and, 
finally,  cardiac  paralysis.  Third,  the  inflammation  of  internal  organs,  among 
which  secondary  pneumonia,  in  particular,  is  a  frequent  cause  of  death,  while 
secondary  pericarditis  and  peritonitis,  as  we  have  said,  are  seen  in  but  very 
few  cases.  We  must  bear  in  mind, '  however,  that  in  individuals  otherwise 
healthy  the  severe  sequelae  just  mentioned  may  also  be  recovered  from.  The 
most  extreme  dropsy  may  be  reabsorbed,  and  we  sometimes  see  recovery,  espe- 
cially in  children,  after  the  worst  uraemic  symptoms. 

Treatment.— With  regard  to  prophylaxis,  the  reader  should  be  reminded 
that  in  all  diseases  which  experience  has  shown  to  be  prone  to  lead  to  secondary 
nephritis— for  instance,  scarlet  fever— the  kidneys  should  be  guarded  as  much 
as  possible,  from  the  start,  by  suitable  diet  (milk)  ;  by  promoting  the  secretion 
of  the  kidneys  ("flushing  the  kidneys"),  by  administering  an  abundance  of 
liquids,  such  as  mineral  waters,  milk,  and  lemonade;  and  by  stimulating  the 
cardiac  activity  by  warm  clothing,  warm  baths,  and  rubbing  with  alcohol. 

If  nephritis  has  already  developed  we  can  scarcely  hope  to  influence  directly 
the  inflammatory  process.  The  remedies  recommended  for  this  purpose  are 
tannin,  uva  ursi,  fuchsin,  and  methylene  blue,  but  to  an  unprejudiced  observer 
they  seem  absolutely  useless.  Strontium  lactate,  in  doses  of  4  gr.  (gm.  0.25) 
three  times  a  day,  in  powder  or  solution,  might  be  worthy  of  mention.    Several 


758  DISEASES   OF   THE   URINARY   ORGANS 

reliable  observers  claim  to  have  seen  a  good  effect  upon  the  albuminuria  from 
its  use.  We  expect  as  little  result  at  present  from  "  external  antiphlogistics  ,T 
as  from  the  internal  remedies  mentioned — that  is,  from  local  bloodletting,, 
applications  of  ice  to  the  region  of  the  kidneys,  etc.  Only  in  the  rare  cases, 
where  severe  pain  in  the  region  of  the  kidneys  comes  on  at  the  beginning  of 
nephritis,  in  an  otherwise  robust  individual,  are  we  at  present  justified  in 
trying  leeches  or  a  few  dry  cups.  The  warm  baths,  to  be  described  more  fully 
below,  have  perhaps  an  indirect  favorable  action  on  the  process  in  the  kidneys, 
since  they  produce  a  hyperemia  of  the  skin,  and  thus  lessen  the  flow  of  blood 
to  the  kidneys. 

Although  we  must  accordingly  admit  that  there  is  scarcely  any  remedy  at 
our  service  which  has  a  direct  therapeutic  influence  upon  the  diseased  kidneys,, 
the  treatment  of  nephritis  may  nevertheless  produce  very  significant  results, 
since  both  a  number  of  hygienic  measures  and  the  fulfillment  of  certain  symp- 
tomatic indications  are  of  the  greatest  importance. 

Among  the  general  hygienic  measures  we  must  mention  first  strict  confine- 
ment to  bed.  In  the  severe  cases  its  necessity  is  self-evident ;  but,  even  in  the 
milder  cases,  which  run  their  course  without  any  severe  subjective  symptoms,, 
constant  rest  in  bed  is  necessary  throughout.  In  this  way  we  not  only  avoid 
the  unfavorable  action  of  cold  upon  the  external  skin,  but  we  also  stimulate 
the  activity  of  the  skin,  which  must  act  vicariously  for  the  kidneys  by  the  uni- 
form warmth  of  the  bed;  while  any  useless  muscular  exertion,  which  would 
tax  the  heart's  capacity  for  work,  is  also  avoided  by  staying  in  bed.  In  gen- 
eral it  is  advisable  to  cover  the  patient  quite  warmly,  so  as  to  keep  him  in  a 
constant  slight  perspiration. 

The  regulation  of  the  diet  is  very  important.  All  those  foods  and  drinks 
which  may  irritate  the  kidneys  are  to  be  strictly  avoided,  especially  spices,  very 
sour  substances,  strong  tea  and  coffee,  or  alcoholic  drinks.  Milk  has  for  a 
long  time  proved  itself  to  be  by  far  the  most  suitable  and  best  food.  It  has. 
won  for  itself  the  reputation  of  a  remedy  in  renal  disease,  and  the  best  results 
have  often  been  seen  from  a  methodical  "  milk  cure  " — that  is,  from  feeding 
the  patient  almost  exclusively  with  milk.  The  great  aversion  of  some  patients 
toward  milk,  however,  is  sometimes  an  obstacle  to  its  use.  We  may  often  be 
aided,  then,  by  making  the  milk  more  acceptable  to  the  patient  by  the  addition 
of  a  little  coffee,  cocoa,  a  little  cognac,  or  soda  water.  Among  other  foods  to 
be  recommended  are  buttermilk,  milk  gruel  with  rice  or  groats,  and  flour 
gruel.  We  should  be  very  cautious  about  giving  meat  as  long  as  there  are 
severe  symptoms.  Less  harmful  are  light  broths  made  from  pigeons,  fowls, 
or  veal.  We  should  also,  in  genera],  restrict  the  amount  of  eggs.  On  theoret- 
ical grounds  a  restriction  of  the  amount  of  salt  ingested  is  to  be  recommended 
(vide  supra,  page  744).  As  a  matter  of  fact,  a  salt-poor  diet  is  preferable, 
especially  in  cases  of  beginning  or  more  pronounced  oedema.  Perhaps  the 
frequently  tested  value  of  milk  depends  in  part  on  its  slight  salt  content.  As 
regards  the  administration  of  liquids,  we  believe  their  abundant,  but  not  ex- 
cessive, ingestion  to  be  advantageous  in  every  case  of  acute  nephritis,  and, 
despite  all  theoretical  objections,  even  when  dropsy  is  present.  For  bever- 
ages, besides  milk  we  may  give  Seltzer,  Wildinger,  or  Fachinger  water,  tea, 
lemonade,  and  other  watery  fruit  drinks.  Alcoholic  beverages  must  be  en- 
tirely withheld,  or,  at  the  most,  we  may  allow  a  little  claret.     The  stronger 


ACUTE   NEPHRITIS  759 

wines  are  given  only  when  the  heart  becomes  weak,  and  even  then  their  a 
fulness  is  dubious. 

The  chief  object  in  the  symptomatic  treatment  consists  in  preventing  the 
injurious  results  of  the  defective  elimination  of  the  water  and  the  solid  con- 
stituents of  the  urine,  or  in  remedying  these  results  if  they  have  occurred. 
This  purpose  can  be  attained  only  by  exciting,  as  far  as  possible,  the  activity 
of  other  organs  which  in  this  respect  may  act  vicariously  for  the  kidney-. 
The  skin  deserves  the  first  attention  here,  through  which,  by  means  of  the 
sweat-glands,  large  amounts  of  water  and  also,  to  a  certain  extent,  the  solid 
constituents  of  the  urine,  which  have  been  retained,  may  be  eliminated.  The 
diaphoretic  treatment  of  renal  diseases  has,  therefore,  been  generally  in  vogue 
for  a  long  time.  If  the  patient's  general  condition  permits,  we  always  begin 
with  it  as  early  as  possible,  even  before  there  have  been  any  signs  of  oedema, 
uraemic  symptoms,  etc.  To  produce  diaphoresis,  hot  baths  are  especially  use- 
ful and  also  hot  packs.  The  former  are  given  at  from  95°  to  100°  F.  (35°  to 
38°  C),  or  even  hotter.  The  patient  stays  about  a  quarter  or  half  an  hour  in 
the  bath,  is  then  rapidly  dried  somewhat,  wrapped  up  in  bed  in  a  previously 
warmed  sheet,  and  well  covered  up  to  the  neck  with  blankets.  In  order  to 
make  the  procedure  somewhat  easier  for  the  patient,  it  is  a  good  plan  to  cover 
the  forehead  with  a  cold  compress,  always  to  wipe  the  sweat  carefully  from 
the  face,  and  frequently  to  give  a  little  swallow  of  fresh  cold  water.  The 
production  of  sweat  is  even  better  excited  during  the  pack  if  the  patient  takes 
some  hot  drink,  hot  milk  with  soda  water  or  hot  elder  tea.  It  sometimes 
seems  to  aid  diaphoresis  if  an  internal  diaphoretic  be  given  at  the  same  time, 
the  best  being  5  to  10  gr.  of  Dover's  powder  (gm.  0.3  to  0.5),  or  a  teaspoonfrd 
or  two  (5  to  10  c.c.)  of  liquor  ammonii  acetatis  [U.  S.  P.]  (spiritus  Minde- 
reri)  in  a  cup  of  elder  tea.  We  have  found  a  good  rubbing  of  the  whole  body 
with  dilute  warm  French  brandy  of  service  before  the  pack.  The  pack  may  last 
two  or  three  hours.  Of  late  years,  particularly  in  severe  cases  with  marked 
dropsy,  we  have  almost  entirely  abandoned  baths,  and  in  their  stead  employed 
with  the  best  results  the  hot,  wet  pack,  or  dry  heat  (vide  infra).  For  the 
pack,  the  patient  is  completely  wrapped  up  in  a  hot,  wet  sheet ;  on  both  sides 
are  arranged  several  jugs  filled  with  hot  water,  and  likewise  enveloped  in 
moist  cloths ;  then  the  patient  is  covered  with  several  dry  blankets  and  is  given 
two  or  three  cups  of  some  hot  drink.  The  duration  of  a  pack  of  this  sort  is 
about  two  or  three  hours.  Dry  heat  may  be  applied  either  by  special  appliances 
(sweat  boxes,  "patent  sweat  beds"),  or  by  the  simple  introduction  of  heated 
air  under  the  bedclothes.  This  latter  method  is  the  most  convenient  and  re- 
liable. In  our  clinic  we  formerly  almost  exclusively  used  a  simple  tin  pipe 
bent  at  an  angle  and  fastened  upon  a  board,  with  its  upper  end  introduced 
under  the  bedclothes,  which  should  be,  if  possible,  somewhat  raised  up,  while 
under  its  lower  open  end  a  lighted  alcohol  lamp  is  placed  upon  the  floor;  the 
warm  air  rises  and  is  conducted  beneath  the  bedclothes,  where  the  heat  becomes 
so  great  that  the  upper  end  of  the  pipe  must  always  be  wrapped  in  a  cloth 
wet  in  cold  water  (see  Fig.  98).  At  present,  on  account  of  its  convenience 
and  safety,  the  incandescent  electric-light  bath,  which  acts  as  a  most  excellent 
diaphoretic,  has  superseded  all  other  appliances.  Where  it  can  be  used,  we 
consider  it  as  one  of  the  most  useful  adjuvants  in  the  treatment  of  all  types 
of  nephritis. 


760 


DISEASES   OF   THE   URINARY   ORGANS 


In  this  way  we  succeed  in  many  cases  in  causing  a  considerable  sweat,  so 
that  the  patient  loses  several  pounds  in  weight  at  each  pack,  and  an  existing 
dropsy  may  sometimes  be  made  to  disappear  completely  in  a  comparatively 
short  time.  On  the  other  hand,  however,  we  cannot  deny  that  it  is  very  hard 
sometimes  to  make  patients  sweat,  even  when  there  is  oedema  of  the  skin,  and 


Fig.  98. — Simple  hot-air  apparatus  for  diaphoresis.     (Erlangen  Medical  Clinic.) 

also  that  many  patients  do  not  bear  these  sweating  treatments  at  all.  The 
latter  is  especially  true  if  the  patient  has  dyspnoea,  and  if  signs  of  cardiac 
weakness  have  already  set  in.  In  such  cases  we  should  employ  merely  warm 
baths,  brief  packs,  or  hot  alcohol  rubs. 

Of  internal  diaphoretics  there  is  still  one  remedy  to  be  mentioned,  the 
hydrochlorate  of  pilocarpin,  prepared  from  jaborandi.  This  is  best  employed 
subcutaneously,  ^  to  |  gr.  at  one  dose  (gm.  0.01  to  0.02),  but  the  drug  may 
also  be  given  internally  in  pills  in  the  same  dose.  Its  effect  consists  in  the 
production  of  a  rather  profuse  perspiration,  and  likewise  a  marked  increase 
in  the  salivary  secretion,  which  latter  is  often  a  great  annoyance  to  the  patient. 
For  this  reason,  and  because  it  sometimes  induces  cardiac  weakness,  pilocarpin 
is,  on  the  whole,  scarcely  to  be  recommended.  We  ourselves  employ  it  only 
occasionally  when  the  hot  baths  are  not  used  or  when  they  do  not  have  a  sat- 
isfactory effect. 

Next  to  the  skin,  the  intestinal  mucous  membrane  is  the  organ  from  which 
we  may  soonest  expect  to  produce  a  vicarious  elimination  of  water,  and  also 
of  urea.  It  is  sometimes,  therefore,  of  a  certain  service  to  prescribe  drastic 
cathartics  in  nephritis  with  a  diminished  secretion  of  urine,  especially  if  there 
is  a  tendency  to  constipation,  besides  the  dropsy,  dyspnoea,  etc.  The  drastic 
cathartics  chiefly  used  are  infusion  of  senna,  extract  of  colocynth,  gamboge  in 
2-gr.  powders  (gm.  0.1),  tamarinds,  Epsom  salts,  etc. 

Finally,  it  may  be  asked  whether  we  should  not  excite  the  secretory  func- 
tion of  the  kidneys  themselves  by  the  exhibition  of  diuretics.  Certainly  the 
employment  of  vigorous  diuretics  is  opposed  by  the  consideration  that  we 


ACUTE    NEPHRITIS  701 

might  still  further  irritate  and  consequently  damage  the  renal  epithelium. 
The  milder  diuretics,  particularly  the  acetates  of  potassium  and  of  sodium, 
in  doses  of  about  1  to  2.5  drachms  (gin.  5  to  10)  in  the  course  of  twenty-four 
hours,  are  usually  well  borne  and  are  often  efficient.  From  diuretin  in  doses 
of  gr.  vijss.  to  xv  (gin.  0.5  to  1)  thrice  daily,  and  the  related  remedies, 
agurin,  theophyllin,  we  have  often  seen  good  results.  On  the  other  hand,  we 
would  warn  against  the  use  of  calomel,  as  very  disagreeable  symptoms  of  mer- 
curial poisoning,  such  as  stomatitis,  are  apt  to  occur. 

If  extreme  dropsy  exists,  which  cannot  be  reduced  by  the  above-mentioned 
methods,  and  which  is  very  distressing  to  the  patient,  the  attempt  can  be 
made  to  remove  the  dropsical  fluid  directly  by  mechanical  means  from  the 
subcutaneous  connective  tissue.  For  this  purpose  we  usually  use  the  so-called 
Southey  or  Curschmann  capillary  trocars.  These  are  inserted  into  dependent 
portions  of  the  dropsical  skin,  and  fastened  with  adhesive  plaster;  the  fluid 
gradually  trickles  away.  In  this  way  several  quarts  of  oedematous  fluid  can  be 
withdrawn  in  twenty-four  hours,  and  great  relief  often  given  to  the  patient. 
Instead  of  the  capillary  trocars,  some  physicians  recommend  simple  scarifica- 
tions of  the  skin  made  longitudinally  in  the  dependent  parts  (scrotum  and 
posterior  surface  of  the  thigh  and  calf).  From  these  the  dropsical  fluid  is 
allowed  to  escape  into  pads  made  of  peat  (gauze),  or  similar  substances.  Ab- 
solute antisepsis  and  asepsis  are  demanded,  for  there  is  a  great  tendency  to 
erysipelatous  inflammation. 

When  uraemia  is  threatening,  and  often  even  when  it  has  broken  out,  we 
may  try  to  produce  an  elimination  of  the  injurious  products  of  tissue  meta- 
morphosis from  the  body  in  the  well-known  ways  above  described,  by  sweating 
or  drastic  purgatives.  Besides  this,  the  uraemic  symptoms,  however,  often 
demand  a  special  symptomatic  treatment.  If  very  violent  and  frequent  uraemic 
convulsions  appear,  we  consider  it  advisable  to  try  to  suppress  the  attacks  by 
chloroforming  the  patient.  At  any  rate,  it  seems  to  us  to  be  better  to  use 
chloroform  in  uraemia  than  to  give  narcotics  internally,  because  with  this  we 
can  watch  the  action  of  the  remedy  better,  especially  with  regard  to  the  pulse 
and  respiration.  Chloroform  is  also  generally  used  by  the  obstetricians  as  the 
main  remedy  in  the  eclampsia  of  pregnancy.  4If  the  attacks  are  not  very  fre- 
cpient, but  if  there  is  marked  somnolence  or  coma,  tepid  baths  with  cold  shower 
baths  are  often  employed  with  distinct  advantage.  Cool  baths  are  also  service- 
able when  there  is  a  great  increase  of  the  temperature.  If  we  are  treating  a 
robust  individual  with  a  full  pulse,  and  during  severe  uraemia  there  is  a  de- 
cided redness  or  cyanosis  of  the  face,  venesection  may  be  indicated.  This 
sometimes  has  a  striking  and  instant  effect,  as  has  lately  been  confirmed  by 
various  observers.  Great  attention  is  to  be  paid  to  the  condition  of  the  heart. 
As  soon  as  the  pulse  becomes  small  and  weak,  energetic  stimulants,  such  as 
strophanthus  or  subcutaneous  injections  of  camphor,  must  be  used.  If  the 
signs  of  cardiac  weakness  appear  before  the  beginning  of  severe  uraemic  symp- 
toms, digitalis  preparations  (digalen,  etc.)  must  be  used.  Through  their 
action  in  raising  the  blood  pressure — it  being  advisable  under  some  circum- 
stances to  combine  acetate  of  potassium  with  them — free  diuresis  sometimes 
comes  on,  and  with  it  a  disappearance  of  the  danger  from  uraemia ;  but  mean- 
win  le  we  must  watch  for  symptoms  of  the  toxic  action  of  digitalis.  The 
tincture  nervina  Bestucheffii  [nearly  equivalent  to  the  tincture  of  the  chlorid 


762  DISEASES  OF   THE'  URINARY   ORGANS 

of  iron,  U.  S.  P.]  may  also  be  sometimes  used  to  advantage  in  uraemia.  We 
are  not  apt  to  interfere  with  urgemic  vomiting  or  urgemic  diarrhea,  because 
these  symptoms,  as  we  have  said,  are  to  be  regarded  as  a  form  of  self-help  by 
the  organism.  Only  when  such  symptoms  are  very  distressing  do  we  give 
cracked  ice,  morphin,  opium,  cocain,  chloroform,  etc.  If  the  vomitus  contains 
ammonia,  it  is  a  good  plan  to  give  10  or  15  drops  of  dilute  hydrochloric  acid 
in  water  several  times  a  day.  An  abundance  of  liquids  is  always  to  be  pre- 
scribed upon  the  appearance  of  urgemic  symptoms,  because  in  this  way  it  is 
probable  that  the  poisonous  blood  is  diluted  and  also  the  excretion  of  the  toxins 
promoted.  We  would  also  briefly  mention  here  that  in  severe  nephritis  with 
lasting  anuria  and  threatening  or  already  developed  uraemia  (especially  in  the 
eclampsia  of  pregnancy),  the  bold  attempt  has  repeatedly  been  made  to  free 
the  swollen  kidney  tissue  from  its  internal  pressure,  and  thus  to  restore  the 
suppressed  urinary  secretion  by  operative  splitting  of  the  kidney  capsule  and 
decapsulation  of  the  kidney.  This  therapeutic  measure  has  as  yet  received 
little  support,  although  a  number  of  surprisingly  good  results  have  been  ob- 
tained. At  any  rate  the  ingenious  suggestion  of  Edebohls  deserves  further 
consideration. 

In  severe  cases  the  patient's  dyspnoea  often  demands  prompt  relief.  If  the 
dyspnoea  be  caused,  or  at  least  increased,  by  hydrothorax,  and  we  do  not  suc- 
ceed in  removing  the  hydrothorax  in  any  other  way,  it  is  necessary  to  evacuate 
it  by  puncture.  In  acute  nephritis,  indeed,  we  may  hope  by  this  means  some- 
times to  preserve  the  patient's  life  until  improvement  sets  in.  Great  ascites 
must  also  be  relieved  by  tapping.  Against  "  renal  pneumonia  "  our  remedies 
are  powerless.  Tepid  baths,  shower  baths,  and  wet  packs  sometimes  procure 
relief.  In  "  urgemic  asthma  "  morphin  injections  may  act  beneficially.  If  pul- 
monary oedema  ensues,  the  heart  again  is  chiefly  to  be  considered.  We  may 
try,  besides  the  remedies  already  mentioned,  large  mustard  plasters,  baths,  and 
acetate  of  lead. 

We  accordingly  see  that  many  remedies  are  at  our  service  in  the  treatment 
of  nephritis,  the  choice  of  which  in  the  individual  case  must  be  committed  to 
the  personal  judgment  of  the  physician.  In  the  main,  we  should  always  begin 
with  the  necessary  hygienic  measures,  and,  if  possible,  with  a  methodical 
diaphoretic  treatment,  and  govern  ourselves  otherwise  by  symptomatic  indica- 
tions. After  recovery  has  set  in,  great  caution  is  still  necessary  for  a  long 
time.  The  patient  must  guard  against  physical  overexertion,  errors  in  diet, 
and  exposure  to  cold.  Preparations  of  iron  are  to  be  prescribed  when  there  is 
a  secondary  angemia. 

In  regard  to  the  influence  of  the  onset  of  an  acute  nephritis  on  the  treat- 
ment of  the  primary  disease,  we  may  mention  that  cold  baths  are  in  general 
not  to  be  freely  used,  as  in  typhoid  fever  with  nephritis,  but  still  they  may  be 
tried  if  they  are  otherwise  urgently  desirable.  We  would  also  suggest  that 
certain  internal  remedies,  especially  calomel  and  salicylic  acid,  must  be  used 
•only  with  great  caution  when  there  is  nephritis. 


THE   SUBCHRONIC   ANJ>    CHRONIC   FORMS   OF   NEPHRITIS       7G3 


CHAPTER    III 

THE    SUBCHRONIC    AND    CHRONIC    FORMS    OF    NEPHRITIS,    WITH    THE 
EXCEPTION    OF    THE    GENUINE    CONTRACTED    KIDNEY 

{Chronic  Diffuse  Nephritis,  Chronic  Parenchymatous  Nephritis,  Chronic  Hemorrhagic  Nephritis, 
Large   White  Kidney,  Secondary  Contracted  Kidney) 

iEtiology. — While  the  acute  nephritis  described  in  the  preceding  chapter 
runs  its  course  in  several  days  or  weeks,  and  only  rarely  extends  over  some 
moDths,  we  will  now  speak  of  inflammatory  degenerative  affections  of  the 
kidneys  which  last  at  least  several  months,  and  often  go  on  for  a  year  or  two. 
The  term  "  subacute  "  or  "  subchronic "  is  chosen  for  the  cases  that  last  a 
comparatively  short  time.  As  we  must  once  more  repeat,  there  is  no  sharp 
limit  in  this  respect. 

In  regard  to  the  aetiology  of  these  forms  of  nephritis,  they  do  arise  from  an 
acute  nephritis,  but  this  is  quite  rare.  Formerly  such  an  origin  was  erroneously 
regarded  as  the  rule,  and  this  is  the  reason  why  the  changes  in  the  kidney  in 
these  cases  were  described  as  the  "  second  stage  of  Bright's  disease  "  (Frerichs). 
The  English  clinical  observers  Wilks  and  Johnson,  whom  Bartels  followed  in 
Germany,  first  pointed  out  the  fact  that  in  most  cases  the  disease  shows  a 
•chronic  character  from  the  start,  and  that  we  can  only  exceptionally,  as  after 
scarlet  fever,  recognize  an  acute  "  first  stage."  The  name  "  chronic  paren- 
chymatous nephritis,"  since  frequently  used,  is  chosen  entirely  from  practical 
reasons,  inasmuch  as  it  briefly  states  the  distinction  from  the  genuine  con- 
tracted kidney;  but  it  is  incorrect  in  principle,  as  will  be  shown  from  the 
description  of  the  anatomical  conditions  later.  It  is  more  correct,  therefore, 
to  employ  the  term  "  chronic  diffuse  nephritis,"  because  we  have,  in  fact, 
to  deal  with  what  is  essentially  a  chronic  universal  or  diffuse  disease  of  the 
kidneys,  as  contrasted  with  the  "  contracted  kidney "  in  which  there  are 
always  bits  of  normal  tissue  interspersed  between  the  numerous  separate  foci 
of  disease. 

If  we  look  for  the  aetiological  conditions  in  cases  that  have  a  chronic  course 
from  the  beginning,  we  can  often  discover  nothing  definite  at  all.  The  disease 
seems  to  have  developed  "  of  itself  "  in  previously  healthy  persons.  Most  prob- 
ably we  have  here  some  toxic  or  infectious  agency  that  acts  on  the  kidneys, 
whose  detection,  however,  is  at  present  impossible.  A  certain  importance  seems 
sometimes  to  belong  to  frequent  exposure  to  cold  and  wet,  to  damp  dwellings, 
and  the  like.  That  hard  drinkers,  particularly  beer  drinkers,  are  especially 
liable  to  nephritis  seems  to  the  author  indubitable,  because  of  his  personal  ob- 
servations (vide  supra).  Of  course,  one  will  always  inquire  particularly  about 
previous  attacks  of  acute  nephritis,  and  about  other  diseases  (tuberculosis, 
syphilis,  malaria )  ;  but  still  it  is  in  only  a  small  number  of  cases  that  a  definite 
aetiology  can  be  demonstrated. 

Persons  in  early  middle  life  are  most  frequently  affected  by  the  disease,  and 
men  more  often  than  women.  In  children  and  old  people  the  disease  is  quite 
rare. 

Pathological  Anatomy. — There  is  no  essential  distinction  between  the  ana- 
tomical lesions  of  the  kidney  in  acute  and  in  chronic  nephritis.     The  changes 


764  DISEASES  OF  THE  URINARY  ORGANS 

that  are  seen  in  both  are  essentially  the  same,  only  they  develop  and  extend 
more  slowly  in  the  chronic  forms ;  and  they  also,  during  their  longer  duration, 
lead  to  certain  sequelae  in  the  kidney,  which  cannot  develop  at  all  in  acute 
nephritis,  owing  in  part  to  the  lack  of  time.  Even  in  chronic  nephritis  the 
individual  cases  differ  from  one  another  in  many  respects.  First  this  and  then 
that  histological  process  is  especially  prominent,  and  thus  lends  certain  pecul- 
iarities to  the  macroscopic  appearance  of  the  kidneys.  Certain  sequela? — such 
as  contractions — have  also  developed  but  little  in  many  cases  that  soon  end 
fatally,  but  they  develop  far  more  in  other  cases  of  longer  duration.  Hence  it 
happens  that  we  can  quite  well  regard  certain  anatomical  forms  that  are  more 
frequently  observed  as  types,  although  we  must  never  lose  sight  of  the 
important  fact  that  there  is  a  pathological  unity  in  all  these  forms  and  t}^pes. 
Then  we  shall  not  lose  the  clew  to  the  understanding  of  the  morbid  process  if 
the  individual  case  does  not  always  harmonize  with  the  scheme  of  the  text- 
books. 

We  distinguish  the.  three  following  chief  anatomical  types  of  subchronic 
and  chronic  nephritis : 

1.  Chronic  Hemorrhagic  Nephritis  in  the  Form  oe  the  Large  Eed 
or  Variegated  Kidney. — The  kidney  is  at  least  of  normal  size,  and  often  a 
little  or  a  good  deal  enlarged.  It  feels  firmer  than  normal ;  its  capsule  is  often 
adherent  to  the  surface  in  some  places.  The  surface  looks  either  uniformly  a 
more  gray-red  or  more  mottled,  while  dark-red  spots  alternate  with  lighter 
gray  or  even  yellow  spots.  The  red  spots  on  the  surface  cannot  be  wholly 
wiped  off,  and  thus  they  prove  to  be  hemorrhages.  The  gray  or  yellow  parts 
correspond  to  the  anaemic  or  fatty-degenerated  portions.  On  section,  the  cortical 
substance  is  usually  wider  than  normal,  its  normal  boundary  is  obliterated, 
and  its  color  is  a  uniform  gray-red,  or  mottled  and  striated. 

Under  the  microscope  we  find  in  part  the  same  changes  as  in  acute  nephritis 
— parenchymatous  and  fatty  degeneration  of  the  epithelium,  casts  or  hemor- 
rhages in  the  uriniferous  tubules,  inflammatory  oedema  or  granular  infiltration 
of  the  interstitial  tissue,  the  capsules  of  the  glomeruli  sometimes  thickened, 
the  epithelium  of  the  glomeruli  sometimes  proliferated  or  desquamated,  etc. 
The  special  characteristic  of  this  chronic  form,  in  contrast  with  acute  nephritis, 
is  that  in  many  places  a  complete  destruction  of  the  uriniferous  tubules  has 
occurred,  and  that  a  genuine  interstitial  connective  tissue,  more  or  less  rich 
in  cells,  has  taken  their  place.  In  this  lies  the  anatomical  evidence  of  the  longer 
duration  of  the  disease,  since  the  two  processes — both  the  complete  atrophy  of 
the  epithelium,  and  especially  the  secondary  proliferation  of  connective  tissue 
— of  course  need  a  certain  time  for  their  development.  The  atrophy  and  the 
consequent  proliferation  of  connective  tissue  usually  predominate  in  some  parts, 
while  in  others  nothing  but  fresher  inflammatory  and  degenerative  changes 
are  perceived. 

2.  The  Inflammatory  Fatty  Kidney,  or  the  Large  White  Kidney 
(yellow  would  be  more  exact). — In  this  form  of  chronic  nephritis  the  kidney  is 
usually  enlarged,  or  at  least  of  normal  size.  Its  outer  surface  is  smooth  and  of 
a  yellow  or  an  alternating  yellow  and  gray-yellow  color  throughout.  The 
broader  cortical  substance  shows  a  yellow  and  usually  somewhat  mottled 
appearance,  while  the  pyramids  almost  always  appear  considerably  reddened. 
Hemorrhages  are  also  almost  always  present  in  this  form,  usually,  of  course,. 


THE   SUBCHRONIC   AND   CHRONIC   FORMS   OF   NEPHRITIS       765 

in  smaller  numbers  than  in  the  variegated  kidney,  but  they  are  sometimes 
quite  abundant,  as  in  the  hemorrhagic  fatty  kidney. 

The  microscope  shows  the  great  affinity  between  this  form  of  nephritis  and 
the  preceding.  We  have  almost  precisely  the  same  changes,  including  always  a 
partial  destruction  of  renal  tissue  with  a  subsequent  increase  of  interstitial 
connective  tissue.  The  macroscopic  appearance  of  the  kidney  is  due  to  the  fact 
that  it  is  anaemic,  and  that  the  fatty  degeneration  preponderates  in  the  epi- 
thelium. It  is  worthy  of  note  that  in  these  kidneys  marked  changes  in  the 
glomeruli  are  usually  present. 

3.  The  Secondary  Contracted  Kidney. — While  in  the  two  forms  of 
nephritis  thus  far  described  the  outer  surface  of  the  kidney  is  still  smooth,  and 
the  kidney,  on  the  whole,  is  somewhat  enlarged,  we  have  to  do  here  with 
kidneys  of  about  normal  size,  on  whose  surface  there  are  granulations,  which 
as  yet  are  slight,  but  which  still  are  already  plain.  This  granulation  signifies 
nothing  more  than  that  the  destruction  of  the  renal  tissue  has  here  advanced 
farther,  and  that  the  newly  formed  connective  tissue  has  in  part  undergone 
cicatricial  contraction.  These  kidneys,  therefore,  represent  a  later  stage  of  the 
two  forms  first  named.  They  usually  come  under  observation  when  the  nephritis 
has  lasted  about  a  year  and  a  half  or  two  years,  or  even  somewhat  longer.  The 
first  beginnings  of  granulation  may,  of  course,  show  themselves  earlier,  while, 
on  the  other  hand,  when  the  process  lasts  a  longer  time,  a  completely  contracted 
kidney  may  develop. 

The  color  of  these  kidneys  is  usually  reddish  or  mottled,  the  red  spots  corre- 
sponding to  the  sunken  atrophic  parts,  and  the  gray  or  yellowish  spots  to  the 
elevated  parts.  Yellow  kidneys,  however,  may  also  show  at  times  decided 
granulations.  Microscopically,  we  find  already  marked  atrophy  of  the  renal 
parenchyma,  with  a  corresponding  increase  of  the  interstitial  connective  tissue. 

Formerly  these  kidneys  were  called  the  "  transition  between  the  second 
and  third  stages  of  Bright's  disease."  As  follows  from  the  above,  they  are  to 
be  regarded  only  as  a  more  advanced  form  of  chronic  nephritis.  Since  the 
kidneys,  in  spite  of  their  granulation,  have,  on  the  whole,  a  normal  size,  we  can 
infer  from  this,  and  from  the  clinical  course,  that  they  were  previously  enlarged. 
Therefore  the  name  of  "  secondary  contracted  kidney "  is  quite  suitable,  in 
opposition  to  the  genuine  contracted  kidney,  which  represents  a  much  more 
chronic  form  of  renal  atrophy.  In  the  latter  the  contraction  takes  place  in  an 
extremely  chronic  manner  in  a  kidney  which  was  previously  normal,  while  in 
the  "  secondary  contracted  kidney  "  the  cicatricial  process  develops  in  a  kidney 
which  was  previously  the  subject  of  diffuse  disease. 

Of  other  pathological  lesions,  apart  from  the  changes  in  the  kidney,  we  will 
mention  here  only  the  hypertrophy  of  the  left  ventricle,  which  is  found  (vide 
infra)  in  all  the  above-mentioned  forms  of  nephritis.  The  chronic  parenchym- 
atous nephritis  without  cardiac  hypertrophy,  assumed  by  Bartels  in  his  time, 
does  not  exist.  Such  cases  were  probably  instances  of  unrecognized  amyloid 
disease.  Exceptionally  it  may  happen  that  when  a  patient  with  chronic 
nephritis  is  very  much  debilitated  and  enfeebled,  the  cardiac  hypertrophy  is 
not  developed. 

Clinical  History. — Only  in  the  comparatively  rare  cases  when  the  renal 
affection  begins  acutely,  do  the  symptoms  of  chronic  nephritis  follow  imme- 
diately on  the  first  acute  stage.     In  most  cases,  however,  the  disease  develops 


766  DISEASES   OF   THE   URINARY  ORGANS 

slowly  and  gradually  from  the  start,  as  we  have  said,  so  that  it  is  usually 
impossible  to  determine  accurately  the  moment  when  the  disease  begins.  Still, 
we  may  assume  that  the  onset  is  decidedly  more  rapid  in  chronic  diffuse 
nephritis  than  in  genuine  contracted  kidney. 

The  first  signs  of  the  disease  consist  of  certain  general  symptoms — pallor, 
dullness,  loss  of  appetite,  nausea  and  headache,  and  later  of  oedema.  The 
latter  is  often  the  first  symptom  which  sends  the  patient  to  the  physician, 
since  in  the  beginning  he  is  apt  to  pay  little  attention  to  the  symptoms  first 
named.  The  oedema  usually  appears  first  in  the  ankles  and  legs,  more  rarely 
,at  an  early  period  in  the  face.  It  often  disappears  at  first  after  a  night's  rest, 
but  always  develops  afresh  during  the  day,  gradually  increasing  in  intensity. 
The  patient  himself  now  sometimes  notices  a  change  in  the  urine,  either  an 
abnormal  color  or  cloudiness  or  a  diminished  amount.  The  accurate  examina- 
tion of  the  urine  by  the  physician  first  establishes  the  diagnosis. 

In  regard  to  the  more  special  symptomatology  of  chronic  nephritis,  we 
meet  exactly  the  same  symptoms  as  have  been  described  in  the  preceding  chap- 
ter on  acute  nephritis.  The  characteristic  distinction  is  based  merely  upon 
the  whole  course  of  the  affection  and  the  order  of  development  of  the  differ- 
ent symptoms,  and  not  upon  the  symptoms  themselves. 

The  urine  almost  always  is  diminished.  Of  course  the  figures  vary  con- 
siderably both  in  different  cases  and  at  different  times  in  the  same  case.  A 
small  amount  of  urine,  10  to  25  ounces  (300  to  700  c.c.)  a  day,  is  almost  al- 
ways an  unfavorable  sign,  while  a  free  diuresis  signifies  an  absorption  of  the 
dropsy  and  an  improvement  of  the  condition.  There  is  also  a  persistent  in- 
crease in  the  amount  of  urine  when  the  chronic  nephritis  passes  into  a  sec- 
ondary contracted  kidney.  Under  such  circumstances  the  daily  amount  of 
urine  may  rise  to  1,500  or  2,000  c.c.  or  more. 

The  specific  gravity  of  the  urine  is  often  increased  to  about  1.015  to  1.025, 
corresponding  to  the  amount  of  albumen  and  of  other  solid  constituents.  It 
is,  of  course,  correspondingly  lower  when  there  is  a  more  abundant  elimination 
of  water  by  the  kidneys. 

The  amount  of  albumen  in  the  urine  is  quite  marked  in  all  severe  cases, 
being  one  third  to  three  fourths  of  its  volume.  It  amounts  to  about  one  and 
■one  half  to  three  per  cent  by  weight,  so  that  the  patient's  daily  loss  of  albu- 
men may  reach  0.5  to  1  ounce  (gm.  15  to  30). 

The  examination  of  the  sediment,  which  is  usually  abundant,  is  of  the 
greatest  importance  for  the  accurate  determination  of  the  form  of  the  ana- 
tomical changes  in  the  kidneys.  Above  all,  the  question  arises  as  to  the  pres- 
ence or  absence  of  blood  in  the  urine.  If  abundant,  hematuria  may  be  recog- 
nized by  the  naked  eye  from  the  color  of  the  urine.  The  detection  of  smaller 
amounts  of  blood  can  be  made  only  by  the  aid  of  the  microscope.  It  goes 
without  saying  that  the  amount  of  blood  in  the  urine  varies  considerably  in 
the  different  cases,  and  in  the  same  case  the  urine  often  contains  much  more 
blood  during  certain  periods  in  the  course  of  the  disease  than  at  other  times. 
The  portions  of  urine  passed  at  different  times  taken  separately  often  show 
quite  marked  variation  in  this  respect;  the  day's  urine  usually  contains  more 
blood  than  the  night's.  From  the  detection  of  renal  hemorrhages,  of  course 
in  connection  with  other  symptoms,  we  can  always  make  with  certainty  the 
•diagnosis  of  a  "  chronic  hemorrhagic  "  nephritis. 


THE   SUBCHRONIC   AND   CHRONIC    FORMS   OF    NEPHRITIS       767 

In  most  cases  easts  are  quite  abundant  in  the  sedimenl  of  the  mine,  hut 
naturally  their  amount  and  variety  undergo  very  greai  variations  in  differ- 
ent cases  and  at  different  times  in  the  same  case.  They  are  the  direci  sign 
of  the  presence  of  an  inflammatory  exudative  process  in  the  kidneys,  although 
the  deposits  on  the  casts  are  more  important  for  the  diagnosis  of  the  special 
form  of  renal  disease  than  are  the  casts  themselves.  Those  formed  constitu- 
ents of  the  sediment  are  most  characteristic  in  this  respect  which  point  di- 
rectly to  the  processes  of  fatty  degeneration  in  the  kidneys:  the  fatty  granules 
and  fatty  granular  cells,  free  or  attached  to  the  casts.  The  number  of  these 
elements  is  especially  great  in  the  chronic  inflammatory  fatty  kidney,  the 
"  large  white  kidney."  The  usually  clear,  nonhemorrhagic  urine  may  in  some 
cases  have  even  a  fatty  lustrous  surface.  Renal  epithelium  is,  on  the  whole, 
more  rarely  present  in  the  sediment  in  chronic  nephritis  than  in  acute,  but  it 
occurs  in  some  cases. 

Of  the  other  symptoms,  the  one  that  usually  most  strikes  the  eye  is  dropsy. 
It  usually  comes  on,  as  we  have  said,  in  the  beginning  of  the  disease,  and 
slowly  or  rapidly  reaches  a  great  extent  and  intensity.  A  medium  or  even 
a  high  degree  of  general  dropsy  may  often  persist  almost  unchanged  for 
months.  In  other  cases  it  shows  either  spontaneous  variations  or  variations 
influenced  by  treatment;  it  decreases  for  a  time  only  to  increase  anew.  The 
severer  and  more  comparatively  acute  the  case,  the  greater  in  general  is  the 
dropsy.  In  the  more  chronic  cases,  in  secondary  contracted  kidney,  its  in- 
tensity may  be  slight  for  a  time  or  even  permanently.  The  dropsy  may  even 
be  absent  in  some  cases,  as  we  learn  especially  from  the  observations  reported 
by  Wagner  under  the  name  of  "  chronic  hemorrhagic  Bright's  disease  without 
oedema"  (vide  infra).  In  regard  to  the  different  localizations  of  the  dropsy, 
and  to  dropsy  of  the  internal  cavities,  hydrothorax,  ascites,  and  hydroperi- 
cardium,  and  their  results,  the  same  holds  true  as  in  acute  nephritis. 

Of  the  internal  organs,  the  condition  of  the  heart  lays  claim  to  the  most 
interest.  In  all  cases  of  chronic  nephritis  in  which  we  do  not  have  to  do  with 
especially  weak  and  run-down  patients,  who  cannot  save  the  necessary  nu- 
tritive material  for  the  formation  of  a  cardiac  hypertrophy,  we  find  a  pro- 
nounced and  often  a  very  marked  hypertrophy  of  the  left  ventricle,  either 
with  or  without  a  coexisting  dilatation  of  its  cavity.  The  detection  of  cardiac 
hypertrophy  during  the  patient's  life  is  sometimes  difficult,  especially  when 
there  is  general  dropsy,  but  the  diagnosis  can  usually  be  correctly  made  with 
proper  attention  to  the  abnormally  tense  radial  pulse,  the  accentuated,  valvu- 
lar aortic  second  sound,  and  the  displacement  outward  of  the  apex  beat,  or 
at  least  its  increased  strength.  We  often  find  in  the  cadaver,  and  can  some- 
times make  out  during  life,  a  hypertrophy  of  the  right  ventricle  (vide  supra, 
page  742). 

A  second  important  sequel  of  chronic  nephritis  consists  of  the  changes  in 
the  retina — albuminuric  retinitis.  Although  very  rare  in  acute  nephritis, 
these  changes  are  present  in  the  majority  of  the  cases  of  this  class.  Some- 
times the  patient's  subjective  visual  disturbance  (dimness  of  vision,  defects 
in  the  field  of  vision)  points  to  a  disease  of  the  retina,  but  the  existence  of 
disease  can  be  established  with  certainty  only  by  ophthalmoscopic  examina- 
tion. The  albuminuric  retinitis  usually  appears  on  both  sides.  It  generally 
begins  with  a  mild  optic  neuritis;  then  in  most  cases  we  find,  first,  retinal 


768  DISEASES   OF   THE   URINARY   ORGANS 

hemorrhages,  and,  second,  white  spots  and  streaks,  especially  in  the  vicinity 
of  the  optic  nerves.  The  origin  of  the  spots,  which  may  appear  and  disap- 
pear again,  is  not  yet  entirely  clear.  At  any  rate,  they  are  circumscribed  fatty 
degenerations  of  the  special  retinal  elements.  The  degree  of  amblyopia  de- 
pends, of  course,  chiefly  upon  the  localization  of  the  changes,  whether  in  the 
macula  lutea  or  other  parts. 

We  need  say  little  in  regard  to  the  other  symptoms,  since  they  agree  es- 
sentially with  those  of  acute  nephritis.  The  general  anaemia  is  very  pro- 
nounced in  many  cases,  but  it  is  less  marked  in  the  very  chronic  forms.  The 
cerebral  symptoms,  especially  the  headache  and  the  mild  vertigo,  may  depend 
in  part  upon  the  cerebral  anaemia;  otherwise  they  are  due  to  uraemia  (vide 
infra).  Cerebral  hemorrhages  have  been  observed  in  a  very  few  cases.  Hem- 
orrhages on  the  inner  surface  of  the  dura  mater  are  more  frequent,  but  they 
are  usually  without  clinical  significance.  The  mouth,  larynx,  and  pharynx 
usually  show  nothing  particular,  except  accidentally  complicating  inflamma- 
tions. We  must,  however,  remember  the  occasional  occurrence  of  a  very  dis- 
tressing or  even  dangerous  oedema  of  the  soft  palate,  or  of  the  arytaeno- 
epiglottic  ligaments — oedema  of  the  glottis.  Forms  of  bronchitis  and 
pneumonia  occur  similar  to  those  seen  in  acute  nephritis.  Bronchitis  and 
chronic  oedema  of  the  lungs  also  make  their  appearance  in  the  more  advanced 
stages  of  the  disease,  as  a  result  of  cardiac  insufficiency.  Finally,  we  must  re- 
member the  hindrance  to  respiration  from  hydrothorax,  and  also  from  uraemic 
d}rspncea.  The  changes  in  the  heart  have  already  been  spoken  of.  Endocar- 
ditis or  pericarditis  may  occur,  but  they  are  very  rare. 

As  to  digestive  disturbances,  loss  of  appetite  is  a  very  common  symptom. 
Very  persistent  vomiting  is  usually  to  be  regarded  as  a  chronic  uraemic  symp- 
tom. The  bowels,  as  a  rule,  are  constipated,  but  there  may  also  be  severe 
diarrhea,  as  in  acute  nephritis.  In  severe  cases,  especially  in  the  last  stages 
of  the  disease,  ulcerative  and  dysenteric  processes  have  repeatedly  been  ob- 
served in  the  large  intestine  and  the  ileum.  Peritonitis  may  occur,  but  it  is 
at  all  events  extremely  rare.  The  liver  and  spleen  usually  show  no  pe- 
culiarities. 

Urasmic  symptoms,  both  of  the  milder  chronic  variety  and  also  in  their 
severest  acute  form,  may  come  on  at  any  time,  although  they  do  not  by  any 
means  attain  their  full  development  in  all  cases,  and  are  somewhat  rarer  than 
in  genuine  contracted  kidney. 

The  temperature  remains  normal,  as  a  rule,  as  long  as  it  is  not  influenced 
by  complicating  inflammations,  or  by  the  appearance  of  uraemia. 

Course,  Duration,  and  Termination  of  Chronic  Nephritis. — In  general,  the 
whole  course  of  chronic  nephritis  presents  quite  a  great  uniformity.  The 
different  symptoms  may  show  certain  variations  within  long  periods,  but  the 
patient  often  presents  almost  the  same  appearance  day  after  day  for  months. 
The  duration  of  the  disease  varies  greatly,  from  three  to  six  months,  in  the 
subacute  cases,  to  two  or  three  years,  or  even  more,  in  the  very  chronic  cases. 
The  cases  of  long  duration  are  almost  all  cases  of  secondary  contracted  kid- 
ney. They  sometimes  show  in  their  clinical  relations  the  transition  from  the 
enlarged  to  the  granular  kidney,  since  the  picture  in  many  of  its  details  is 
more  like  that  in  the  genuine  contracted  kidney:  the  oedema  decreases,  dis- 
appears completely,  or  at  least  continues  in  a  lesser  degree;  the  amount  of 


THE   SUBCHRONIC   AND   CHRONIC   FORMS   OF    NEPHRITIS       769 

urine  becomes  more  abundant,  and  the  specific  gravity  and  the  amount 
of  albumen  become  correspondingly  less.  The  condition  thus  lasts  for  a  long 
time  until  it  grows  worse  again,  through  uraemia  or  disturbance  of  the  com- 
pensation in  the  heart. 

The  final  termination  of  chronic  nephritis  is  in  most  cases  unfavorable. 
In  the  severe  forms  death  ensues  in  from  three  months  to  a  year,  either  in 
consequence  of  general  dropsy  or  from  uraemia,  from  complicating  inflamma- 
tions, etc.  The  conditions  when  the  nephritis  goes  on  to  secondary  contraction 
are  comparatively  more  favorable,  inasmuch  as  the  patient  may  then  find  him- 
self in  a  tolerable  state,  for  a  time  at  least.  Complete  recoveries  doubtless 
occur  in  chronic  nephritis,  but  they  are  rare.  The  longer  the  disease  lasts 
beyond  the  first  six  months  the  less  likely  is  recovery.  The  development  of  ■ 
secondary  contraction  may  simulate  recovery,  or,  at  any  rate,  the  subjective 
condition  of  the  patient  may  be  almost  perfect.  Even  after  signal  improve- 
ment, however,  relapses  are  always  to  be  feared.  There  are  even  genuine  acute 
attacks  in  the  course  of  chronic  nephritis. 

Different  Forms  of  Chronic  Diffuse  Nephritis.  Diagnosis. — By  means  of 
careful  examination  of  the  urine  in  all  suspicious  cases — for  example,  those 
presenting  oedema,  anosmia,  and  similar  symptoms — we  may  in  general  be 
certain  of  making  a  correct  diagnosis  of  chronic  nephritis,  but  all  experienced 
observers  will  acknowledge  that  the  diagnosis  of  the  particular  form  of  chronic 
nephritis  is  difficult  and  uncertain,  even  when  the  examination  of  the  case 
is  most  painstaking.  Still,  the  following  schematic  resume  may  at  least  fur- 
nish some  indications: 

Chronic  Hemorrhagic  Nephritis  (large  variegated  or  mottled  kidney) . — 
Duration  from  six  to  eighteen  months.  ■  Urine  hemorrhagic ;  usually  quite 
rich  in  red  blood  corpuscles  and  casts.  (Edema.  Cardiac  hypertrophy. 
Eetinal  changes.     Quite  frequently  uraemia. 

Inflammatory  Fatty  Kidney  (large  white  kidney). — Duration  also  six  to 
eighteen  months,  but  usually  somewhat  shorter  than  in  the  preceding  form. 
Urine  not  at  all,  or  only  slightly,  hemorrhagic.  Frequently  many  white 
blood  corpuscles,  and  especially  signs  of  fatty  degeneration  in  the  kidneys, 
fatty  granular  cells,  fat  drops  in  the  urine,  etc.  Large  amount  of  albumen 
in  the  urine.  Marked  oedema.  Cardiac  hypertrophy.  Very  often  retinal 
changes.     Death  by  uraemia  frequent. 

Secondary  Contracted  Kidney. — Longer  duration  of  the  disease,  from  a 
year  and  a  half  to  three  years.  At  first  the  symptoms  of  the  preceding  forms ; 
later,  urine  more  abundant,  less  oedema,  etc.  Death  from  an  increase  of  the 
dropsical  symptoms  due  to  cardiac  insufficiency,  uraemia,  etc. 

Chronic  Hemorrhagic  Nephritis  without  (Edema. — This  form  has  been 
already  mentioned  (page  767),  but  it  should  receive  somewhat  further  con- 
sideration. Up  to  this  time  it  has  been  too  little  regarded,  although  we  our- 
selves have  observed  not  a  few  cases  of  this  variety  of  chronic  nephritis.  The 
disease  has  a  rather  chronic  course.  For  a  long  time  the  patient  is  but  slightly 
inconvenienced,  particularly  if  he  has  good  care.  The  urine  is  usually  quite 
abundant,  and  contains  very  little  albumen,  but  has  always,  or  almost  always, 
small  amounts  of  blood  mixed  with  it,  and  this  continues  for  many  months  or 
even  longer.  From  time  to  time  there  will  appear  a  more  or  less  considerable 
haematuria,  so  that  the  urine  has  an  abundant  dark,  brownish-red  sediment. 


770  DISEASES  OF   THE   URINARY   ORGANS 

This  is  especially  likely  to  occur  if  the  mode  of  life  has  heen  indiscreet,  but  it 
may  also  happen  without  exciting  cause.  The  urinary  sediment  is  composed  of 
red  blood  corpuscles,  some  of  which  are  entire  and  some  already  disintegrated 
together  with  a  moderate  number  of  hyaline  casts.  The  latter  usually  have  red 
blood  globules  or  granules  of  hematoidin  and  detritus  adherent  to  them.  The 
amount  of  urine  temporarily  diminishes,  but  it  soon  increases  again.  Little,  if 
any,  increase  in  the  size  of  the  heart  can  be  demonstrated;  oedema  is  entirely 
absent,  nor  have  we  yet  observed  retinitis  in  association  with  this  form  of  ne- 
phritis. Uraemia  does  occur,  but  it  is  rare.  The  course  of  the  disease  is  very 
tedious,  as  we  have  said.  Whether  recovery  may  take  place  is  uncertain.  Usu- 
ally apparent  recovery  is  followed  by  the  sudden  appearance  of  a  fresh  hemor- 
rhage. It  is  probable  that  in  most  cases  the  final  result  is  a  secondary  con- 
tracted kidney. 

With  regard  to  the  aetiology  of  this  form  of  chronic  nephritis,  it  is  our 
opinion  that  in  most  cases  there  is  a  chronic  septic  infection  or  intoxication; 
at  any  rate,  it  is  noticeable  that  such  patients  not  very  infrequent]y  give  a 
history  of  some  suppurative  process. 

Treatment. — The  treatment  of  chronic  nephritis  corresponds  in  all  its  de- 
tails so  closely  to  that  of  acute  nephritis  that  we  can  refer  almost  entirely  to 
the  preceding  chapter. 

The  main  thing  here  also  is  regimen  and  symptomatic  treatment.  The 
patient  must  always  keep  himself  warm,  wear  flannels,  or  stay  in  bed.  The 
diet  must,  in  general,  conform  to  the  rules  prescribed  in  the  discussion  of  acute 
nephritis.  For  a  time  we  may  try  a  diet  in  which  milk  predominates.  A  diet 
lacking  in  salt  is  particularly  indicated  in  the  cases  with  a  tendency  to  oedema. 
It  is  always  advantageous  to  give  an  abundance  of  liquids,  except  that  alcoholic 
beverages  should  be  avoided  so  far  as  possible.  It  is  well  to  pay  careful  atten- 
tion to  the  skin — bathing,  or  sponging  with  warm  water  and  alcohol.  Under 
some  circumstances  climatic  treatment,  in  Italy,  Egypt,  etc.,  are  indicated  in 
the  more  chronic  forms.  We  see  good  results  occasionally,  in  particular,  from 
the  warm,  dry  climate  of  Upper  Egypt;  but  we  must  not  expect  too  much  of 
this  kind  of  treatment,  which  generally  involves  great  sacrifices. 

The  treatment  of  dropsy  follows  entirely  the  methods  previously  described, 
and  so  does  the  treatment  of  any  uraemic  symptoms.  If  there  is  persistent 
haematuria,  ergotin  may  be  tried,  but  it  seldom  seems  to  do  any  good. 

If  the  graver  symptoms  of  nephritis  are  absent,  we  confine  ourselves  to  a 
general  dietetic  treatment,  prescribing  warm  baths,  massage,  and,  if  anaemia 
be  present,  preparations  of  iron.  In  cases  of  this  character,  such  baths  as 
Briickenau,  Wildungen,  and  sea  baths  may  be  recommended. 


CHAPTEE    IV 

CONTRACTED    KIDNEY 

(Genuine  Contracted  Kidney.     Granular  Atrophy  of  the  Kidney.     Granular  Kidney.     Chronic 

Interstitial  Nephritis) 

Definition  and  iEtiology. — The  genuine  contracted  kidney  is  the  result  of 
an  extremely  chronic  and  very  slowly  but  constantly  progressive  atrophy  of  the 


CONTRACTED   KIDNEY  771 

renal  tissue.  The  term  "  chronic  nephritis  "  is  also  used  for  contracted  kidi 
but  the  special  inflammatory  processes  are  very  subordinate  here,  for  the  ana- 
tomical change  consists  essentially  in  nothing  but  a  simple  degenerative  atrophy 
of  the  renal  parenchyma,  and  in  a  corresponding  gradual  increase  of  the  inter- 
stitial connective  tissue.  From  a  general  pathological  point  of  view  th< 
is  to  be  regarded  as  wholly  analogous  to  the  corresponding  changes  in  the  liver 
in  cirrhosis  of  that  organ,  in  the  spinal  cord  in  the  chronic  degeneration-  of 
the  different  systems  of  fibers,  etc.  In  all  these  cases  we  have  a  primary  de- 
struction of  the  special  tissue  elements  as  a  result  of  some  deleterious  action. 
and,  following  a  general  pathological  law  (Weigert),  a  partial  replacement  of 
the  parts  destroyed  by  a  newly  formed  cicatricial  connective  tissue. 

In  the  "genuine"  contracted  kidney  the  atrophy  of  the  renal  parenchyma 
begins  in  a  previously  healthy  kidney.  Cell  after  cell  of  epithelium,  islet  after 
islet  of  tissue,  are  slowly  attacked,  while  other  parts  still  remain  intact.  It 
was  therefore  an  error  of  the  older  pathologists  to  regard  the  contracted  kidney 
as  the  "  third  stage  of  Bright's  disease,"  as  if  every  granular  kidney  were  first 
found  in  the  stage  of  acute  inflammation,  and  then  passed  into  the  stage  of 
chronic  enlargement,  and  lastly  into  that  of  contraction.  This  theory,  of 
course,  suits  certain  cases  in  part,  for  chronic  nephritis  at  least  may  often 
finally  pass  into  contraction,  but  these  "  secondary  contracted  kidneys  "  (vide 
supra)  can  clinically,  and  almost  always  anatomically,  be  differentiated  from 
the  genuine  contracted  kidnevrs.  The  contracted  kidney  may  arise  from  an 
acute  nephritis  in  some  cases,  and  careful  investigation  indicates  that  such 
cases  are  not  very  rare;  but  then  the  process  hardly  ever  passes  through  the 
three  stages  mentioned  above,  for  the  acute  nephritis  apparently  recovers.  A 
slight  remnant  of  it  is  left — a  little  fire,  as  it  were,  cmoldering  under  the  ashes ; 
its  work  of  destruction  advances,  wholly  in  secret,  and  perhaps  only  after  many 
years  do  the  symptoms  of  a  pronounced  renal  contraction  appear. 

If  we  inquire  into  the  causes  which  produce  the  atrophy  of  the  renal  tissue 
in  the  ordinary  cases  of  contracted  kidney,  which  are  chronic  from  the  first, 
we  are  very  often  unable  to  make  out  any  special  aetiolog3r.  Of  course,  one  of 
the  first  things  to  consider  in  this  disease  is  chemical  or  toxic  agents,  whether 
these  are  introduced  directly  as  such  into  the  body,  or  whether  they  are  manu- 
factured in  the  body  because  of  abnormalities  in  metabolism,  or  as  a  result  of 
infectious  processes. 

Experience  teaches  us  that  there  are  three  chemical  substances  to  be  men- 
tioned which  may  favor  the  development  of  contracted  kidney :  alcohol,  lead, 
and  uric  acid.  Chronic  alcoholism  is  often  to  be  regarded  as  the  most  probable 
cause  of  renal  contraction,  especially  in  people  who  have  "  lived  well "  other- 
wise, and  have  become  corpulent.  In  these  cases  contracted  kidney  is  to  be 
viewed  as  a  sort  of  atrophy,  due  to  wearing  out,  or  to  strain.  It  is  difficult 
to  decide  how  much  influence  should  be  ascribed  to  the  alcohol  itself  and  how 
much  to  the  excessive  ingestion  of  food.  The  specific  effect  of  alcohol  is  al- 
most indubitable  in  those  cases  in  which  contracted  kidney  and  hepatic  cir- 
rhosis are  both  present,  a  combination  repeatedly  observed.  The  connection 
between  contracted  kidney  and  chronic  lead  poisoning,  in  typesetters,  painters, 
etc.,  is  also  incontestable.  It  is  a  remarkable  circumstance,  and  one  not  yet 
fully  explained,  that  in  these  cases  we  very  often  see  at  the  same  time  genuine 
gout   (arthritis  uratica  saturnina).     If  we  make  careful  inquiries  into  the 


772  DISEASES   OF   THE   URINARY   ORGANS 

history  and  previous  symptoms  of  the  patient,  almost  invariably  we  will  be 
able  to  determine  that  previously  attacks  of  genuine  articular  gout  have  oc- 
curred. Gout,  however,  alone,  without  any  coexisting  chronic  lead  poisoning, 
often  leads  to  the  development  of  contracted  kidney,  "  gouty  kidne}*',"  in  which 
we  probably  have  to  do  with  the  noxious  action  of  an  abnormal  amount  of 
uric  acid  on  the  renal  parenchyma;  but  it  always  seems  to  be  especially  un- 
favorable to  have  an  accumulation  of  several  injurious  factors — for  instance, 
lead  poisoning  associated  with  chronic  alcoholism. 

Infectious  influences  are,  probably,  first  to  be  considered  in  those  cases 
where  the  contracted  kidney  can  be  referred  to  a  former  acute  infectious 
nephritis,  as  after  scarlet  fever.  We  may  also  mention  here  the  appearance  of 
contracted  kidney  sometimes  observed  after  severe  acute  articular  rheumatism. 
We  may  perhaps  imagine  a  similar  connection  in  the  cases  where  contracted  kid- 
ney is  found  combined  with  chronic  endocarditis  (valvular  heart  disease),  or 
with  chronic  arthritis  not  of  gouty  origin.  Of  the  chronic  infectious  diseases, 
which  sometimes  have  a  connection  with  the  origin  of  contracted  kidney,  we 
may  mention  malaria  and  syphilis.  The  latter  ought  especially  to  be  consid- 
ered more  than  it  is  at  present,  because  we  may  have  either  an  immediate  action 
of  syphilitic  toxins,  or  a  renal  atrophy  as  the  result  of  a  specific  disease  of  the 
renal  arteries. 

We  must  here  devote  a  little  time  to  a  consideration  of  the  connection  be- 
tween contraction  and  primary  disease  of  the  vessels,  which  has  been  much 
discussed.  It  is  true  that  we  often  find  general  arteriosclerosis,  and  also 
atheroma,  especially  in  the  renal  arteries,  in  the  bodies  of  persons  who  have 
died  from  contracted  kidney,  but  this  frequent  coincidence  cannot  be  remark- 
able in  such  cases,  because  contracted  kidney  is  seen  chiefly  in  elderly  persons, 
and  those  in  whom  atheroma  of  the  arteries  is  also  a  very  common  symptom. 
The  theory  advanced  by  the  English  authors,  Gull  and  Sutton  and  others, 
that  the  vascular  disease,  "  arteriocapillary  fibrosis,"  always  represents  the 
primary  process,  to  which  the  renal  atrophy  is  only  secondary,  is,  however, 
utterly  untenable.  We  often  find  the  most  pronounced  contraction  of  the 
kidneys  without  any  vascular  changes  sufficient  to  explain  the  atrophy;  and 
where  the  latter  can  be  found  in  the  small  renal  arteries,  we  usually  have  not  a 
primary  but  a  secondary  process — namely,  the  well-known  obliterating  arteritis, 
which  is  seen  in  almost  all  chronic  inflammations  and  degenerative  atrophies 
of  various  organs. 

Of  course,  it  cannot  be  denied  that  primary  disease  of  the  arteries  in  the 
kidneys  may  check  the  flow  of  blood  to  certain  portions  of  the  tissue,  and  thus 
occasion  secondary  atrophy  in  limited  areas  (arteriosclerotic  contracted  kid- 
ney), just  as,  for  example,  interstitial  myocarditis  results  from  primary  ar- 
teriosclerosis of  the  coronary  arteries.  This  is  particularly  true  of  the  so-called 
senile  kidney — that  is,  the  granulated  kidney  of  old  persons,  due  to  atherom- 
atous changes  in  the  blood  vessels,  and  perhaps  also  certain  other  cases  of 
nephritis  subsequent  to  syphilis,  and  especially  the  rare  cases  of  unilateral 
contracted  kidney,  which  have  been  seen  chiefly  in  association  with  syphilis. 

Finally,  we  have  yet  to  call  special  attention  to  the  fact  that  we  not  infre- 
quently observe  cases  of  contracted  kidney,  more  particularly  in  younger  per- 
sons and  in  women,  in  which  the  most  careful  investigation  fails  to  disclose 
any  causal  factor,  and  the  disease  appears  to  develop  altogether  spontaneously. 


CONTRACTED   KIDNEY  773 

We  are  inclined  to  ascribe  these  cases,  at  least  in  part,  to  a  congenital  lack  of 
power  of  resistance  in  the  tissues  of  the  kidney.  Kidneys  of  thi-  character 
are  not  equal  to  the  ordinary  functional  demands  on  them  for  any  length  of 
time.  In  a  certain  sense  we  may  well  compare  such  cases  of  "  primary  pro- 
gressive atrophy  "  of  the  kidneys  to  ft  progressive  muscular  atrophy  " ;  all  the 
more  readily  as  our  own  experience  shows  that  a  family  or  hereditary  predis- 
position can  sometimes  be  made  out  in  such  cases  of  renal  disease.  Even  in 
cases  in  which  it  is  certain  that  extraneous  causes  are  involved,  we  must  always 
take  into  consideration  the  individual  predisposition  and  the  power  of  resist- 
ance of  the  tissues. 

With  relation  to  the  age  and  sex  of  patients  with  contracted  kidney,  it  has 
already  been  repeatedly  stated  that  .the  disease  occurs  mainly  in  later  life. 
The  explanation  of  this  fact  lies  in  the  peculiar  circumstances  which  occasion 
the  renal  process.  For  the  same  reason,  also,  the  male  sex  is  much  oftener 
attacked  than  the  female;  yet  the  causes  which  lead  to  contracted  kidney  are 
so  numerous  that  it  is  easy  to  understand  why  the  disease  is  not  infrequently 
seen  even  in  younger  individuals  and  in  women.  Contracted  kidney  does  occur 
in  children,  though  rarely.  In  all  cases  in  youthful  persons  we  must  make 
careful  inquiry  as  to  any  previous  attack  of  acute  nephritis,  subsequent  perhaps 
to  scarlet  fever,  diphtheria,  or  measles. 

The  relations  of  contracted  kidney  to  amyloid  disease  of  the  kidney  (so- 
called  amyloid-contracted  kidney),  and  to  chronic  disease  of  the  urinary 
passages,  particularly  of  the  pelvis  of  the  kidney,  will  be  discussed  later  in  the 
appropriate  chapters. 

Pathological  Anatomy. — In  the  genuine  contraction  of  the  kidney,  both 
kidneys  are  always  diminished  in  about  the  same  degree.  Their  size  is  some- 
times reduced  to  one  half  or  even  one  third  of  the  normal,  so  that  it  is  almost 
difficult  to  find  the  little  kidney  in  the  very  abundant  and  thick  fatty  capsule 
that  is  often  present.  The  kidneys  feel  firm  and  dense,  and  show  on  their 
surface  a  very  plain,  coarse  or  fine,  uniform  or  irregular,  granulation.  On 
pulling  off  the  somewhat  thickened  fibrous  capsule,  these  granulations  become 
more  prominent,  and  the  capsule  usually  adheres  quite  firmly  to  the  depressed 
portions.  The  raised  portions  are  almost  always  darker  and  redder — that  is, 
richer  in  blood — than  the  lighter  and  grayer  depressions.  Whether  the  whole 
kidney  appears  more  red  or  more  white  depends  only  upon  the  amount  of  blood 
in  the  organ,  and  there  is  no  reason  for  separating  the  "  small  red  "  from  the 
"  small  white  "  contracted  kidney. 

On  section  of  the  contracted  kidney  we  find  the  cortex  very  thin,  and  pale 
atrophic  streaks  alternating  with  the  darker  portions.  The  pyramids  are  also 
rather  small,  and,  as  a  rule,  are  darker  than  the  cortex.  In  the  pelvis  of  the 
kidney,  which  is  often  somewhat  dilated,  there  are  sometimes  a  number  of  uric- 
acid  concretions.  Striated  uric-acid  infarctions  in  the  pyramids  are  a  very 
characteristic  mark  of  the  gouty  contracted  kidney.  The  microscope  shows  an 
advanced  destruction  of  the  renal  parenchyma,  which  is  replaced  by  a  cicatri- 
cial connective  tissue  in  which  the  nuclei  are  still  numerous  or  else  have  al- 
ready become  scanty.  We  can  always  make  out  signs  of  degeneration  and 
atrophy  of  the  epithelium,  and  the  formation  of  casts  in  the  uriniferous  tubules 
which  still  remain,  but  which  are  already  diseased.  Atrophy,  thickening  of 
the  capsule,  etc.,  are  found  in  many  of  the  glomeruli.  The  uriniferous  tubules 
49 


774  DISEASES   OF   THE   URINARY   ORGANS 

that  are  still  preserved  in  some  places  are  often  in  part  dilated.  We  cannot, 
here  go  more  fully  into  the  manifold  histological  details,  especially  the  forma- 
tion of  cysts,  the  changes  in  the  vessels  (vide  supra),  the  deposition  of  lime 
salts,  etc.    Hemorrhages  are  only  very  rarely  present. 

Thus  the  contracted  kidney  may  be  regarded  as  the  form  of  chronic 
nephritis  with  by  far  the  longest  course  (lasting  from  three  to  five  years.,  and 
even  much  longer),  and  also  the  form  with  the  widest  extent.  Its  essential 
nature  can  in  no  way  be  contrasted  with  "  chronic  parenchymatous  nephritis  " 
as  a  "  chronic  interstitial  nephritis  " ;  for  we  always  find  interstitial  processes 
in  the  former,  which  have  reached  a  far  higher  degree  in  the  contracted  kidney 
only  because  the  slow  atrophy  of  tissue  is  compatible  with  a  much  longer  dura- 
tion of  life,  and  hence  can  attain  a  much  greater  extent. 

The  anatomical  changes  in  the  other  organs  of  the  body  besides  the  kidneys 
will  be  spoken  of  in  connection  with  the  symptomatology  of  contracted  kidney. 

Clinical  Symptoms. — Except  in  the  comparatively  rare  cases  where  we  can 
refer  the  origin  of  a  contracted  kidney  to  a  previous  acute  or  chronic  nephritis, 
the  clinical  symptoms  of  contracted  kidney  develop  as  gradually  and  insidiously 
as  the  anatomical  process  itself.  There  is  no  doubt  that  a  contraction  of  the 
kidney  may  exist  for  years  without  calling  the  patient's  attention  to  his  disease 
by  a  single  serious  subjective  symptom.  This  is  evident  from  the  chance  dis- 
coveries on  autopsy  of  a  contraction  of  the  kidney  in  people  who  have  lost  their 
lives  in  some  other  way,  but  especially  from  the  cases  where  the  severest  symp- 
toms, such  as  uraemia,  cerebral  hemorrhage,  etc.,  which  often  lead  immediately 
to  death,  suddenly  come  on  in  persons  previously  regarded  as  perfectly  healthy, 
while  the  autopsy  shows  a  quite  far  advanced  contraction  of  the  kidney  as  the 
special  cause  of  these  symptoms.  The  less  prominent  the  subjective  symptoms 
of  renal  contraction  are  in  the  earlier  stages  of  the  disease,  the  more  we  should 
consider  the  objective  changes,  which  in  fact  usually  permit  the  diagnosis  of 
the  disease  quite  early  on  careful  examination  of  the  patient. 

The  condition  of  the  urine  is  most  important  in  this  respect.  As  soon  as 
changes  have  taken  place  in  the  epithelium  in  different  parts  of  the  kidneys, 
the  results  previously  spoken  of  must  make  themselves  manifest  in  the  secre- 
tion of  the  urine,  although  still  in  a  slight  degree,  and  the  diseased  portions 
will  secrete  a  urine  diminished  in  amount  and  in  solid  constituents,  but  con- 
taining albumen.  Since,  however,  many  normal  uriniferous  tubules  and 
glomeruli  are  still  present,  and  since  the  whole  process,  as  we  have  seen,  de- 
velops only  very  slowly,  the  body  gains  time  for  the  development  of  one  of 
those  apt  compensatory  arrangements  which  we  recognize  in  so  many  patholog- 
ical processes,  and  which  we  must  regard  in  a  teleological  sense.  This  com- 
pensatory process  consists  of  an  increase  in  the  arterial  pressure,  coming  on 
as  gradually  as  the  renal  contraction  itself,  and  constantly  increasing,  and  of 
a  hypertrophy  of  the  left  ventricle  dependent  upon  it.  The  blood  therefore 
courses  through  the  many  normal  glomeruli  of  the  contracting  kidney  under 
an  increased  pressure,  and  the  consequence  is  that  in  these  portions  the  secre- 
tion of  the  urine,  especially  of  the  water,  is  much  more  abundant.  It  is  pos- 
sible, also,  that  the  incipient  disease  of  the  glomerular  walls  tends  to  increase 
their  permeability,  and  thus  contributes  to  the  polyuria.  At  any  rate,  it  is  a 
fact  that  in  cases  of  contracted  kidney  there  is  usually  an  abnormally  large 
amount  of  pale,  watery  urine  of  low  specific  gravity,  containing  merely  a  trace 


CONTRACTED   KIDNEY  775 

of  albumen  (originating  from  the  diseased  portions  of  the  organ).  The  daily 
amount  of  urine  is  often  70  to  120  ounces  (2,000  to  3,500  c.c.)  or  more;  the 
urine  looks  light  yellow  and  clear,  contains  scarcely  any  morphological  con- 
stituents, has  a  specific  gravity  of  1.010  to  1.005  or  even  lower,  and  gives,  on 
heating,  only  a  slight  precipitate  of  albumen,  the  amount  excreted  in  the 
twenty-four  hours  being  about  0.5  to  1  drachm  (gm.  2  to  5).  On  careful 
microscopical  examination  of  the  urine,  we  usually  succeed  in  finding  a  few 
hyaline  casts,  which  only  exceptionally  may  be  more  abundant.  The  urine 
also  frequently  contains  some  white,  and  more  rarely  a  few  red,  blood  cor- 
puscles. In  rare  but  definitely  attested  cases  it  may  happen  that  for  a  time, 
or  even  during  the  main  part  of  the  disease,  the  urine  contains  no  albumen  at 
all,  or  only  a  trace  of  it.  This  is  probably  explained  by  the  fact  that  the 
diseased  glomeruli  have  wholly  ceased  secreting,  and  that  therefore  the  urine 
is  secreted  only  by  the  healthy  portions  of  the  kidney.  As  to  the  character  of 
the  urine  in  arteriosclerotic  contracted  kidney,  vide  infra. 

It  is  apparent  of  how  great  significance  this  abundant  secretion  of  water, 
as  a  result  of  the  abnormally  high  blood  pressure,  must  be  for  the  whole  morbid 
process ;  for,  in  spite  of  the  renal  disease,  there  is  now  absolutely  no  retention 
of  water  in  the  body,  and  we  therefore  understand  why  there  is  often  no  oedema 
in  contracted  kidney,  even  after  a  course  of  years.  The  secretion  of  the  solid 
constituents  of  the  urine  is  not  quite  in  such  a  favorable  condition  as  the 
secretion  of  water.  It  is  self-evident  that  the  percentage  of  the  former  de- 
creases with  the  increased  amount  of  urine,  but  the  whole  amount  of  urea, 
uric  acid,  phosphoric  acid,  etc.,  eliminated  is  also  at  times  somewhat  less  than 
normal  in  relation  to  the  food.  This  diminution,  however,  is  not  very  great, 
as  long  as  the  work  of  the  heart  is  sufficient,  and  at  certain  times,  especially 
in  the  earlier  periods  of  the  disease,  a  normal  amount  may  be  secreted.  We 
accordingly  see  that  the  symptoms  dependent  upon  an  accumulation  of  the 
urinary  constituents  in  the  blood  do  not  appear  at  all  for  a  long  time.  Thus 
it  happens  that  the  patient  may  still  feel  perfectly  well  up  to  a  time  when 
the  objective  examination  of  the  urine  indicates  marked  pathological  changes. 
Many  patients,  of  course,  notice  the  polyuria,  but  often  no  special  attention 
is  paid  to  it,  and  it  is  attributed  to  drinking  a  good  deal  of  fluid.  The  patient 
gets  accustomed  to  it,  even  if,  as  often  happens,  he  has  to  pass  his  urine  much 
more  frequently  than  formerly,  and  even  during  the  night. 

We  need  not  go  into  detail  here  in  regard  to  the  special  causes  of  cardiac 
hypertrophy  (compare  page  740).  It  was  with  regard  to  contracted  kidney 
that  Traube  advanced  his  mechanical  theory  of  cardiac  hypertrophy,  which, 
however,  rested  upon  the  considerations  previously  mentioned,  and  therefore 
was  properly  replaced  by  the  chemical  theory,  which  was  also  very  applicable 
to  this  form  of  renal  disease.  In  its  clinical  relations  it  is  an  important  fact 
that  the  cardiac  hypertrophy  causes  no  subjective  symptoms  at  all  as  long  as 
the  heart  can  suffice  for  the  work  put  upon  it  without  strain,  a  condition 
which  is  perfectly  analogous  to  that  of  any  fully  compensated  valvular  disease. 
We  can  usually  recognize  the  condition  correctly  only  by  a  careful  physical 
examination  of  the  heart  and  the  vascular  apparatus,  although  in  contracted 
kidney  the  percussion  and  palpation  of  the  heart  are  often  rendered  difficult 
by  a  coexisting  pulmonary  emphysema.  We  can  often  perceive,  however,  the 
displacement  and  the  increased  strength  of  the  apex  beat,  the  extension  of 


776  DISEASES   OF   THE   URINARY  ORGANS 

the  cardiac  dullness  to  the  left,  and  almost  invariably  the  abnormal  tension 
of  the  radial  pulse  and  the  accentuation  of  the  aortic  second  sound.  In  the 
later  stages  of  the  disease  a  hypertrophy  of  the  right  ventricle  is  often  added 
to  that  of  the  left  (compare  page  742).  Complete,  or  almost  complete,  absence 
of  the  cardiac  hypertrophy  is  observed,  as  we  have  said,  only  in  weak  and 
cachectic  patients. 

As  long,  therefore,  as  the  high  arterial  pressure  kept  up  by  the  cardiac 
hypertrophy  regulates  the  renal  secretion  in  the  way  above  described,  the  con- 
dition of  the  patient,  as  a  rule,  shows  no  special  abnormality.  At  most  it  hap- 
pens that  certain  cerebral  symptoms  now  appear,  especially  attacks  of  headache 
and  occasional  vertigo,  which,  unless  they  are  ursemic,  are  probably  to  be  re- 
ferred to  active  cerebral  hyperemia.  Frequent  nosebleed  also  sometimes  re- 
sults from  the  abnormally  high  blood  pressure. 

The  clinical  picture  is  completely  transformed,  however,  upon  the  appear- 
ance of  the  first  signs  of  incipient  cardiac  insufficiency — that  is,  the  moment 
that  the  hypertrophy  of  the  left  ventricle  ceases  to  be  sufficient  to  overcome 
the  obstacles  to  the  secretion  of  urine  occasioned  by  the  deficiency  in  the  renal 
parenchyma.  The  disturbance  is  evident  either  when  the  left  ventricle  itself 
grows  weak,  or  when  the  gradual  advance  of  the  diseased  process  has  reached 
such  a  point  that  even  the  most  vigorous  efforts  of  the  heart  are  no  longer 
sufficient  to  bring  about  compensation.  In  the  latter  case  the  symptoms  which 
appear  are  to  be  regarded  as  uraemic,  in  the  broadest  sense  of  that  word.  The 
pulse  is  frequent,  but  it  still  remains  unusually  full  and  hard.  On  the  other 
hand,  in  case  there  is  a  diminution  in  the  cardiac  energy,  the  pulse  becomes 
more  compressible,  smaller,  more  frequent,  and  sometimes,  toward  the  ter- 
mination of  the  disease,  irregular.  The  heart  sounds  remain  pure,  but  the 
first  sound  often  becomes  indistinct.  When  there  is  a  decided  disturbance  of 
•compensation  we  hear  a  well-marked  bruit  de  galop.  In  all  these  cases  the. 
symptoms  result  from  the  disturbance  to  the  circulation,  and  from  the  conse- 
quent retention  of  urinary  constituents. 

Ordinarily,  the  subjective  symptoms  of  contracted  kidney  begin  very  grad- 
ually, then  disappear  for  a  time,  then  appear  again,  and  grow  worse  slowly  but 
steadily.  Apart  from  the  feeling  of  general  languor  and  weariness,  it  is  usu- 
alty  the  dyspnoea  which  first  calls  attention  to  the  disease.  The  patient  grows 
short  of  breath,  is  much  disturbed  by  even  slight  physical  exertion,  and  is 
perhaps  subject  to  attacks  of  palpitation.  Not  infrequently  the  dyspnoea  oc- 
curs, in  the  later  stages  of  the  disease,  in  distinct  paroxysms,  which  suggest 
asthma.  This  nephritic  asthma  has  long  been  recognized.  It  does  not  have 
the  same  origin  in  every  case ;  often  it  is  undoubtedly  the  result  of  the  attacks 
of  cardiac  weakness,  and  is  then  a  merely  cardiac  asthma  and  corresponds  in 
its  individual  symptoms  to  the  dyspnoea  of  heart  disease.  In  other  cases 
the  asthma  seems  to  be  connected  with  the  retention  of  the  products  of  metabo- 
lism (uraemic  asthma,  vide  supra).  The  clinical  picture  is  most  peculiar  in 
those  cases  in  which  the  dyspnoea  is  associated  with  the  signs  of  acute  pul- 
monary oedema,  and  is  attended  with  the  expectoration  of  a  large  amount  of 
foamy,  serous  sputum,  which  is  often  tinged  with  blood.  These  conditions, 
which  may  pass  off  and  reappear  at  stated  intervals,  are  mainly  those  to  which 
the  name  of  humid  asthma  was  formerly  given.  It  may  seem  questionable 
whether  we  should  regard  the  pulmonary  oedema  in  such  cases  as  a  purely 


CONTRACTED   KIDNEY  777 

congestive  transudation  due  to  cardiac  weakness,  or  as  an  cedema  occasioned 
by  nephritis  and  in  a  certain  degree  inflammatory.  In  the  last  stage  of  the 
disease  there  is  often  constant  dyspnoea,  and  this  may  be  the  chief  complaint 
of  the  patient.  It  is  in  such  cases  often  referable  to  various  causes  acting 
simultaneously;  for  instance,  pulmonary  congestion,  diffuse  bronchitis,  pneu- 
monia (vide  infra),  and  hydrothorax. 

Another  result  of  beginning  cardiac  failure  in  the  later  course  of  the  dis- 
ease may  be  oedema  of  various  portions  of  the  body.  This  is  certainly  in 
many  cases  to  be  regarded  as  a  purely  congestive  oedema,  particularly  when 
associated  with  contracted  kidney;  but,  on  the  other  hand,  we  cannot  always 
exclude  conditions  which  occasion  nephritic  cedema  (vide  supra).  It  has,  in- 
deed, been  repeatedly  observed  that  dropsy  may  be  entirely  absent  in  con- 
tracted kidney;  but  this  is  the  case  only  when  death  ensues  from  some  inter- 
current attack  before  the  pronounced  cardiac  insufficiency.  Otherwise  oedema 
is  by  no  means  rare  in  contracted  kidney.  It  usually  appears  first  in  the 
ankles,  the  eyelids,  or  the  prepuce,  disappears  again  when  the  patient  remains 
at  rest,  and,  after  a  longer  or  a  shorter  pause,  comes  on  anew,  until  finally,  in 
the  last  period  of  the  disease,  a  high  degree  of  general  dropsy  may  develop. 

Among  the  disturbances  of  the  internal  organs  we  must  mention  first  the 
cerebral  symptoms.  While  at  first,  as  we  have  said,  these  have  more  of  an  active 
hyperaemic  character,  the  frequent  and  very  violent  headaches  that  come  on 
later  in  part  are  of  a  urasmic  nature  and  in  part  depend  upon  the  passive  hy- 
peremia, or  the  arterial  anaemia  of  the  brain.  The  pain  sometimes  shoots  into 
the  back  of  the  neck,  and  sometimes  is  localized  chiefly  in  one  half  of  the  head ; 
it  is  often  associated  with  symptoms  of  vertigo,  with  a  gloomy  or  morose  mood, 
with  troubled  sleep,  etc.  The  stasis  is  usually  also  apparent  in  the  abdominal 
organs.  Chronic  dyspeptic  disturbances  appear,  the  appetite  fails,  the  bowels 
become  irregular,  and  we  can  even  make  out  a  moderate  enlargement  of  the 
liver.  The  influence  which  the  altered  activity  of  the  heart  exerts  upon  the 
function  of  the  kidneys  themselves  is,  however,  particularly  important.  From 
what  has  been  previously  said  of  the  dependence  of  the  secretion  of  urine  upon 
the  arterial  pressure,  it  follows  directly  that  any  compensatory  activity  of  the 
still  normal  renal  territory  must  at  once  experience  a  reduction,  as  soon  as 
the  blood  pressure  falls.  Corresponding  to  this  we  see,  in  fact,  that  the  secre- 
tion of  urine  also  usually  suffers  a  decline  at  the  same  time  with  the  other 
symptoms  of  stasis.  The  amount  of  urine  is  less  abundant :  it  drops  to  40  or 
50  ounces  (1,500  to  1,000  c.c),  and  even  lower;  the  specific  gravity  rises,  rarely 
to  a  high  figure,  but  still  up  to  1.010  or  1.012,  or  over.  The  urine  often  retains 
its  light  color  for  quite  a  long  time,  but  it  may  finally  more  and  more  resemble 
the  genuine  urine  of  stasis.  The  point,  however,  which  is  especially  to  be 
considered,  is  the  simultaneous  and  increasing  retention  of  the  solid  con- 
stituents of  the  urine  in  the  blood,  and  the  consequent  possibility  of  the  onset 
of  ursemic  symptoms. 

It  must  be  stated  that,  in  contracted  kidney,  the  immediate  exciting  causes 
of  ursemia  are  not  always  clear.  Thus,  it  is  a  well-known  and  very  important 
fact,  clinically,  that  very  severe  and  often  fatal  uremic  convulsions  may  some- 
times attack  the  patient  quite  suddenly,  apparently  when  in  the  best  of  health. 
Cases  have  been  repeatedly  seen,  by  other  observers  and  by  ourselves,  where 
the  daily  amount  of  urine  has  shown  no  discoverable  diminution  in  the  days 


778  DISEASES   OF   THE   URINARY   ORGANS 

preceding  the  uraemia.  Probably  the  explanation  of  this  is  that  for  a  long  time 
very  minute  amounts  of  toxic  material  are  daily  retained  in  the  blood,  and  that 
these  of  themselves  occasion  no  noticeable  disturbance  until  suddenly  the 
severe  symptoms  of  uraemia  develop  as  a  cumulative  result  of  long-continued, 
though  slight,  injurious  influences.  These  cases  of  suddenly  developing 
uraemia  always  remind  us  of  the  similar  phenomena  in  chronic  poisoning  from 
lead  or  mercury.  In  these  cases,  also,  after  a  long-continued  absorption  of 
trifling  amounts  of  poison,  the  symptoms  of  intoxication  may  finally  appear 
abruptly.  In  other  cases  of  uraemia  associated  with  contracted  kidney,  the  con- 
dition of  the  heart  is  of  great  importance.  The  uraemic  symptoms  develop  in 
different  ways,  according  to  the  slowness  or  rapidity  with  which  the  cardiac 
insufficiency  causes  diminution  in  the  urinary  secretion.  If  the  amount  of 
urine  is  slowly  diminished,  we  observe  the  s}rmptoms  of  chronic  uraemia  (page 
739),  consisting  of  headache,  vomiting,  diarrhea,  severe  pruritus  of  the  skin, 
etc.,  but  these  symptoms  are,  of  course,  often  combined  with  the  immediate 
symptoms  of  stasis,  and  are  not  always  to  be  easily  and  distinctly  separated 
from  them.  Such  a  condition  of  chronic  uraemia,  in  patients  with  contracted 
kidney,  often  presents  a  very  mournful  picture,  since  the  unrestrainable  and 
constantly  recurring  vomiting,  the  headache,  and  the  general  mental  anxiety 
may  last  for  weeks.  The  severe  acute  uraemia  either  is  preceded  by  chronic 
uraemic.  symptoms,  or  comes  on  at  once  in  the  severest  form,  with  general  and 
often-recurring  convulsions,  and  coma.  The  uraemia  may  pass  off  again,  even 
in  contracted  kidney,  but  quite  frequently  it  is  the  immediate  cause  of  death 
(vide  infra). 

Besides  the  symptoms  so  far  described,  we  must  now  mention  also  a  number 
of  anatomical  complications  which  may  appear  in  the  course  of  contraction  of 
the  kidney.  From  its  diagnostic  and  clinical  importance  the  albuminuric 
retinitis,  already  known  to  us  from  the  preceding  chapter,  takes  the  first 
place.  It  may  come  on  at  any  time  in  the  course  of  the  disease;  but  it  often 
develops  so  early  that  the  patient,  up  to  this  time,  knows  nothing  at  all  of 
his  other  disease.  He  merely  consults  an  oculist,  who  often  first  recognizes, 
from  the  ophthalmoscopic  image  (see  page  767),  the  special  seat  of  the  primary 
disease.  Even  in  the  cases  where  no  subjective  visual  disturbance  is  present, 
the  retinal  examination  sometimes  discloses  retinitis.  In  general,  the  con- 
tracted kidney  is  that  form  of  renal  disease  in  which  retinal  changes  are 
decidedly  most  frequent. 

Another  rarer  but  clinically  important  complication  consists  of  the  hemor- 
rhages in  internal  organs,  whose  cause  is  to  be  found  either  in  the  increased 
arterial  pressure,  or  in  an  abnormal  weakness  of  the  walls  of  the  vessels — 
arteriosclerosis  in  older  persons,  defective  nutrition  of  the  vascular  walls  in 
young  and  anaemic  patients.  Hemorrhages  into  the  brain  are  comparatively 
the  most  frequent.  They  cause  both  mild  and  severe  apoplectic  attacks,  which 
pass  off  completely  or  leave  a  hemiplegia  behind,  and  sometimes  they  are  the 
direct  cause  of  death.  Besides  the  hemorrhages  into  the  brain  itself,  there  may 
also  be  hemorrhages  on  the  inner  surface  of  the  dura  mater — hematoma. 
Nosebleed  is  also  of  significance ;  in  many  patients  it  is  frequent  and  very  stub- 
born ;  we  have  ourselves  seen  two  cases  where  the  fatal  termination  was  caused 
directly  by  an  unrestrainable  nosebleed.  Hemorrhages  into  the  other  organs 
are  more  rare,  but  they  have  been  observed  in  the  skin,  the  stomach,  the  intes- 


CONTRACTED   KIDNEY  779 

tines,  and  the  lungs.  In  a  few  cases,  indeed,  a  sort  of  hemorrhagic  diath 
seems  to  develop.  We  must  remind  the  reader  again,  in  this  connect  ion,  of  the 
general  truth  that  in  renal  disease  all  the  internal  organs  display  a  somewhat 
increased  tendency  to  secondary  inflammation;  thus  the  mucous  membranes 
often  present  an  accompanying  catarrhal  inflammation,  such  as  chronic  laryn- 
gitis, bronchitis,  gastric  catarrh,  and  intestinal  catarrh.  These  catarrhal 
troubles  are  in  part  to  be  regarded  as  due  to  congestion,  but  in  part  they  cer- 
tainly result  from  the  retention  of  the  products  of  metabolism.  In  serous 
membranes  we  often  observe  pleurisy,  pericarditis,  etc.  The  surface  of  the 
body  sometimes  displays  a  tendency  to  obstinate  eczema.  Of  the  inflammations 
of  internal  organs,  pneumonia  is  the  most  frequent  and  important.  Some 
cases  are  croupous  or  lobar,  and  some  are  of  that  diffuse  lobular  variety  which 
is  peculiar  to  all  sorts  of  nephritis.  We  have  already  mentioned  that  the  kid- 
ney itself  may  suffer  from  inflammatory  exacerbations,  in  addition  to  the 
chronic  disease. 

Very  great  variations  appear  in  regard  to  the  general  nutrition.  In  most 
cases  where  the  disease  develops  quite  gradually  in  persons  in  middle  or  ad- 
vanced life,  the  general  nutrition  for  a  long  time  shows  no  striking  anomaly. 
The  patient  is  often  very  well  nourished,  and  even  corpulent,  at  the  period 
when  the  first  cardiac  symptoms  begin.  To  the  more  practiced  and  attentive 
■eye,  of  course,  he  shows  a  certain  appearance  of  suffering,  which  later  becomes 
more  pronounced.  He  becomes  emaciated,  and  has  a  sallow  and  often  cyanotic 
complexion.  Marked  anaemia  usually  develops  only  in  younger  individuals, 
who  then  show  the  pallor  characteristic  of  so  many  patients  with  renal  disease. 

We  desire  to  append  a  few  remarks  with  regard  to  arteriosclerotic  con- 
tracted kidney.  This  may  pursue  precisely  the  characteristic  course  of  the 
ordinary  disease,  but  in  many  cases  its  symptoms  are  very  obscure.  If  we 
examine  carefully,  from  day  to  day,  the  urine  of  old  persons  who  present  other 
signs  of  general  arteriosclerosis,  we  shall  be  likely  to  find  at  many  times  a 
small  trace  of  albumen,  and  at  other  times  none  at  all.  In  such  cases  we  may 
foe  almost  certain  that  there  is  an  arteriosclerotic  contracted  kidney.  Still,  the 
renal  symptoms  are  usually  of  minor  importance  in  the  clinical  picture  of 
senile  marasmus,  senile  emphysema,  senile  dementia,  or  the  other  changes  of 
old  age. 

General  Course,  Duration,  and  Termination. — The  most  important  pecul- 
iarities in  the  course  of  renal  contraction  have  already  been  spoken  of  above. 
We  have  stated  that  the  disease  may  be  latent  for  a  long  time ;  that  the  severest 
symptoms — such  as  uraemia  or  apoplexy — sometimes  come  on  suddenly  and 
unexpectedly;  that  in  other  cases  the  disturbances  of  compensation  in  the 
heart,  dyspnoea,  palpitation,  or  slight  oedema,  are  the  first  symptoms;  that, 
under  some  circumstances,  certain  complicating  conditions,  such  as  retinitis, 
or  frequent  nosebleed,  first  direct  suspicion  to  a  renal  disease,  and  suggest  an 
examination  of  the  urine;  while,  finally,  in  a  last  class  of  cases,  only  general 
disturbances,  loss  of  appetite,  pallor,  general  physical  weakness,  and  similar 
symptoms  induce  the  patient  to  consult  a  physician.  It  is  usually  hard  to 
decide  how  long  the  disease  has  lasted  before  a  diagnosis  is  made.  We  must 
especially  inquire  into  the  existence  of  polyuria,  which  patients  may  not  notice, 
however,  even  if  it  exists. 

The  further  course  may  vary  according  to  the  onset  of  complications,  the 


780  DISEASES   OF   THE   URINARY  ORGANS 

external  conditions  under  which  the  patient  lives,  etc.  In  general,  as  we  must 
repeatedly  emphasize,  much  depends  upon  the  heart's  capacity  for  work  and 
its  staying  qualities.  If  death  does  not  ensue  sooner  from  some  intercurrent 
disease,  the  last  stage  of  the  disease  almost  always  presents  itself  under  the 
picture  of  cardiac  insufficiency  with  predominant  symptoms  of  dyspnoea  and 
general  dropsy. 

As  has  been  said,  we  usually  cannot  determine  with  any  accuracy  the 
duration  of  the  disease.  It  may,  at  any  rate,  last  many  years,  probably  even 
ten  years  or  more,  although  there  may  be  many  variations  in  its  course.  It  is 
not  impossible  that,  during  the  earlier  period  of  the  disease,  there  may  be 
a  cessation  in  the  process  of  renal  atrophy,  but  it  is  hard  to  decide  with  cer- 
tainty. At  all  events,  the  disease  must  generally  be  termed  absolutely  incura- 
ble, although  life  may  not  only  be  preserved  for  a  long  time,  but  the  patient 
may  even  exist  without  much  discomfort.  We  need  not  refer  especially  here 
to  the  different  intercurrent  attacks,  the  possibility  of  which  must  always  be 
kept  in  mind  in  regard  to  prognosis. 

Diagnosis. — The  diagnosis  of  contracted  kidney  can  be  made'  with  cer- 
tainty only  by  examining  the  urine.  We  must,-  therefore,  dwell  again  on  the 
necessity  of  making  this  examination  in  all  suspicious  cases,  because  only  in 
this  way  can  we  avoid  overlooking  the  condition.  The  suspicion  of  a  develop- 
ing renal  contraction  should  demand  an  examination  of  the  urine,  especially 
in  all  cases  where  the  patient  complains  of  frequent  headache,  of  congestive 
conditions,  of  palpitation  and  dyspnoea,  asthmatic  attacks,  disturbances  of 
vision,  general  dullness,  and  dyspeptic  symptoms,  without  finding  any  other 
reason  for  these  symptoms.  The  polyuria,  the  clear  urine  of  low  specific  grav- 
ity, containing  a  slight  amount  of  albumen,  in  connection  with  the  signs  in 
the  circulatory  apparatus,  the  tense  pulse,  and  the  hypertrophy  of  the  left 
ventricle,  permit  us  to  recognize  the  disease  correctly  in  most  cases.  If 
retinal  changes  are  present,  they  may  sometimes  be  of  much  aid  in  confirming 
the  diagnosis.  The  serological  conditions — lead,  gout,  alcoholism,  etc. — of 
course  also  merit  attention. 

The  diagnosis  presents  great  difficulty  in  the  quite  rare  cases  where  albu- 
minuria is  absent.  In  these  cases  we  are  sometimes  able  to  reach  the  correct 
interpretation  of  the  morbid  condition  only  by  repeated  examinations  of  the 
urine.  Otherwise  we  can  scarcely  avoid  mistaking  it  for  chronic  affections  of 
the  heart,  such  as  myocarditis  or  idiopathic  hypertrophy. 

The  diagnosis  is  also  very  difficult  if  the  patient  does  not  come  under  ob- 
servation until  the  stage  of  fully  developed  disturbance  of  compensation.  The 
characteristic  features  of  the  urine  of  contracted  kidney  are  then  absent,  the 
urine  is  scantier,  darker,  richer  in  albumen,  and  it  is  often  scarcely  possible 
to  decide  whether  we  have  a  primary  renal  affection  with  secondary  cardiac 
hypertrophy  or  a  primary  heart  disease  with  a  secondary  congested  kidney. 
If  general  arteriosclerosis  or  marked  pulmonary  emphysema  is  present  at  the 
same  time,  the  judgment  as  to  the  condition  is  still  more  difficult.  In  such 
cases  a  correct  diagnosis  is  possible  only  by  very  carefully  balancing  all  the 
different  symptoms,  and  considering  the  whole  course  of  the  disease. 

Finally,  the  diagnosis  of  contracted  kidney  is  very  difficult  in  cases  where 
the  first  examination  of  the  patient  is  made  during  a  sudden  attack  of  uraemia 
or  after  an  apoplectic  seizure.     Here  the  albuminuria  is  the  symptom  which 


CONTRACTED   KIDNEY  781 

points  most  to  the  existence  of  a  renal  disease,  although,  in  spite  of  this  symp- 
tom, the  judgment  as  to  the  condition,  and  its  differentiation  from  other  acute 
cerebral  affections,  often  presents  great  difficulties. 

We  must  devote  a  few  words  to  those  not  very  infrequent  cases  in  which  a 
small  amount  of  albumen  is  found,  often  quite  by  chance,  in  the  urine  of 
youthful  individuals  who  are  apparently  in  perfect  health;  thereupon  the 
question  is  propounded,  which  is  often  of  extreme  practical  importance, 
whether  we  are  dealing  with  a  so-called  physiological  or  intermittent  albu- 
minuria (vide  supra,  page  725),  or  with  an  actual  renal  disease — viz.,  an  un- 
suspected contracted  kidney.  The  diagnosis  is  never  easy.  In  the  first  place, 
it  is  necessary  to  make  careful  observations  for  a  considerable  period,  at  the 
same  time  varying  the  conditions  as  to  nourishment  (nitrogenous  diet,  milk 
diet,  use  of  beer)  and  activity  (complete  physical  rest,  persistent  exercise) ; 
then  we  must  carefully  investigate  all  the  possible  etiological  circumstances, 
such  as  previous  disease  and  mode  of  life,  and  finally  take  into  consideration 
the  associated  phenomena — for  instance,  of  the  circulatory  apparatus,  the 
retina,  etc.  From  a  practical  point  of  view  it  is  advisable  to  be  most  cautious 
in  all  these  cases,  and,  at  any  rate,  to  give  such  advice  as  to  regimen  with  the 
aim  of  preventing  damage  to  the  kidneys,  as  if  there  were  an  actual  renal 
disease. 

Treatment. — As  soon  as  the  diagnosis  of  renal  contraction  is  established, 
the  whole  hygienic  condition  of  the  patient  must  be  regulated  so  as  to  pre- 
vent the  advance  of  the  affection  in  every  possible  way.  In  this  respect  two 
indications  are  to  be  fulfilled — to  guard  against  any  irritation  which  may 
have  an  injurious  action  on  the  kidneys  and  to  relieve  the  work  of  the  heart 
as  much  as  possible,  in  order  to  keep  off  cardiac  insufficiency  as  long  as  we  can. 
The  diet  must  be  carefully  regulated,  and  must  be  of  scant  measure  or  abun- 
dant and  strengthening,  according  to  the  patient's  physical  constitution.  In 
these  cases,  too,  milk  is  a  food  of  great  value,  but  it  should  not  be  prescribed 
unnecessarily  for  corpulent  patients.  The  determination  as  to  the  amount 
of  salt  in  the  food  must  depend  on  the  considerations  already  pointed  out. 
The  use  of  meat  is,  in  general,  to  be  limited,  while  easily  digestible  dishes 
made  from  cereals  and  eggs,  and  vegetables  and  fruits,  are  to  be  recommended. 
Whether  the  so-called  white  meats  (poultry,  veal,  lamb),  as  so  many  at  pres- 
ent assume,  are  really  less  injurious  than  the  so-called  dark  meats  (beef, 
venison),  cannot  be  positively  proved,  but,  notwithstanding,  this  view  will 
usually  be  remembered  in  practice.  Alcoholic  drinks  should  be  permitted 
only  in  small  quantity.  Mineral  waters  (Fachingen,  Wildungen,  Wernazer 
water,  etc.)  and  water  with  lemon  juice  or  the  juice  of  other  fruits,  etc.,  serve 
as  beverages.  Great  care  of  the  skin  is  an  important  matter.  We  should 
recommend  the  regular  employment  of  warm  baths  or  salt  baths,  and  daily 
sponging  of  the  whole  body  with  brandy  or  warm  vinegar.  All  physical  over- 
exertion is  to  be  avoided,  although  moderate  methodical  exercise  is  to  be 
recommended  for  corpulent  patients.  We  should  always  provide  for  regular 
evacuation  of  the  bowels  by  appropriate  remedies,  dietetic  prescriptions,  fruits, 
bitter  mineral  waters,  etc.  The  general  condition  is  often  materially  im- 
proved by  proper  air  and  recreation,  and  in  this  way  resort  to  a  bath  may  be 
of  service,  chosen  according  to  the  individual  conditions,  such  as  Briickenau, 
Marienbad,  Carlsbad,  Kissingen,  Nauheim,  Ems,  or  Baden-Baden.     In  ap- 


782  DISEASES   OF   THE   URINARY   ORGANS 

propriate  cases  a  winter  residence  in  the  south  is  advisable — e.  g.,  in  the  Ei- 
viera  or  Egypt. 

If  disturbances  of  compensation  appear,  we  must  be  still  more  strict  in  our 
dietary,  and  must  enjoin  the  utmost  physical  rest,  at  the  same  time  employ- 
ing other  treatment  according  to  the  symptoms  which  may  be  present.  Above 
.all,  we  must  endeavor  to  impart  new  vigor  to  the  heart  by  means  of  digitalis 
and  digitalis  preparations — digalen,  digipuratum — though  unfortunately  such 
efforts  often  prove  unavailing.  The  minutiae  of  treatment  in  this  connection 
are  almost  precisely  the  same  as  in  chronic  heart  disease  (q.  v.)  and  in  other 
renal  diseases.  The  treatment  of  the  dyspnoea  and  chronic  uraemia,  which 
develop  in  the  last  stages  of  the  disease,  is  apt  to  be  most  unsatisfactory;  but 
we  can,  sometimes,  at  least,  remove  the  symptoms  by  various  external  appli- 
cations upon  the  chest  and  the  head  (ice  bags  or  hot  compresses),  by  various 
drugs  to  combat  the  nervous  symptoms,  bromid  of  potassium,  antipyrin,  ni- 
troglycerin, and  by  the  combination  of  cardiac  stimulants,  such  as  digitalis 
and  strophanthus,  with  diuretics,  such  as  caffein,  diuretin,  agurin,  theophyllin, 
theocin,  etc.  In  the  worst  cases  narcotics  are  indispensable,  particularly  sub- 
cutaneous injections  of  morphin.  As  yet  we  are  unable  to  exert  a  direct  bene- 
ficial influence  by  drugs  upon  the  interstitial  process  in  the  kidneys.  The  only 
ones  recommended  for  this  purpose  and  worth  a  trial  are  the  preparations  of 
iodin — viz.,  iodid  of  potassium  or  iodid  of  sodium,  in  daily  amounts  of  3 
•to  8  gr.  (gm.  0.2  to  0.5),  and,  in  anaemic  patients,  iodid  of  iron.  We  do  not 
need  to  go  minutely  into  the  treatment  of  the  numerous  complications  which 
occur. 

The  prophylaxis  of  renal  contraction  is  evident;  we  should  avoid  so  far  as 
we  can  the  known  serological  conditions. 


CHAPTEE   V 
AMYLOID    KIDNEY 

etiology. — The  amyloid  kidney  is  invariably  associated  with  the  more  or 
less  extensive  amyloid  degeneration  of  other  organs  in  the  body.  In  its  clin- 
ical relations,  however,  it  claims  the  most  interest  of  all  amyloid  diseases, 
since  it  has  by  far  the  greatest  significance  for  the  whole  clinical  picture  of 
amyloid  degeneration. 

As  is  well  known,  we  understand  by  amyloid  degeneration  a  peculiar 
change  which,  under  certain  pathological  conditions,  is  observed  in  the  con- 
nective tissue,  and  especially  in  the  smaller  vessels.  The  walls  of  the  vessels 
are  thickened,  they  have  a  lustrous,  homogeneous  appearance,  and  they  show 
peculiar  reactions  on  treatment  with  certain  coloring  agents.  These  reac- 
tions are  due  to  the  presence  of  an  albuminoid  substance — amyloid — which 
either  is  deposited  in  the  tissue  from  the  blood,  or,  as  is  much  more  probable, 
is  developed  in  that  spot  from  the  albuminoid  substances  there  present.  In 
marked  amyloid  degeneration  the  diseased  organs  often  show  macroscopically 
an  altered,  "  bacon-like  "  appearance,  and  assume  a  characteristic  red-brown 
color  on  treating  the  affected  parts  with  Lugol's  solution  of  iodin,  changing 


AMYLOID   KIDNEY  783 

to  violet  on  the  addition  of  sulphuric  acid.  The  microscopic  examination 
alone  affords  more  accurate  conclusions  as  to  the  presence  and  distribution  of 
the  degeneration.  For  this  purpose  we  usually  stain  the  tissues  with  methyl 
violet  or  gentian  violet.  The  amyloid  portions  thus  take  on  a  very  charac- 
teristic and  clearly  defined  red  color.  In  this  way  we  can  discover  that  the 
amyloid  degeneration  hegins  everywhere  in  the  walls  of  the  small  vessels, 
that  the  interparenchymatous  connective  tissue  may  also  be  affected  later, 
hut -that  the  parenchymatous  cells  proper,  liver  cells,  renal  epithelium,  etc., 
almost  always  remain  perfectly  free.  The  latter  often  show  atrophic  and 
fatty  degenerative  changes  (vide  infra),  but  little  if  any  amyloid  degen- 
eration. 

Nothing  is  known  as  to  the  special  causes  which  effect  this  peculiar  meta- 
morphosis of  the  albumen  of  the  connective  substance  into  amyloid.  We  know 
only  that  there  are  a  number  of  primary  diseases  in  which  experience  has 
shown  that  amyloid  degeneration  quite  frequently  develops  as  a  secondary 
condition  in  the  different  organs.  These  conditions  have,  for  the  most  part, 
the  common  characteristic  of  being  associated  with  general  cachexia  and  de- 
bility, and  of  being  connected  with  some  localized  chronic  morbid  process  in 
some  part  of  the  body,  from  which  abnormal  chemical  matters  may  be  con- 
stantly carried  into  the  blood.  We  suppose  that  the  normal  albuminous 
material  is  transformed  into  amyloid  by  means  of  such  influences.  With 
regard  to  the  relations  which  may  exist  between  the  so-called  hyaline  degen- 
eration of  Eecklinghausen,  and  amyloid  disease,  the  investigations  are  not 
yet  complete. 

The  conditions  in  which  amyloid  degeneration  in  general,  and  conse- 
quently amyloid  disease  of  the  kidney  also,  are  chiefly  observed,  are  the  fol- 
lowing, arranged  in  about  the  order  of  their  frequency: 

1.  Chronic  pulmonary  tuberculosis,  particularly  the  ordinary  ulcerative 
phthisis.  Tubercular  ulcers  of  the  intestines,  with  or  without  coexisting 
marked  pulmonary  tuberculosis,  may  also  lead  to  amyloid  disease. 

2.  Long-continued  chronic  suppuration  in  the  bones  or  soft  parts,  es- 
pecially chronic  fungous  processes  with  fistulas  into  the  bones  or  joints,  em- 
pyema with  fistulas,  vertebral  caries,  etc. 

3.  Constitutional  syphilis,  chiefly  the  cases  with  ulcerative  and  usually 
tertiary  processes  in  the  bones  and  mucous  membranes. 

4.  Other  ulcerative  processes,  or  processes  associated  with  chronic  suppu- 
ration: saccular  bronchiectases,  chronic  intestinal  ulcers  (for  example,  of 
dysenteric  origin),  purulent  pyelocystitis,  vesicovaginal  fistulas,  ulcerated  new 
growths,  such  as  cancer,  etc. 

5.  In  rare  cases  amyloid  degeneration  has  also  been  observed  in  other 
chronic  diseases,  as  in  malaria,  gout,  and  other  chronic  articular  affections. 
In  the  medical  clinic  at  Leipsic  we  once  saw  a  case  of  marked  amyloid  kidney 
in  a  girl  of  twenty-one  with  aortic  insufficiency. 

6.  Finally,  in  a  small  class  of  cases,  -of  which  we  have  ourselves  seen  some 
examples,  no  discoverable  cause  at  all  may  be  found  at  the  autopsy  for  quite 
extensive  amyloid  degeneration.  In  such  cases,  therefore,  there  seems  to  be 
a  primary  intoxication  with  resultant  amyloid  disease. 

Pathological  Anatomy. — With  regard  to  the  anatomical  lesions  of  amyloid 
disease  in  other  organs,  we  shall  refer  to  handbooks  on  pathological  anatomy. 


784  DISEASES   OF   THE   URINARY   ORGANS 

As  to  amyloid  liver,  see  page  714.  Here  we  shall  discuss  merely  the  patho- 
logical anatomy  of  amyloid  kidney. 

In  very  slight  and  limited  amyloid  degeneration  of  the  kidneys,  the 
latter  present  a  perfectly  normal  appearance  to  the  naked  eye.  Careful 
microscopic  examination  alone  shows  amyloid  degeneration  of  the  walls 
of  different  vessels  in  the  cortex,  and  especially  in  the  medullary  sub- 
stance. 

The  commonest  and  most  characteristic  form  of  amyloid  kidney  is  the  so- 
called  large  white  amyloid  kidney  (waxy  kidney,  lardaceous  kidney).  The 
kidney  is  usually  enlarged,  and  the  surface  is  smooth  and  of  a  grayish-white 
or  yellowish  color,  and  usually  somewhat  mottled.  On  section,  the  cortex  is 
wide  and  also  of  a  yelloAvish-white  color,  and  the  glomeruli  may  often  be 
recognized  with  the  naked  eye  as  dull,  lustrous,  translucent  points.  Hemor- 
rhages are  scarcely  ever  seen.  The  medullary  substance  may  be  also  pale,  or 
darker.  In  many  cases  the  cortex  may  itself  have  a  darker  reddish  or  mottled 
appearance,  which  is  due  merely  to  the  greater  amount  of  blood  in  the  organ. 
The  pale-yellow  color  is  due  either  to  the  ansemia  or  to  the  fatty  degeneration,, 
while  the  amyloid  spots  show  a  more  translucent  character  with  a  bacon-like 
luster. 

If  we  examine  the  kidney  microscopically,  we  find  first  the  amyloid  de- 
generation, which,  in  varying  extent  and  combination,  affects  most  frequently 
the  glomeruli  and  also  the  capillaries  of  the  cortex,  the  vasa  recta,  and  some- 
times the  membrana?  propria?  of  the  uriniferous  tubules.  In  pure  amyloid 
kidney  the  rest  of  the  renal  tissue  is  normal,  but  in  many  cases  we  find 
changes  in  the  epithelium — fatty  degeneration,  desquamation,  and  disintegra- 
tion— and  also  not  infrequently  interstitial  cellular  infiltration.  We  see, 
therefore,  that  amyloid  degeneration  of  the  kidney  is  not  infrequently  asso- 
ciated with  degenerative  changes  of  an  inflammatory  nature.  Thus  we  ob- 
serve, not  infrequently,  the  combination  of  chronic  diffuse  nephritis  (large 
white  kidney)  with  amyloid. 

If  the  process  has  lasted  for  a  long  time,  it  leads,  as  in  ordinary  nephritis, 
to  a  complete  atrophy  of  tissue  in  some  parts,  with  a  corresponding  increase 
of  connective  tissue.  Then  the  renal  tissue  sinks  in  at  the  affected  spots,  and 
there  is  a  decided  unevenness  to  the  surface  of  the  kidney.  There  is  even  a 
completely  developed  red  or  white  contracted  kidney,  in  which  we  find  abun- 
dant amyloid,  and  which  is,  therefore,  termed  amyloid  contracted  kidney. 
In  this  form  the  parenchymatous  and  interstitial  changes  correspond  pre- 
cisely to  those  in  ordinary  contracted  kidney,  only  the  amyloid  degeneration 
is  added  to  them. 

At  present  differences  of  opinion  prevail  as  to  the  precise  connection  be- 
tween amyloid  and  the  inflammatory  degenerative  processes  in  the  kidney. 
In  our  opinion  there  is,  in  most  cases,  an  actual  combination  of  both  condi- 
tions, they  being  coeffects  of  simultaneously  acting  causes.  We  have  seen 
that  in  tuberculosis,  chronic  suppuration,  etc.,  genuine  nephritis  may  develop, 
as  well  as  amyloid  disease,  so  it  cannot  be  surprising  that  sometimes  with  these 
diseases  both  sequela?,  nephritis  and  amyloid,  should  develop  side  by  side,  and 
that  we  should,  consequently,  find  in  the  kidney  not  only  the  changes  asso- 
ciated with  an  inflammatory,  large,  white  kidney,  a  secondary  contraction,  or 
a  genuine  contracted  kidney,  but  also  a  more  or  less  extensive  amyloid  de- 


AMYLOID   KIDNEY  785 

generation.  On  the  other  hand,  it,  of  course,  cannot  he  questioned  that  the 
disturbance  of  circulation,  which  must  arise  in  conM-queiice  of  a  marked  amy- 
loid degeneration  of  the  vessels,  is  of  influence  on  the  nutrition  of  the  renal 
tissue,  and  that,  therefore,  many  changes  in  it,  especially  fatty  degeneration 
of  the  epithelium,  are,  under  some  circumstances,  the  direct  result  of  the 
amyloid  disease. 

Clinical  History. — If  we  consider  the  great  diversity  which  the  distribu- 
tion of  the  amyloid  change  in  the  kidneys  shows,  and  its  manifold  combina- 
tions with  inflammatory  processes,  it  is  clear  from  the  outset  that  we  cannot 
get  up  a  uniform  picture  of  the  symptoms  of  amyloid  disease  in  general.  To 
this  we  must  add  that  the  symptoms  of  amyloid  disease,  which  is  almost  al- 
ways a  secondary  condition,  are  also  modified  in  various  ways  by  the  primary 
disease. 

We  must  first  state  that  many  cases,  where  the  amyloid  change  in  the  kid- 
neys is  of  comparatively  slight  extent,  cannot  be  recognized  by  any  clinical 
symptom.  The  albuminuria  in  particular  ma}r  be  entirely  absent,  as  has  been 
repeatedly  proved  (Eosenstein,  Litten,  and  others).  That  in  such  cases  the 
vasa  recta  and  not  the  glomeruli  are  chiefly  affected  by  the  amyloid  degenera- 
tion has  been  affirmed  but  not  proved. 

Except  in  these  instances,  however,  the  urine  secreted  from  the  amyloid 
kidneys  shows  marked  changes,  which,  of  course,  present  considerable  varia- 
tions according  to  the  form  of  the  individual  case.  The  amount  of  urine  is 
most  frequently  about  normal,  or  somewhat  diminished — in  some  cases  much 
diminished — but  in  others  it  is  decidedly  increased,  so  that  the  patient  may 
pass  80  "to  120  ounces  (2,500  to  3,500  c.c.)  in  the  twenty-four  hours.  We 
quite  frequently  see  considerable  variations  in  the  amount  of  the  urine  in  the 
same  patient  at  different  times.  All  these  differences  are  easily  explained  if 
we  remember  how  many  circumstances  may  affect  the  amount  of  urine — the 
presence  or  absence  of  inflammatory  changes  in  the  kidney,  the  presence  or 
absence  of  cardiac  hypertrophy,  coexisting  perspiration,  diarrhea,  oedema, 
fever,  etc. 

The  color  of  the  urine  is  almost  always  light  yellow.  Only  exceptionally, 
in  amyloid  nephritis,  does  it  contain  an  abundant  sediment;  usually  it  is  en- 
tirely, or  almost  entirely,  clear.  The  very  considerable  amount  of  albumen 
in  the  urine,  which  is  often  one  or  two  per  cent,  is  also  characteristic  of  amy- 
loid kidney.  In  many  cases,  indeed,  particularly  in  the  combination  of 
amydoid  with  contracted  kidney,  the  amount  of  albumen  is  smaller,  although 
usually  decidedly  more  abundant  than  in  pure  interstitial  nephritis.  Sen- 
ator has  pointed  out  that  the  comparative  amount  of  the  globulin  which  is 
contained  in  the  urine  besides  the  serum  albumen  is  often  particularly  large 
in  amyloid  kidney.  The  specific  gravity  of  the  urine  varies  very  much  ac- 
cording to  the  amount  of  water  and  albumen  in  it.  It  may  be  increased  (1.015 
to  1.020)  or  diminished  (1.010  to  1.005). 

If  we  examine  the  urine  under  the  microscope,  we  usually  find  only  a  few 
hyaline  casts,  and  also  most  frequently  a  small  number  of  white  blood  cor- 
puscles. In  general,  it  is  very  characteristic  of  amyloid  kidney  that  there 
is  an  abundance  of  albumen,  contrasting  with  the  scanty  or  scarcely  appreci- 
able microscopic  sediment.  In  the  combination  of  amyloid  with  more  marked 
nephritic  changes  the  sediment  is  more  abundant,  so  that  the  urine  is  cloudy. 


786  DISEASES   OF   THE   URINARY   ORGANS 

The  microscope  then  shows  more  numerous  hyaline  or  moderately  fatty  casts,, 
more  abundant  white  blood  corpuscles,  sometimes  a  little  renal  epithelium, 
and  in  quite  rare  cases  even  red  blood  corpuscles.  Amyloid  reaction  is  said 
to  occur  in  the  casts,  but  it  is  very  rare,  and  therefore  of  no  value  in 
diagnosis. 

The  other  morbid  symptoms  which  are  observed  in  amyloid  kidney  depend 
either  upon  the  change  in  the  kidneys  themselves,  or  upon  coexisting  amy- 
loid degeneration  in  other  organs;  or,  lastly,  upon  the  primary  disease.  The 
symptoms  of  the  latter  are,  of  course,  extremely  varied,  but  in  many  cases, 
they  may  be  entirely  subordinate. 

In  regard  to  the  directly  resulting  symptoms  of  amyloid  kidney,  their 
occurrence  is  of  interest,  especially  in  comparison  with  the  analogous  condi- 
tions in  acute  nephritis.  Dropsy  of  a  moderate,  or  even  a  severe  degree,  is 
often  present  in  amyloid  kidney,  but  it  may  also  be  entirely  absent.  We  must 
remember  that  an  oedema  independent  of  a  renal  affection  may  be  produced 
by  marantic  venous  thrombosis.  Ursemic  symptoms  are  distinctly  rare  in 
amyloid  kidney,  but  they  are  sometimes  observed,  especially  in  their  milder 
forms,  such  as  vomiting.  It  is  a  very  important  point  that  hypertrophy  of 
the  left  ventricle  is  absent  in  most  cases  of  amyloid  kidney.  This  is  explained 
partly  by  the  fact  that  the  disease  usually  affects  feeble,  cachectic  individuals 
who  have  no  superfluous  material  for  the  manufacture  of  cardiac  hypertrophy, 
and  partly  by  the  fact  that  in  pure  amyloid  kidney  there  is  no  appreciable 
retention  of  urinary  constituents  in  the  blood.  This  latter  fact  explains,  also, 
the  infrequency  of  ursemic  symptoms  (vide  supra).  If,  however,  the  amyloid 
degeneration  is  combined  with  genuine  nephritic  changes,  the  condition  of 
things  is  altered.  In  amyloid  contracted  kidney  we  have  repeatedly  observed 
hypertrophy  of  the  left  ventricle. 

Albuminuric  retinitis  hardly  ever  appears  in  pure  amyloid  kidney.  In 
the  amyloid  contracted  kidney  it  has  sometimes  been  observed,  however,  in 
cases  where  there  has  probably  been  originally  a  pure  contracted  kidney,  with 
amyloid  coming  on  later.  The  secondary  inflammations  in  the  internal  organs, 
such  as  renal  pneumonia,  and  the  hemorrhages,  such  as  cerebral  hemorrhage, 
are  also  rare. 

The  patient's  general  condition  is  dependent  in  part  upon  the  renal  dis- 
ease, and  in  part  upon  amyloid  degeneration  in  other  organs,  but  mainly  upon 
the  primary  disease.  The  patient  with  amyloid  kidney  is  usually,  therefore, 
cachectic,  and  shows  in  high  degree  a  pallid,  anaemic  color  of  the  skin.  If, 
also,  general  dropsy  develops,  we  have  an  external  appearance  very  charac- 
teristic of  amyloid  disease;  still,  in  some  few  cases  of  syphilis,  bronchiectasis, 
and  unilateral  pulmonary  contracture,  the  general  nutrition  remains  tolerably 
good  for  a  considerable  time. 

The  symptoms  which  point  to  a  coexisting  amyloid  degeneration  in  other 
organs  besides  the  kidneys  are  of  great  diagnostic  significance.  The  symp- 
toms in  the  liver  (enlargement,  abnormal  firmness,  and  a  hard,  sharp  lower 
edge  to  the  organ),  the  spleen  (enlargement  and  hardness),  and  intestines 
(obstinate  diarrhea  not  yielding  to  any  remedy)  are  clinically  important  in 
this  respect.  The  interpretation  of  the  diarrhea  is,  of  course,  usually  difficult, 
since  it  may  often  depend  upon  tubercular  intestinal  ulcers  as  well  as  upon 
amyloid  disease  of  the  intestines. 


AMYLOID   KIDNEY  787 

We  can  scarcely  make  general  statements  in  regard  to  the  whole  course  and 
the  duration  of  amyloid  kidney,  since  the  form  of  the  primary  disease  i-  to  he 
especially  considered  in  these  cases.  In  regard  to  the  time  that  it  takes  for  an 
amyloid  degeneration  to  develop  in  an  existing  primary  disease,  the  degenera- 
tion is  certainly  present  sometimes  after  a  few  months.  Of  course,  it  is  hardly 
ever  possible  to  determine  its  onset  accurately,  since  the  first  beginnings  of 
amyloid  degeneration  in  the  kidneys  do  not  usually  permit  themselves  to  be 
recognized  at  once  by  the  appearance  of  albuminuria  (vide  supra).  The 
duration  of  amyloid  kidney  varies  very  much  according  to  the  severity 
of  the  case;  it  may  last  only  a  few  weeks  or  months  before  death,  while 
other  cases  have  certainly  lasted  for  a  year,  especially  in  amyloid  contracted 
kidney. 

Prognosis. — The  prognosis  of  amyloid  kidney  is  in  most  cases  utterly  un- 
favorable, which  is  due  mainly  to  the  incurability  of  the  primary  disease ;  but 
trustworthy  observers  have  repeatedly  proved  that,  when  the  primary  disease 
is  curable,  as  with  syphilis  and  many  chronic  suppurations,  an  already  devel- 
oped amyloid  kidney  may  exceptionally  be  completely  restored. 

Diagnosis. — The  diagnosis  of  amyloid  kidney  can  be  made  with  consider- 
able certainty  when  the  evident  signs  of  a  renal  affection  are  added  to  those 
of  a  disease  which  we  know  by  experience  to  promote  the  development  of 
amyloid  degeneration.  Whether  in  such  cases  we  have  a  pure  amyloid  or  a 
pure  nephritis,  or  a  combination  of  the  two,  can  be  decided  with  some  certainty 
only  from  the  condition  of  the  urine;  a  clear  urine,  containing  but  few  mor- 
phological elements,  but  rich  in  albumen,  points  to  pure  amyloid,  while  a 
large  number  of  casts  and  red  and  white  blood  corpuscles  in  the  urine  points 
to  the  presence  of  inflammatory  changes  in  the  kidney.  The  diagnosis  of 
amyloid  contracted  kidney  is  justified  when  the  symptoms  of  contracted  kidney 
(abundance  of  pale  urine,  secondary  cardiac  hypertrophy)  are  seen  in  associa- 
tion with  such  morbid  conditions  as  are  likely  to  occasion  amyloid  disease. 
Of  great  importance,  as  we  have  already  pointed  out,  is  the  comparatively 
large  amount  of  albumen  and  the  consequently  somewhat  higher  specific  gravity 
of  the  urine.  Of  many  cases  of  amyloid  kidney  it  is  very  characteristic,  and 
so  of  diagnostic  value,  that  there  is  a  rapid  and  frequent  variation  in  the 
amount  of  urine  and  the  percentage  of  albumen   (Wagner). 

A  very  material  support  for  the  diagnosis  of  amyloid  kidney,  and  there- 
fore one  which  should  always  be  looked  for,  is  the  discovery  of  amyloid 
degeneration  in  other  organs.  We  have  briefly  mentioned  above  the  most 
important  symptoms  in  the  liver,  the  spleen,  and  the  intestines  referable  to 
this  point. 

Treatment. — Only  the  treatment  of  the  primary  disease  can,  of  course,  be 
considered,  both  as  a  prophylactic  and  also  as  a  causal  indication.  In  many 
surgical  cases,  and  also  in  the  cases  of  amyloid  in  syphilis,  there  is  a  possi- 
bility of  this  (as  by  iodid  of  potassium),  but  otherwise  we  try  to  improve  the 
primary  disease  as  far  as  we  can. 

In  other  respects  the  treatment  is  purely  hygienic  and  symptomatic.  We 
must  try  to  strengthen  the  patient  as  much  as  possible  by  good  food  and  the 
exhibition  of  preparations  of  iron  and  quinin.  The  use  of  iodid  of  iron  or 
small  doses  of  iodid  of  sodium  is  to  be  recommended.  In  a  symptomatic 
point  of  view  the  same  remedies  are  used  as  in  other  renal  diseases. 


788 


DISEASES   OF   THE   URINARY   ORGANS 


We  insert  here  a  synopsis  of  the  condition  of  the  urine  and  of  the  left 
ventricle  in  the  most  important  varieties  of  renal  disease. 


Amount  of 

Specific 

Amount  of 

Morphological  Constit- 

Condition of 

Urine. 

Gravity. 

Albumen. 

uents- 

Left  Ventricle. 

1.  Acute  nephritis. .  . 

Diminished. 

High. 

Consider- 

Numerous        casts; 

Not   hyper- 

able. 

blood  corpuscles ; 
epithelium. 

trophied. 

2.  Chronic   diffuse 

Normal     or 

High. 

Consider- 

Numerous        casts ; 

Hypertro- 

somewhat 

able. 

blood      corpuscles ; 

phied. 

diminished 

epithelium ;  fatty 
degeneration  of  the 

3.  Contracted 

cells. 

Increased. 

Low. 

Slight. 

Few      casts  ■      small 

Hypertro- 
phied. 

number    of    blood 

corpuscles. 

4.  Amyloid  kidney .  . 

Variable, 

Variable. 

Consider- 

Few casts. 

Not   hyper- 

normal,  or 

able. 

trophied. 

increased. 

5.  Amyloid  con- 

tracted kidney  . 

Increased. 

Rather  low. 

Moderate. 

Few  casts . 

Hypertro- 
phied. 

6.  Passive  conges- 

tion   

Diminished. 

High. 

Absent     or 

Few     casts;     blood 

Generally 
prima  ry 

scanty. 

corpuscles. 

heart    dis- 

ease. 

CHAPTER    VI 


PURULENT    NEPHRITIS    AND    PERINEPHRITIS 


1.     PURULENT   NEPHRITIS 

iEtiology. — Although  in  the  forms  of  nephritis  so  far  described  the 
occurrence  of  large  numbers  of  nuclei  in  the  interstitial  tissue  has  been 
repeatedly  mentioned,  none  of  them  ever  come  to  genuine  suppuration 
— that  is,  to  a  purulent  liquefaction  of  tissue,  a  true  abscess  formation. 
The  origin  of  a  purulent  nephritis  is,  rather,  always  associated  with  the 
entrance  of  perfectly  definite  morbid  irritants  into  the  kidneys.  These  are 
invariably  organized,  and  their  special  peculiarity  is  to  excite  a  purulent 
inflammation. 

There  are  two  chief  ways  through  which  the  morbid  irritants  may  reach 
the  kidneys — the  arterial  blood  current  and  the  urinary  passages.  The  first- 
mentioned  means  of  entrance  is  to  be  considered  in  all  the  cases  of  purulent 
nephritis  which  come  on  as  one  symptom  of  pyasmic  processes  and  certain 
forms  of  ulcerative  endocarditis  (see  pages  138  and  373  on  the  point).  Far 
more  rarely  purulent  nephritis  develops  in  this  way  as  a  complication  in  other 
diseases,  such  as  dysentery.  Purulent  nephritis  also  occurs  in  actinomycosis 
(Israel). 

The  excitants  of  inflammation  take  the  second  path  in  those  cases  where  a 
purulent  nephritis  follows  an  inflammation  of  the  lower  urinary  passages,  the 


PURULENT   NEPHRITIS   AND   PERINEPHRITIS  789 

pelvis  of  the  kidney,  the  bladder,  etc.  Here  the  bacteria,  which  almost  always 
enter  directly  into  the  urinary  passages  (the  urethra  and  bladder)  from  with- 
out, pass  gradually  upward  from  the  bladder  through  the  ureter  to  the  pelvis 
of  the  kidney;  from  this  they  enter  the  apertures  of  the  collecting  tubes  and 
the  uriniferous  tubules  of  the  kidney,  everywhere  exciting  a  purulent  inflam- 
mation. We  therefore  term  these  forms  of  purulent  nephritis — with  regard  to 
their  origin — purulent  pyelonephritis. 

We  must  remark  in  conclusion  that  a  purulent  nephritis  and  perinephritis 
(vide  infra)  may  arise  in  direct  wounds  of  the  kidney  from  infection  of  the 
wound. 

Pathology. — Purulent  nephritis  shows  quite  characteristic  peculiarities 
and  differences  according  to  its  mode  of  origin.  (We  omit  traumatic  ab- 
scesses here.) 

The  renal  abscesses  in  pyaemia  and  analogous  diseases  are  usually  focal 
suppurations,  which  only  exceptionally  attain  a  great  extent,  but  which  are  usu- 
ally to  be  recognized  with  the  naked  eye  as  numerous  little  yellowish  dots  or 
lines,  scattered  over  the  whole  kidney,  about  half  a  millimeter  or  a  millimeter 
in  diameter.  On  microscopic  examination,  these  nodules  prove  to  be  genuine 
little  abscesses,  in  whose  territory  the  renal  tissue  proper  is  completely  de- 
stroyed. In  the  middle  of  them  we  often  find  the  originating  colony  of  micro- 
cocci, the  "  micrococci  embolus,"  seated  in  a  central  vessel.  The  conditions 
are  still  plainer  if  we  examine  an  earlier  stage  of  the  process.  We  find  vessels 
(the  loops  of  the  glomeruli,  or  the  encircling  capillaries),  which  are  com- 
pletely plugged  with  micrococci,  and  in  whose  vicinity  the  renal  tissue  is  still 
perfectly  normal.  We  further  see  analogous  spots  where  the  renal  tissue  is 
already  necrosed  in  the  vicinity  of  the  colony  of  micrococci,  and  is  infiltrated 
with  emigrated  cells.  These  nodules  show,  finally,  a  continuous  transition  to 
the  completed  abscess,  which  is  often  surrounded  by  a  hyperaemic  or  even  a 
hemorrhagic  areola. 

In  purulent  pyelonephritis  the  renal  abscesses  appear  somewhat  different. 
The  abscesses  also  have  a  characteristic  striated  appearance,  corresponding  to 
the  distribution  of  the  inflammation  along  the  straight  tubules.  They  often 
extend  from  the  point  of  the  renal  papilla  through  the  cortex  to  the  surface 
of  the  organ,  so  that  from  the  outside  we  see  the  abscesses,  showing  through 
as  yellowish  points.  The  broader  abscesses  arise  from  the  confluence  of  neigh- 
boring strige.  The  microscope  shows  that  the  purulent  inflammation  arises 
from  the  vessels  of  the  interstitial  tissue,  in  whose  territory  the  uriniferous 
tubules  are,  of  course,  destroyed.  The  clusters  of  micrococci  form  the  most 
interesting  feature.  These  settle  originally  in  the  uriniferous  tubules,  and  are 
the  special  cause  of  the  necrosis  of  epithelium  and  the  inflammation.  Pyelo- 
nephritis, indeed,  was  one  of  the  first  diseases  for  which  a  bacterial  origin  was 
discovered  (Klebs). 

Clinical  Symptoms. — We  can  speak  very  briefly  here  in  regard  to  the  clin- 
ical symptoms  of  purulent  nephritis,  since  they  can  never  be  sharply  separated 
from  the  symptoms  of  the  primary  disease.  The  pysemic  renal  abscesses,  and 
the  abscesses  in  ulcerative  endocarditis,  hardly  ever  cause  special  clinical  symp- 
toms, so  that  their  presence  is  first  recognized  on  the  autopsy  table.  Since 
the  abscesses  do  not,  as  a  rule,  communicate  with  the  uriniferous  tubules,  there 
is  usually  no  great  amount  of  pus  in  the  urine. 
50 


790  DISEASES   OF   THE   URINARY   ORGANS 

The  clinical  symptoms  of  pyelonephritis  also  depend  less  upon  the  nephritic 
abscesses  than  upon  the  previous  and  accompanying  pyelitis  and  cystitis.  We 
will  therefore  return  to  renal  abscesses  in  the  description  of  these  diseases. 

2.    PERINEPHRITIC    (PARANEPHRITIC)    ABSCESS 

Perinephritic  abscess  is  the  name  given  to  suppurations  in  the  vicinity  of 
the  kidney,  especially  in  its  fatty  capsule  or  in  the  perirenal  connective  tissue. 
Apart  from  any  traumatic  origin  for  such  abscesses,  they  develop  most  fre- 
quently as  a  result  of  purulent  nephritis  or  purulent  pyelitis.  The  escape  of 
pus,  which  involves  the  surrounding  tissue  in  the  inflammation,  may  come 
from  the  ureter  or  pelvis  of  the  kidney,  or  from  the  kidney.  The  special  form 
of  primary  disease  differs  very  much;  it  may  be  either  simple  purulent 
pyelitis,  or  pyelitis  from  renal  calculi,  or  sometimes  tubercular  processes  and 
new  growths  that  finally  suppurate,  such  as  cancer  or  echinoeocci.  The  peri- 
renal suppuration  may  also  take  its  start  from  the  other  organs  in  the  neigh- 
borhood. Thus  cases  have  been  seen  in  which  the  perinephritis  followed  a 
perityphlitic  abscess,  a  hepatic  abscess,  or  a  psoas  abscess  after  vertebral  dis- 
ease. Perinephritic  suppuration  may  also  be  due  to  actinomycosis.  It  is  a 
very  important  fact,  however,  that  paranephritic  abscesses  may  develop  as  a 
primary  disease  in  persons  in  apparently  perfect  health,  particularly  in  middle- 
aged  men,  and  this  without  any  discoverable  cause.  It  is  usually  absolutely 
impossible  to  determine  how  and  by  what  path  the  inflammatory  germs  reach 
the  perirenal  connective  tissue  unless  possibly  they  migrate  from  the  intestine. 
These  cases  of  abscess  are  very  important  from  a  clinical  standpoint,  because 
the  symptoms  are  at  first  difficult  of  interpretation.  There  is  fever,  usually 
of  a  decidedly  intermitting  pyasmic  type,  and  there  are  also  dull,  indefinite 
pains  in  the  loins  or  abdomen,  constipation,  and  constitutional  symptoms. 
The  cause  of  all  these  symptoms  is  gradually  made  apparent  by  the  develop- 
ment of  distinct  local  changes. 

In  almost  all  cases  of  perinephritic  abscess  the  accumulation  of  pus  finally 
becomes  so  great  that  a  swelling  appears,  usually  in  the  lumbar  region,  and 
this  grows  more  and  more  prominent;  at  first  it  is  scarcely  noticeable,  but 
later  the  skin  becomes  cedematous  there,  it  constantly  protrudes  more  and 
more,  it  assumes  an  inflammatory  hypersemic  redness  until,  finally,  a  definite 
fluctuation  shows  the  advance  of  the  abscess  up  to  the  skin.  In  other  cases 
the  inflammatory  swelling  extends  forward  into  the  iliac  fossa;  then  there  is 
also  abnormal  resistance  and  dullness  above  Poupart's  ligament.  The  swelling 
may  also  extend  upward  toward  the  diaphragm,  so  that  the  diaphragm  is 
crowded  upward,  giving  rise  to  marked  dyspnoea.  The  relations  of  the  swell- 
ing to  the  descending  colon  are  sometimes  the  same  as  in  new  growths  of  the 
kidney  (compare  Chapter  VIII). 

Besides  the  swelling  there  is  almost  invariably  a  very  great  pain  in  the 
affected  region,  either  spontaneous  or  on  pressure.  If  the  swelling  presses  on 
the  large  nerve  trunks  in  the  vicinity,  it  produces  severe  shooting  pains  in  the 
leg  of  the  same  side,  and  sometimes  a  numb  feeling  and  paresis.  The  leg  is- 
then  often  kept  in  a  position  similar  to  that  in  coxitis. 

The  fever  is  persistent,  and  usually  of  an  intermittent  character  and  as- 
sociated with  rigors.    It  and  the  pain  make  the  patient  thin  and  feeble,  even 


DISTURBANCES  OF   CIRCULATION   IN   THE   KIDNEYS  791 

to  an  extreme  degree.  The  urine  does  not  contain  pus  unless  the  abscess  has 
some  connection  with  the  urinary  passages. 

Recovery  may  occur  if  the  pus  finds  some  way  out  of  the  body.  Apart  from 
operative  interference,  the  most  favorable  termination  is  the  spontaneous  dis- 
charge of  the  pus  into  the  intestine  (colon),  or  into  the  urinary  tract  (pelvis 
of  the  kidney,  bladder).  The  course  of  the  disease  is  much  more  tedious  if 
the  pus  finds  its  way  through  the  skin.  If  renal  abscesses  discharge  outwardly, 
they  most  frequently  point  in  the  loins,  less  often  like  a  psoas  abscess,  below 
Poupart's  ligament.  They  may  also  discharge  into  the  pleural  or  peritoneal 
cavities,  with  a  consequent  empyema  or  quickly  fatal  peritonitis.  In  other 
cases,  if  prompt  surgical  aid  is  impossible,  death  occurs  from  exhaustion. 

Diagnosis. — The  diagnosis  is  made  chiefly  from  the  swelling,  pain,  and 
fever,  and  a  consideration  of  the  ^etiological  factors.  We  can  settle  any  doubts 
in  most  cases  by  exploratory  puncture.  The  condition  may  be  confounded 
with  hydronephrosis,  psoas  abscess,  and  solid  tumors  of  the  kidney. 

Treatment. — The  only  treatment,  apart  from  the  fulfillment  of  any  symp- 
tomatic indications,  is  surgical,  and  consists  in  opening  and  draining  the  ab- 
scess. The  result  depends  chiefly  upon  the  patient's  general  condition,  and 
the  character  of  the  primary  disease.  The  details  are  to  be  found  in  the  text- 
books of  surgery. 


CHAPTER    VII 
DISTURBANCES    OF    CIRCULATION    IN    THE    KIDNEYS 

1.  The  Congested  Kidney. — Although  local  impediments  to  the  flow  of 
venous  blood  from  the  kidneys,  such  as  thrombosis  of  the  renal  veins,  hardly 
ever  attain  a  clinical  significance,  the  participation  of  the  kidneys  in  a  general 
venous  stasis,  as  is  seen  chiefly  in  heart  disease  (compare  page  403),  pulmo- 
nary emphysema,  etc.,  is  of  great  diagnostic  importance,  since  we  possess  in 
the  condition  of  the  urine  quite  an  accurate  measure  of  the  intensity  as  well 
as  of  the  increase  and  decrease  of  the  stasis. 

The  congested  kidney  is  easily  recognized  anatomically.  The  organ  is 
often  somewhat  enlarged,  it  feels  firmer  than  normal,  and  shows,  both  on  its 
surface  and  on  section,  a  dark,  bluish-red  color — "  cyanotic  induration."  The 
medullary  substance  is  usually  darker  than  the  cortex.  Under  the  microscope 
we  see  considerable  dilatation  and  a  tense  fullness  of  the  veins  and  capillaries. 
The  parenchyma  is  normal,  but  in  more  advanced  cases  it  may  show  a  begin- 
ning fatty  degeneration  of  the  epithelium,  which  is  a  result  of  the  defective 
arterial  blood  supply.  At  first  the  interstitial  tissue  is  little  changed,  but  if 
the  congestion  persists  for  a  long  while  there  may  be  a  gradual  destruction  of 
the  renal  parenchyma,  to  a  certain  degree,  with  the  formation  of  an  abun- 
dance of  contractile  interstitial  tissue  (congested  and  contracted  kidney). 

The  clinical  symptoms  of  congested  kidney  concern  only  the  changes  in  the 
urine.  The  amount  of  urine  diminishes,  corresponding  to  the  diminution  of 
the  arterial  pressure  and  the  diminished  rapidity  of  the  blood  current.  Only 
25  to  20  ounces  (800  to  500  c.c),  or  less,  10  to  6  ounces  (300  to  200  c.c),  are 
secreted  daily.     The  urine  is  also  more  concentrated  and  darker  than  normal, 


792  DISEASES  OF   THE   URINARY   ORGANS 

and  often  has  an  abundant  sediment  of  urates.  If  nutritive  disturbances  have 
begun  in  the  epithelium  of  the  glomeruli  as  a  result  of  stasis,  the  urine  is  also 
albuminous,  but  the  amount  of  albumen  in  pure  congested  kidney  is  always 
slight — about  ^  to  ^  of  the  volume.  The  urine  often  contains,  besides,  a  few 
hyaline  casts,  and  a  few  white  and  red  blood  corpuscles,  the  latter  pointing 
to  little  congestive  hemorrhages. 

If  the  changes  mentioned  come  on  as  one  symptom  of  a  general  venous 
stasis,  and  are,  accordingly,  associated  with  cyanosis  and  dropsy,  the  diagnosis 
of  congested  kidney  can  be  made  with  certainty.  If  we  succeed  in  restoring 
the  circulation  by  appropriate  remedies,  such  as  digitalis,  the  urine  at  once 
becomes  more  abundant  and  clearer  and  its  albumen  disappears.  Otherwise 
the  characteristics  of  the  urine  of  passive  congestion  last  until  the  patient's 
death. 

2.  Embolic  Infarction  in  the  Kidneys. — Since  the  renal  infarction,  al- 
though it  has  great  pathological  interest,  is  hardly  ever  of  clinical  significance, 
we  will  limit  ourselves  here  to  a  brief  description  of  the  most  essential  points. 

If  one  of  the  smaller  renal  arteries  is  plugged  by  an  embolus  in  heart  dis- 
ease, the  affected  portion  of  the  organ  cut  off  from  the  circulation  must  perish, 
since  all  the  renal  arteries  are  terminal  arteries.  The  epithelium  undergoes 
the  well-known  changes  of  coagulation  necrosis,  disappearance  of  the  nuclei 
of  the  cells,  and  disintegration,  and  the  tissue  becomes  entirely  or  in  part  a 
hemorrhagic  infarction  (compare  page  403).  In  this  way  arise  the  charac- 
teristic wedge-shaped,  red,  hemorrhagic  infarctions  in  the  kidney,  or  far  more 
frequently  the  yellowish-gray,  ansemic  infarctions  (often  surrounded  by  a 
hemorrhagic  areola),  the  base  of  which  is  at  the  surface  of  the  kidney;  the 
base  may  reach  a  width  of  half  a  centimeter  to  a  centimeter  or  more,  while  the 
apex  extends  a  varying  distance  into  the  cortex,  or  even  into  the  medullary 
substance.  Later  on  the  gradually  disintegrated  tissue  of  the  infarction  is 
absorbed,  round  cells  emigrate  from  without  into  the  region  destroyed,  and  a 
shrunken  connective-tissue  cicatrix  gradually  develops  in  place  of  the  former 
infarction.  Many  kidneys  may  have  such  a  granular  surface  from  numerous 
infarction  cicatrices  that  they  may  be  appropriately  termed  "  embolic  con- 
tracted kidneys." 

The  anatomical  processes  just  briefly  described  cause  in  most  cases  no 
special  clinical  symptoms  at  all.  Sometimes,  however,  a  slight  amount  of 
blood  in  the  urine  seems  to  depend  on  the  development  of  a  hemorrhagic  in- 
farction in  the  kidneys,  so  that  when  a  cause  for  embolic  processes,  such  as 
heart  disease,  is  present,  we  may  entertain  the  suspicion  of  the  development 
of  a  renal  infarction  during  life.  In  rare  cases  the  development  of  a  rather 
large  infarction  of  the  kidneys  is  associated  with  a  sudden  and  violent  pain 
in  that  region,  with  marked  subsequent  hsematuria  or,  as  we  observed  in  one 
case,  hemoglobinuria. 

The  embolic  processes  in  the  kidney  never  demand  special  treatment. 


NEW   GROWTHS  IN   THE  KIDNEYS  793 

CHAPTEE    VIII 
NEW    GROWTHS    IN    THE    KIDNEYS 

1.  Congenital  Sarcomatous  Mixed  Growths  of  the  Kidney. — Of  the  primary 
forms  of  tumor  occurring  in  the  kidney,  those  tumors,  often  of  great  size,  that 
are  not  rarely  observed  in  young  children  especially  claim  our  interest.  In 
former  times,  they  were  often  regarded  either  as  sarcomata  or  as  carcinomata. 
We  now  know  that  we  have  to  deal  with  new  growths  which  owe  their  origin 
to  embryonic  disturbances  of  development,  and  which,  therefore,  present  a 
varied  formation  even  in  one  and  the  same  tumor,  being  at  one  time  more 
of  a  sarcomatous  character  and  composed  of  spindle  or  round  cells,  at  another 
more  adenomatous  or  carcinomatous.  It  is  an  especially  interesting  fact  that 
in  these  tumors  tissue  elements  may  appear  which  are  normally  never  present 
in  the  kidney,  and  whose  presence  can  be  explained  only  on  the  theory  of 
"  scattered  germs."  Thus,  striped  muscle  fibers  have  been  repeatedly  found 
in  tumors  of  that  character,  to  which  the  name  striocellular  myosarcoma  or 
rhabdomyoma  is  applied;  in  other  cases  cartilaginous  tissue,  mucoid  tissue, 
etc.,  have  also  been  found.  This  theory  obtains  a  further  interesting  confirma- 
tion from  our  own  observation  of  the  development  of  left-sided,  and,  probably, 
congenital  renal  sarcoma  in  two  brothers.  Both  children  died  when  between 
two  and  three  years  of  age,  and  the  autopsy  gave  almost  precisely  the  same 
lesions  in  both:  numerous  metastases  in  the  liver  and  lungs,  besides  a  new 
growth  almost  as  large  as  a  child's  head  in  place  of  the  left  kidney.  But  these 
tumors  may  also  attain  a  very  considerable  size  without  forming  metastases. 

2.  Renal  Sarcoma  and  Carcinoma. — Genuine  renal  sarcoma  and  particularly 
carcinoma  are  also  not  rarely  observed.  The  carcinoma  may  originate  in  part 
from  the  tissue  itself,  and,  in  part,  from  the  membranous  lining  of  the  pelvis 
of  the  kidneys  without  giving  rise  to  metastases.  The  sarcomata  are,  in  part, 
angiosarcomata  and  endotheliomata,  etc.  Benal  cancer  is  also  remarkably  fre- 
quent, comparatively  speaking,  in  children  under  four  years  of  age,  and  about 
equally  common  in  the  two  sexes.  Of  course,  we  find  renal  cancer  in  persons 
of  more  advanced  years;  in  some  cases  of  this  sort  renal  calculi  seem  to  occa- 
sion the  development  of  carcinoma.  This  is  like  the  relation  between  gall- 
stones and  cancer  of  the  biliary  passages.  Usually  only  one  kidney  is  affected, 
chiefly  the  left,  as  it  seems,  but  the  new  growth  has  sometimes  been  found  in 
both  kidneys.  In  its  character,  renal  cancer  belongs  either  to  the  denser  or 
to  the  softer,  medullary  form.  It  may  permeate  the  whole  kidney  and  change 
it  to  a  large  tumor,  weighing  15  or  20  pounds  (5  or  10  kgm.).  Softening 
and  hemorrhage  very  often  take  place  within  the  tumor.  The  proliferation 
has  been  repeatedly  observed  to  extend  to  the  neighboring  parts,  especially 
the  pelvis  of  the  kidney,  and  metastases  also  form  in  other  organs,  as  in  the 
lymph-glands,  liver,  or  lungs.  It  should  also  be  mentioned  that  several  times 
renal  cancer  and  cancer  of  the  testicle  have  been  combined. 

3.  Benign  Kidney  Tumor. — The  only  benign  form  of  kidney  tumor  that 
has  any  particular  clinical  interest  is  the  rare  one  of  lipoma,  since  it  may 
develop  into  a  large-sized  tumor.  Besides  this,  we  would  mention  the  interest- 
ing cystic  tumors  of  the  kidneys   (cystic  degeneration),  which  probably  have 


794  DISEASES   OF   THE   URINARY   ORGANS 

some  connection  with  anomalies  of  embryonic  development.  Their  occur- 
rence as  a  congenital  anomaly,  their  occasional  appearance  as  a  family  disease, 
and,  finally,  their  frequent  association  with  other  disturbances  of  develop- 
ment (anomalies  of  the  ureters  and  of  the  renal  vessels,  simultaneous  for- 
mation of  cysts  in  the  liver,  etc.),  all  point  to  this  conclusion.  Some  kidney 
cysts,  which  do  not  proceed  from  the  uriniferous  tubules,  but  from  atypical 
proliferations  of  glands,  are  to  be  regarded  as  adenocystomata.  Kidney  cysts 
may  develop  into  rather  large  tumors,  and  may  be  unilateral  or  bilateral. 

4.  Hypernephroma. — Clinically,  the  so-called  hypernephroma — i.  e.,  growths 
originating  in  scattered  suprarenal  cells,  and  therefore  lying  beneath  the 
kidney  capsule  ("  Grawitz  tumors  ") — are  not  to  be  separated  from  genuine 
tumors  of  the  kidney.  They  may  form  large  tumors  whose  histological  struc- 
ture allows  their  origin  from  the  suprarenal  cells  to  be  plainly  recognized.  In 
consequence  of  the  large  amount  of  fat  in  them,  these  swellings  generally  pre- 
sent a  yellowish-white  soft  surface  on  section,  and  a  tendency  to  disintegra- 
tion and  to  hemorrhages. 

Symptomatology. — The  clinical  symptoms  of  new  growths  in  the  kidneys 
may  first  become  noticeable  through  the  appearance  of  a  swelling.  Tumors 
of  the  kidney,  in  children,  may  attain  a  considerable  size  (vide  supra),  caus- 
ing a  distention  of  the  entire  abdomen.  But  even  when  smaller,  upon  careful 
palpation,  renal  tumors  often  enough  are  distinctly  felt  in  the  lumbar  and 
lower  lateral  abdominal  regions.  Bimanual  palpation  is  most  advisable,  the 
one  hand  pressing  forward  from  behind  and  below  in  the  region  of  the  kid- 
ney, while  the  other  presses  against  it  from  above  and  in  front.  In  this  man- 
ner it  is  often  possible  to  get  the  entire  tumor  between  the  two  hands.  A 
particularly  characteristic  factor  in  diagnosis  is  the  ballottement  renal  de- 
scribed by  Guyon :  when  a  gentle  thrust  is  made  in  the  renal  region  the  tumor 
is  felt  to  strike  softly  upon  the  anterior  abdominal  wall.  The  tumor  feels 
firm  and  sometimes  smooth,  sometimes  uneven ;  it  does  not  usually  move  with 
respiration,  but  this  rule  has  exceptions,  particularly  in  the  case  of  tumors 
of  the  right  kidney.  In  tumors  of  the  left  kidney  some  diagnostic  importance 
attaches  to  the  relation  of  the  new  growth  to  the  descending  colon,  inasmuch 
as  the  latter  is  pushed  forward  by  the  growth  of  the  tumor  and  comes  to  lie 
between  it  and  the  anterior  abdominal  wall.  It  is  quite  often  possible  to 
demonstrate  that  portion  of  the  intestine  which  traverses  the  tumor  by  means 
of  percussion  at  times  after  previous  distention  with  air,  and  sometimes 
also  by  means  of  palpation,  or  by  Rontgen  rays  after  the  introduction  of  bis- 
muth pap.  In  the  case  of  tumors  of  the  right  kidney  there  may  be  corre- 
sponding relations  to  the  ascending  colon,  but  this  is  less  frequent.  Almost 
all  larger  tumors  of  the  kidney  occasion  displacement  of  the  diaphragm  up- 
ward, and  of  neighboring  organs  laterally.  A  number  of  other  clinical  symp- 
toms are  to  be  noted.  These  sometimes  become  noticeable  before  the  appear- 
ance of  a  palpable  tumor,  and  themselves  lead  to  a  more  exact  palpatory 
-examination  of  the  abdomen.  In  a  third  class  of  cases  it  is  altogether  im- 
possible directly  to  demonstrate  the  existence  of  the  tumor,  and  only  the 
accompanying  and  resultant  phenomena  appear.  There  may  often  be  scarcely 
any  tenderness  and  pain,  but  in  some  cases  the  latter  is  violent  and  persistent. 
Often  the  pressure  of  the  tumor  upon  neighboring  nerve  trunks — for  instance, 
the  sciatic — occasions  obstinate  neuralgia,  sometimes  associated  with  paresis. 


NEW   GROWTHS   IN   THE   KIDNEYS  795 

The  state  of  the  urine  is  of  the  greatest  importance.  Not  infrequently,  it 
shows  no  abnormal  conditions  at  all  if  it  is  secreted  by  the  other  healthy  kid- 
ney, or  by  the  normal  parts  of  the  diseased  one.  Very  often,  however,  from 
time  to  time,  blood  appears  in  greater  or  lesser  amount  mixed  with  the  urine. 
In  many  cases  the  hematuria  is  the  first  indication  of  an  existing  kidney 
affection.  It  is,  of  course,  rare  in  congenital  tumors  in  children,  but,  on  the 
other  hand,  quite  frequent  in  sarcoma  and,  above  all,  in  cancer  in  adults,  and 
equally  frequent  in  hypernephroma.  As  has  already  been  mentioned,  it  often 
appears  at  a  time  when  no  tumor  at  all  can  be  felt.  The  hemorrhage  is  asso- 
ciated with  colicky  pains  only  when  large  clots  have  to  pass  through  the 
urinary  passages.  Sometimes,  but  very  rarely,  small  particles  and  shreds  of 
tissue  from  the  disintegrated  new  growth  may  be  found  in  the  urine. 

The  influence  of  the  tumor  on  the  constitutional  condition  varies  greatly. 
The  general  condition  of  children  with  congenital  tumors,  may  remain  good 
for  a  long  time.  In  other  respects  the  symptoms  are  the  same  as  in  all  other 
tumors.  The  appearance  of  mild  symptoms  of  Addison's  disease  repeatedly 
observed  by  us  in  hypernephroma,  is  very  interesting.  "We  should,  therefore, 
carefulty  note  any  anomalies  of  pigmentation  in  the  folds  of  the  hands  and 
fingers,  etc.  We  have  also  seen  peculiar  nervous  conditions  (persistent  som- 
nolence, comatose  state)  in  such  cases.  We  must  also  mention  the  peculiar 
symptom  several  times  observed  in  children  with  congenital  renal  tumors — 
viz.,  an  abnormally  early  development  of  the  pubic  and  axillary  hairs  (Kiihn). 
The  tendency  of  many  renal  tumors  to  form  metastases  in  the  glands,  the 
lungs,  the  brain,  etc.,  is  clinically  important.  I  have  repeatedly  seen  cases  of 
"  brain-tumor,"  which,  at  the  autopsy,  turned  out  to  be  metastases  of  small 
primary  renal  tumors.  In  conclusion,  we  would  mention  that  there  are  cases 
of  bilateral  cystic  kidneys  whose  clinical  picture  resembles  that  presented  by 
contracted  kidney,  viz.,  excretion  of  a  pale  urine  with  only  a  small  amount  of 
albumen,  development  of  cardiac  hypertrophy,  and  finally  uraemia. 

Diagnosis. — The  diagnosis  of  renal  tumors  is,  in  many  cases,  quite  evident, 
but  in  others  very  difficult.  The  position  of  the  new  growth,  its  limited  mo- 
bility, its  relations  to  the  colon,  the  possibility  of  grasping  and  moving  the 
tumor  between  the  hands  on  bimanual  palpation,  one  hand  being  behind  the 
kidney  and  one  in  front,  and,  above  all,  our  knowledge  as  to  the  occurrence 
of  renal  tumors  in  children,  often  suggest  the  correct  interpretation  of  the 
case.  In  older  persons  renal  hemorrhages  which  cannot  be  otherwise  explained 
must  direct  our  suspicions  to  the  possibility  of  a  cancer  of  the  kidney.  Often, 
however,  the  disease  has  been  confounded  with  tumors  of  the  retroperitoneal 
glands  and  of  the  ovaries,  with  large  psoas  abscess,  tumor  of  the  liver,  and 
splenic  tumor.  We  can  only  briefly  call  attention  to  the  importance  of  a 
cystoscopic  examination. 

Prognosis. — The  prognosis  is,  of  course,  unfavorable.  The  disease  some- 
times lasts  only  a  few  months,  sometimes  a  year  or  two,  rarely  longer. 

Treatment. — The  treatment  must  in  most  cases  be  purely  symptomatic. 
The  only  expectation  of  success  lies  in  the  operative  removal  of  the  new 
growth,  the  details  of  which  are  to  be  found  in  recent  monographs  on  renal 
surgery. 


796  DISEASES   OF   THE   URINARY   ORGANS 


CHAPTER    IX 

PARASITES    OF    THE    KIDNEYS   AND    OF    THE    URINARY    PASSAGES— 

CHYLURIA 

1.  Echinococcus  of  the  Kidney. 1 — Echinococcus  cysts  have  been  repeatedly 
found  in  the  kidney,  although  much  more  rarely  than  in  the  liver.  Usually 
only  one  kidney  is  affected,  and  the  parasite  is  generally  situated  in  the  renal 
substance  itself,  only  exceptionally  between  it  and  the  capsule  of  the  kidney. 
The  size  of  the  echinococcus  cysts  may  be  very  considerable,  the  diameter  reach- 
ing to  20  cm.  or  more. 

Clinical  symptoms  usually  first  appear  when  the  tumor  can  be  felt  through 
the  abdominal  walls.  Subjective  symptoms  may  even  then  be  entirely  want- 
ing. Pain  on  pressure  develops  gradually  later.  The  tumor  usually  has  an 
approximately  globular  shape.  Its  relations  to  the  neighboring  organs,  espe- 
cially to  the  colon,  are  the  same  as  we  have  learned  to  recognize  in  the  pre- 
ceding chapter,  in  the  description  of  cancer  of  the  kidney.  The  so-called  hyda- 
tid thrill  which  is  said  to  be  characteristic,  and  which  is  obtained  by  giving 
the  tumor  a  little  push  with  the  flat  of  the  hand,  can  be  distinctly  felt  in  only 
the  rarest  instances. 

It  is  a  comparatively  frequent  occurrence  for  the  echinococcus  cyst  to  burst 
into  the  pelvis  of  the  kidney.  Then  single  echinococcus  cysts,  or  at  least  bits 
of  membrane,  hooklets,  etc.,  are  passed  with  the  urine,  usually  with  severe 
colicky  pains,  which  are  exactly  like  the  renal  colic  from  the  passage  of  a 
calculus.  Such  attacks  may  be  often  repeated,  and  may  form  a  very  severe 
type  of  disease  by  obstructing  the  urinary  passages — the  bladder  and  urethra. 
In  such  cases  the  symptoms  of  a  secondary  pyelitis  and  cystitis  are  often  added. 

Perforations  in  other  directions  are  much  rarer.  The  rupture  of  a  renal 
echinococcus  into  the  lungs  has  sometimes  been  observed,  the  patient  coughing 
up  echinococcus  cysts. 

Sometimes,  especially  after  injuries,  the  sac  of  the  echinococcus  becomes  in- 
flamed, suppurates,  and  leads  to  a  general  pysemic  condition. 

The  diagnosis  of  renal  echinococcus  is  possible  only  when  a  tumor  can  be 
made  out  belonging  to  the  kidney,  and  when  portions  of  echinococcus  are  passed 
with  the  urine,  or  through  an  exploratory  puncture.  It  has  already  been 
stated  that  one  should  be  cautious  about  employing  this  procedure  (see  page 
710).  The  cysts  are  more  frequently  confounded  with  hydronephrosis  (vide 
infra),  and,  in  women,  with  ovarian  tumors. 

The  prognosis  is  not  wholly  unfavorable.  Permanent  recovery  has  been  re- 
peatedly observed,  especially  after  the  rupture,  or  single  or  repeated  evacua- 
tions, of  the  sac  of  the  echinococcus ;  but,  of  course,  echinococcus  of  the  kidney 
may  also  be  attended  with  numerous  dangers,  such  as  suppuration  of  the  sac. 
The  course  of  the  disease  is  always  very  tedious. 

A  radical  treatment  is  possible  only  by  surgical  means.  Symptomatically, 
ice  and  local  bloodletting  are  used  when  there  are  symptoms  of  local  inflam- 
mation ;  and  morphin,  warm  baths,  and  sometimes  mechanical  aids — e.  g.,  the 
catheter — when  there  are  symptoms  of  colic. 

1  In  regard  to  the  general  natural  history  of  the  echinococcus,  compare  p.  708. 


PARASITES  OF  THE   KIDNEYS  AND   URINARY   PASSA< 


797 


2.  Distoma  hematobium  (Bilharzia  hematobia — Blood- fluke). — The  dis- 
toma  hematobium  (see  Fig.  99)  is  a  parasite  which  belongs  to  the  flukes  or 
trematodes,  and  which  occurs  especially  in  Egypt,  Abyssinia,  and  Easl  Africa. 
Infection  is  said  to  take  place  partly  by  means  of  the  drinking  water  and  food, 
and  partly,  perhaps,  by  the  parasite  creeping  into  the  urinary  passages  and 
the  rectum  during  bathing.     Natives  are  much  oftener  attacked  than  Euro- 


Fig.  99. — Distoma  hematobium  (from  Leuckart).  a.  Male  and  female,  the  latter  in  the  gyne- 
cophorus  canal  of  the  former.  Enlarged  ten  diameters.  6.  Egg  with  a  terminal  spine. 
c.  Egg  with  a  lateral  spine.     150  diameters. 

peans.  The  distoma  has  its  chief  abode  in  the  branches  of  the  portal  vein, 
and  particularly  in  the  venous  plexuses  of  the  bladder  and  the  rectum.  Its 
eggs  are  often  deposited  in  great  numbers  in  the  mucous  membrane  of  the 
pelvis  of  the  kidney,  the  ureter,  and  the  bladder,  and  they  excite  in  these 
places  a  severe  inflammation  with  ulceration  and  consequent  strictures,  or  the 
formation  of  concretions.  Similar  violent  inflammation  occurs,  also,  in  the  rec- 
tum and  in  the  sexual  organs.  The  course  of  the  disease  is  very  chronic.  The 
main  symptom  is  persistent  hematuria.  Many  cases  of  so-called  tropical  hema- 
turia are  due  to  the  distoma,  and  later  we  have  the  symptoms  of  local  inflam- 
mation and  of  severe  cystitis.  The  diagnosis  may  be  established  by  the  dis- 
covery of  the  eggs  in  the  urine  or  the  feces.    Treatment  is  merely  sjmiptomatic. 

3.  Strongylus  or  Eustrongylus  Gigas  (Palisade  Worm). — This  is  a  parasite 
occurring  in  the  pelvis  of  the  kidney  in  many  animals — the  dog,  the  wolf,  the 
marten — and  very  rarely  in  man.  In  size  and  color  it  is  not  unlike  an  ordinary 
earthworm.  It  may  produce  symptoms  of  severe  pyelitis,  with  hemorrhages 
and  colicky  pains.     No  well-established  cases  have  been  reported  of  late. 

4.  Filaria  Sanguinis.  Chyluria. — The  blood  filaria  of  man,  belonging  to 
the  roundworms,  has  obtained  a  special  clinical  interest,  since  it  is  recognized, 
from  the  investigations  of  Wucherer  in  Bahia  in  1868,  and  of  Lewis  in  the 
East  Indies  in  1870,  as  the  cause  of  the  tropical  chyluria  and  some  allied  dis- 
eases, such  as  lymph  scrotum,  elephantiasis  Arabum,  and  chylous  ascites. 

The  full-grown  filaria,  "filaria  Bancrofti,"  a  very  thin  worm,  about  3  or 
4  inches  long,  has  been  found  only  a  few  times  in  man.  Its  seat  is  in  the 
larger  lymphatics,  where  is  gives  rise  to  chronic  stasis  of  the  lymph  with  its 
consequences — chronic  hyperplasia  of  the  connective  tissue,  etc.  In  chyluria, 
the  parasites  are  probably  situated  in  the  main  branches  of  the  thoracic  duct 
— at  any  rate,  in  such  a  place  that  a  stasis  of  the  lymph  ensues  in  the  lym- 
phatics of  the  bladder,  or  perhaps,  in  some  cases,  of  the  pelvis  of  the  kidney 
and  the  other  urinary  passages.  If  the  distended  lymph  sac  ruptures,  the 
lymph  or  chyle  is  poured  out  into  the  urinary  passages  and  is  evacuated  with 
the  urine.     Since  this  process  may  be  often  repeated,  the  intermittent  course 


798 


DISEASES   OF    THE   URINARY   ORGANS 


of  chyluria  is  thus  explained.    The  individual  attacks  of  the  disease  may  come 

■on  during  years  at  intervals  of  weeks  or  months.     They  are  often  associated 

with  pain  and  febrile  symptoms. 

The  condition  of  the  urine,  which  in  many  cases  may  look  almost  exactly 

like  milk,  is  most  characteristic.    A  creamy  layer  of  fat  forms  upon  the  surface. 

If  we  shake  the  urine  with  ether,  the  greater  part  of  the  fat  can  be  removed, 

and  the  urine  rendered  clear.  The  fat  in 
the  urine  may  amount  to  two  or  three  per 
cent.  The  chyluria  is  often  associated 
with  a  hematuria  coming  from  the  rup- 
tured veins.  The  urine  then  looks  bloody 
red,  and  shows  under  the  microscope 
many  red  blood  corpuscles  besides  the  fat 
drops.  Large  clots  often  form  in  the  urine. 
The  embryos  of  filaria,  found  in  the 
urine  in  very  many  cases,  although  not 
in  all,  form  the  most  important  diagnos- 
tic feature  in  the  urine.  These  (see  Fig. 
100)  are  objects  TV  to  |  in.  (0.2-0.3 
millimeter)    long,  with  a  diameter  about 

\/f  equal   to  that  of  a  red  blood  corpuscle. 

m  They  are  usually  imbedded  in  a  very  deli- 

IM  cate  sheath,  which  often  projects  at  the 

ff  end  of  the  animal,  and  show  a  constant, 

vigorous  vibrating  motion.  They  have 
also  been  found  in  the  blood  of  the  pa- 
tient, as  well  as  in  the  urine,  and,  strange 
to  say,  especially  during  the  night. 

The  course  of  the  filaria  disease  may 
vary  considerably.  Many  patients  reach 
an  advanced  age;  in  others,  severe  general  symptoms,  like  anaemia  and  ema- 
ciation, finally  come  on.  The  different  forms  in  which  the  disease  occurs 
— chyluria,  elephantiasis,  etc. — are  combined  in  manifold  ways. 

The  region  of  the  geographical  distribution  of  the  disease  lies  almost  wholly 
in  hot  countries.  It  has  so  far  been  most  frequently  observed  in  Brazil,  the 
Antilles,  the  East  Indies,  China,  Japan,  Egypt,  Cape  Colony,  and  Australia. 
Nothing  definite  is  yet  known  of  the  precise  mode  of  invasion  of  the  parasites. 
According  to  Manson's  investigations,  mosquitoes  play  an  important  part  here. 
[This  view  is  now  well  established.] 

In  regard  to  treatment,  apart  from  any  surgical  interference,  we  may  try 
picronitrate  of  potassium,  3  to  8  gr.  (gm.  0.2  to  0.5),  in  pills  or  capsules, 
several  times  a  day  (Scheube). 


Fig.  100. — (From  Scheube.) 
Embryos  of  filaria. 


CHAPTEE    X 

MOVABLE    KIDNEY    (FLOATING    KIDNEY,    REN   MOBILES) 

etiology. — With  some  practice  the  physician  can  frequently  palpate  the 
kidneys,  particularly  the  right  kidney,  even  under  absolutely  normal  condi- 


MOVABLE    KIDNEY  70*.) 

lions  ("palpable  kidney").  This  is  much  oftcncr  the  case  in  women  with 
];i.\  and  yielding  abdominal  walls  than  in  men.  With  every  inspiration  the 
kidney  is  pushed  somewhat  downward.  In  many  cases,  therefore,  the  kidney, 
or  at  least  its  lower  half,  is  felt  only  upon  deep  inspiration.  If  the  kidney  is 
not  only  palpable,  but  also  capable  in  greater  or  less  degree  of  being  moved 
ahout  by  the  hand,  and  if,  consequently,  we  do  not  always  find  the  kidney  in 
the  same  place,  then  we  describe  it  as  an  abnormally  movable  kidney ;  or,  if 
the  case  is  extreme,  a  floating  kidney.  What  may  be  the  causes  of  this  ex- 
treme mobility  of  the  kidney  is  not  settled.  Often  it  may  be  due  to  the  con- 
genital, anatomical  relations  of  the  peritoneum,  and  other  tissues  around  the 
kidney.  This  is  indicated  particularly  by  the  occasional  occurrence  of  mov- 
able kidney  in  children.  Certain  external  mechanical  factors,  however,  un- 
doubtedly play  the  most  important  role.  First  among  these  is  the  distention 
and  relaxation  of  the  abdominal  walls  as  a  result  of  pregnancy;  and,  secondly, 
the  influence  of  clothing,  waistbands,  and  corsets.  This  explains  the  fact  that 
movable  kidney  is  found  mainly  in  women,  and  particularly  in  married  women. 
At  the  same  time,  the  abnormal  mobility  and  downward  displacement  of  the 
kidney  are  often  merely  a  part  of  a  general  "  enteroptosis  "  (see  page  565), 
and  are  therefore  associated  with  gastroptosis,  coloptosis,  and  corset  liver. 
That  the  movable  kidney  is  far  more  often  the  right  than  the  left  is  probably 
due  to  the  fact  that  the  right  kidney  is  originally  less  firmly  fastened,  and  is 
placed  lower,  and  also  that  it  is  affected  by  the  great  mass  of  the  liver  which 
lies  above  it. 

Numerous  other  causative  influences  have  been  mentioned,  but  none  of 
them  is  as  important  as  the  preceding:  they  are,  severe  physical  labor  with 
frequent  tension  of  the  abdominal  muscles,  injuries  involving  the  region  of 
the  kidneys,  diseases  of  the  neighboring  organs,  particularly  displacement  of 
the  uterus,  and,  finally,  emaciation,  causing  absorption  of  the  fat  which  sup- 
ports the  kidneys  and  makes  tense  the  abdominal  walls.  After  death  a  mov- 
able kidney  cannot  be  recognized  unless  it  is  found  in  an  abnormal  position — 
e.  g.,  in  front  of  the  vertebral  column,  or  close  to  the  anterior  abdominal  walls. 
In  such  cases  its  external  edge  may  be  directed  downward  and  its  inner  edge 
upward. 

Symptoms. — The  clinical  importance  of  movable  kidney  is  estimated  very 
differently  by  different  physicians.  Many  conceive  that  it  is  a  very  frequent 
cause  of  manifold  abdominal  disturbances ;  others  are  almost  inclined  to  deny 
it  any  influence  on  the  health.  We  ourselves  believe  that  a  movable  kid- 
ney as  such  may,  in  fact,  excite  disagreeable  symptoms,  but  that  this  is  the 
exceptional  occurrence.  As  we  have  already  mentioned,  palpability  and  slight 
movability  of  the  right  kidney  are  so  frequent  in  women  that,  as  soon  as  one's 
attention  is  directed  to  the  matter,  one  finds  this  condition  in  a  large  propor- 
tion of  all  cases  in  which  there  is  occasion  to  make  a  careful  abdominal  exam- 
ination. The  pains  and  abnormal  sensations  in  the  abdomen,  of  which  women 
so  frequently  complain,  are  difficult  of  interpretation,  and  it  is,  of  course,  very 
seductive  and  convenient  to  refer  them  to  a  movable  kidney;  but  if  we  con- 
sider how  often  we  find  an  exactly  similar  movable  kidney  in  women  who  are 
entirely  free  from  abdominal  symptoms,  we  cannot  avoid  suspicion  as  to  the 
importance  of  the  condition. 

It  is  difficult  to  form  a  characteristic  group  of  symptoms  which  may  be 


800  DISEASES   OF  THE   URINARY   ORGANS 

unhesitatingly  referred  to  movable  kidney.  First,  pain  should  be  named. 
This  is  to  a  certain  extent  local,  but  it  often  radiates  into  the  epigastrium  and 
the  sacral  and  lumbar  regions,  and  sometimes  is  colicky.  Not  infrequently 
the  pain  is  associated  with  nausea.  The  discomfort  is  aggravated  by  any  de- 
cided motion  of  the  patient,  or  by  riding,  driving,  and  the  like;  but  during 
repose  it  becomes  slight,  or  entirely  disappears.  In  rare  cases  we  have  symp- 
toms of  strangulation.  These  occur  periodically,  and  are  said  to  be  especially 
frequent  at  the  time  of  the  menses.  They  consist  of  the  sudden  onset  of 
violent  pain,  chilliness,  which  seldom  amounts  to  a  rigor,  great  tenderness  and 
tenseness  of  the  abdomen,  slight  fever,  vomiting,  and  collapse.  During  this 
time  the  urine  is  usually  scanty,  and  the  amount  does  not  increase  again  till 
the  attack  is  over,  about  three  to  five  days.  The  precise  cause  of  these  symp- 
toms is  supposed  to  be  a  sudden  damming  up  of  the  urine  by  a  kink  or  twist 
in  the  ureter.  This  occasions  acute  hydronephrosis,  and  resultant  phenomena, 
which  last  until  the  urinary  channels  are  free  again.  In  other  cases  an  acute 
swelling  of  the  kidney  and  distention  of  its  capsule  are  said  to  arise  from  a 
kink  in  the  kidney  veins.  We  must  openly  confess  that  we  have  never  ob- 
served a  case  of  that  character  in  which  the  symptoms  could  positively  be  in- 
terpreted as  symptoms  of  strangulation  of  a  movable  kidney,  and  that  the  oc- 
currence of  the  conditions  in  question  has  never  seemed  clearly  proved  to  us. 

The  discovery  of  floating  kidney  by  palpation  is  usually  easy.  The  physi- 
cian examines  the  patient  lying  on  her  back,  applying  his  left  hand  on  the 
right  lumbar  region  and  pressing  forward,  while  his  right  hand  presses  from 
in  front  in  the  opposite  direction.  It  is  then  often  possible,  especially  upon 
deep  inspiration  (vide  supra),  to  catch  the  kidney  between  both  hands,  and 
so  form  an  opinion  as  to  its  position  and  mobility. 

The  next  point  is  to  determine  whether,  in  any  particular  case,  the  symp- 
toms which  may  be  present  are  actually  due  to  the  movable  kidney  which  has 
been  discovered,  or  whether  the  latter  is  an  unimportant  matter.  This  ques- 
tion demands  a  careful  and  complete  physical  examination  and  a  consideration 
of  all  the  symptoms.  In  the  first  place,  we  should  determine  accurately  the 
condition  of  the  stomach  (gastroptosis,  etc.)  and  of  the  intestines  (chronic 
catarrh  of  the  colon,  mucous  colitis,  etc.),  and  we  should  also  think  of  the 
possibility  of  gallstones,  which  may  produce  a  very  similar  group  of  symp- 
toms. Gallstones  are  especially  apt  to  occur  in  women  with  corset  liver  and 
enteroptosis,  and  this  explains  why  a  movable  kidney  is  not  infrequently  found 
in  cases  of  biliary  colic,  although  it  has  nothing  to  do  with  the  attack.  With 
so-called  "  symptoms  of  strangulation,"  the  possibility  of  renal  calculi  must 
be  borne  in  mind. 

In  a  great  majority  of  cases  of  "  floating  kidney  "  we  have  to  do  with  those 
familiar  and  frequent  conditions  of  a  "  nervous  "  character  which  are  termed 
hysteria  or  neurasthenia.  Women  of  this  kind  suffer  very  frequently  from  all 
sorts  of  painful  sensations  in  the  abdomen,  and  from  dyspeptic  disturbances 
and  the  like,  and  of  course  we  very  often  find  in  them  a  movable  kidney.  In 
such  cases  the  abdominal  symptoms  are  also  of  a  nervous  character,  as  can 
usually  be  easily  determined  from  the  general  condition  of  the  patient,  from 
her  psychical  and  cerebral  symptoms,  and  the  indications  of  a  cardiac  neurosis, 
and  also  from  the  results  of  suggestive  treatment.  Still,  a  certain  number  of 
cases  may  be  very  difficult  of  diagnosis.     If  we  find  a  movable  kidney  in  a 


DISEASES   OF  SUPRARENAL   CAPSULES   AND   ADDISON'S   DISEASE     801 

nervous,  hysterical  woman,  it  is  not  always  advisable  to  apprise  the  patient  of 
the  fact,  for  with  a  person  of  this  sort  the  mere  idea  of  possessing  a  "  floating 
kidney  "  is  enough  to  stir  up  a  host  of  subjective  symptoms.  On  the  other 
hand,  it  may  be  said  that  the  floating  kidney  may  serve  as  a  very  handy  instru- 
ment for  suggestive  therapeutics.  If  we  say  to  such  a  patient  that  her  annoy- 
ance would  immediately  vanish  after  the  application  of  a  suitable  bandage,  we 
may  sometimes  attain  great  therapeutic  success,  although  this  is  apt  to  be  but 
temporary. 

Treatment. — If  we  deem  that  the  movable  kidney  requires  treatment,  the 
first  thing  to  recommend  is  the  wearing  of  a  suitable  support.  The  bandages, 
with  special  pads  and  the  like,  we  regard  as  usually  of  no  value,  while  a  good 
elastic  abdominal  bandage,  with  thigh  straps,  or  a  well-fitted.  "  abdominal 
corset,"  is  sometimes  decidedly  efficient,  particularly  in  all  cases  of  general 
enteroptosis.  We  should  also  see  that  the  patient  is  properly  nourished.  If 
she  is  emaciated,  we  should  prescribe  rest  with  the  largest  possible  amount  of 
food,  so-called  overfeeding.  As  more  and  more  fat  is  deposited  in  the  ab- 
domen, the  abdominal  walls  regain  their  tension  and.  the  kidneys  receive  better 
support.  It  is  also  advisable  to  sponge  the  abdomen  with  cold  water  or  brandy, 
or  to  employ  massage,  the  Scotch  douche,  or  electricity. 

If  there  are  any  symptoms  of  strangulation,  we  should,  of  course,  put  the 
patient  to  bed.  and.  order  hot  poultices  and  opium.  We  may  also  make  a  cau- 
tious attempt  to  replace  the  organ.  If  severe  attacks  of  this  sort  recur,  the 
possibility  of  surgical  treatment  should,  be  considered,  (nephrorrhaphy  or 
nephropexy).  In  a  fairly  large  number  of  cases  the  patients  are  said  to  have 
been  entirely  freed  of  their  discomfort  by  this  method.  We  doubt  if  all  these 
cases  would  stand  the  test  of  a  rigid  criticism.  It  is  certain  that  the  operative 
result  is  often  of  a  purely  suggestive  nature. 


APPENDIX 


THE    DISEASES    OF    THE    SUPRARENAL    CAPSULES    AND    ADDISON'S 
DISEASE     (BRONZED    SKIN) 

iEtiology  and  Pathological  Anatomy. — In  the  year  1855  the  English  physi- 
cian Addison  published  for  the  first  time  a  list  of  cases  in  which,  besides  the 
symptoms  of  a  general  bodily  weakness  and  ansemia,  a  peculiar  dark  pigmenta- 
tion of  the  skin  had  gradually  developed.  Since  disease  of  the  suprarenal 
capsule  was  found  at  the  autopsy  in  all  cases,  Addison  concluded  that  this 
was  the  immediate  cause  of  the  bronze  coloring  of  the  skin.  Observations  sim- 
ilar to  Addison's  were  soon  made  in  greater  numbers,  so  that  the  fact  itself 
cannot  be  doubted. 

The  actual  nature  of  Addison's  disease  is,  to  be  sure,  by  no  means  entirely 
cleared  up.  Still,  through  the  newer  discoveries  regarding  the  physiological 
significance  of  the  suprarenals,  our  conceptions  of  the  disease  have  become 
decidedly  more  intelligible.  All  the  more  so  as  the  disease  is  obviously  cor- 
related to  quite  a  number  of  morbid  processes,  which  likewise  depend  upon  a 
disturbance  in  the  so-called  internal  secretions  (the*  suprarenal  bodies,  thyroid 
gland,  thymus  and  pituitary  glands). 


802  DISEASES   OF   THE   URINARY  ORGANS 

The  suprarenal  capsules  are  composed  of  two  entirely  different  tissues,  the 
medullary  and  cortical  substances.  Their  anatomical  intermingling,  however, 
speaks,  in  all  probability,  for  a  close  mutual  physiological  relationship.  The 
cortex  is  composed  of  epithelial  cells  with  a  profuse  network  of  thin-walled 
capillaries.  The  medulla,  on  the  other  hand,  is  certainly  a  part  of  the  sym- 
pathetic system.  Accordingly,  it  consists  for  the  smaller  part  in  typical  sym- 
pathetic ganglion  cells  and  numerous  nonmedullated  nerve  fibers,  and  for  the 
greater  part  in  so-called  chromophile  cells.  These  are  peculiar,  large  branch- 
ing cells,  which  take  on  a  characteristic  brown  stain  with  chromium  salts. 
They  accompany  the  sympathetic  nervous  tissue  all  over  the  body,  and  are 
also  found  in  other  accessory  organs  of  the  sympathetic  system  (carotid  glands, 
coccygeal  gland,  etc.).  Adrenalin  (suprarenin)  is  found  only  in  the  extract 
of  the  medullary  portion,  and  is  derived  from  the  chromophile  cells.  The 
remarkable  action  of  this  substance  in  raising  the  blood  pressure  was  first 
accurately  studied  by  Oliver  and  Schafer  in  1884.  The  so-called  accessory 
adrenals  are,  as  a  rule,  composed  of  only  cortical  substance. 

Brown- Sequard,  in  1856,  was  the  first  to  demonstrate  that  the  supra- 
renal capsules  were  absolutely  essential  to  life.  He  found  that  the  extirpation 
of  both  suprarenals  led  in  a  short  time  to  the  death  of  the  animal  experi- 
mented upon.  Through  numerous  observations  in  recent  years  the  following 
phenomena  have  been  established  as  the  main  results  of  suprarenal  extirpa- 
tion: General  muscular  weakness,  nervous  disturbances  (somnolence,  coma, 
epileptiform  seizures,  dilatation  of  the  pupil,  etc.),  fall  of  blood  pressure, 
abnormal  pigmentation,  lowering  of  the  body  temperature,  general  disturb- 
ances of  nutrition,  etc.  These  symptoms  are  explained  partly  by  the  loss  of 
the  neutralizing  function  of  the  suprarenals  for  certain  poisons  in  the  body, 
and  partly  by  the  loss  of  the  secretory  function  of  the  organ.  The  former 
function  is  supposed  to  reside  mainly  in  the  cortex,  while  the  latter,  as  al- 
ready mentioned,  is  exercised  chiefly  by  the  medulla.  The  main  results  of 
the  physiological  action  of  suprarenal  extract  (adrenalin)  thus  far  established 
are  as  follows : 

1.  Marked  increase  in  the  blood  pressure  due  to  contraction  of  the  smaller 
vessels,  as  a  result  of  direct  peripheral  irritation. 

2.  Strengthening  of  the  cardiac  contraction  and  slowing  of  the  pulse. 

3.  Slowing  of  the  respiration,  which,  at  the  same  time,  becomes  more 
superficial. 

4.  Dilatation  of  the  pupils.  This  can  also  be  demonstrated  in  the  enucle- 
ated eyes  of  frogs. 

5.  Inhibition  of  intestinal  peristalsis,  etc. 

We  are  still  far  removed  from  a  complete  explanation  of  the  clinical  phe- 
nomena of  Addison's  disease  on  the  basis  of  these  physiological  facts.  Still, 
quite  a  number  of  connecting  links  between  the  results  of  experimental  and 
clinical  observation  must  be  recognized.  For  the  time  being  we  must,  how- 
ever, study  from  a  clinical  standpoint  the  symptoms  which  point  toward  a 
disturbance  of  the  function  of  the  suprarenal  bodies  in  a  diseased  individual. 
Even  Addison  himself  pointed  out  the  fact  that  the  actual  nature  of  the 
lesion  in  the  suprarenals  was  by  no  means  always  the  same.  Hence  the  dis- 
ease named  after  him  is,  first  of  all,  to  be  regarded  not  as  a  definite  pathological 
condition,  but  far  more  as  a  peculiar  symptom-complex  due  to  a  loss  of  supra- 


DISEASES   OF   SUPRARENAL   CAPSULES   AND   ADDISON'S   DISEASE     803 

renal  function.     Willi  comparative  frequency  tuberculosis  of  the   mprarenal 

capsules  is  found  to  be  the  basis  of  the  .Addison  symptom-complex.  The  eupra- 
renals  are  then  either  enlarged  and  infiltrated  with  caseated  tuberculous  tissue, 
or  they  are  in  part  already  cicatrized  and  contracted.  Almost  always  other 
tubercular  disease  is  found  coexistent  at  autopsy,  especially  caseation  of  the 
mesenteric  lymph-glands,  pulmonary  tuberculosis,  etc.  Besides  tuberculosis, 
other  morbid  processes,  such  as  neoplasms,  etc.,  may  sometimes  be  found  in 
the  suprarenals.  Eecent  personal  clinical  and  pathological  observations  have 
convinced  us  that  there  exists  a  special  peculiar  form  of  Addison's  disease  in 
which  at  autopsy  only  an  extreme  atrophy  of  the  suprarenal  bodies  [&  found. 
In  these  cases  both  suprarenals  are  converted  into  thin  parchment-like 
structures,  in  which  the  actual  parenchyma  has  almost  entirely  degenerated. 
In  somewhat  the  same  manner  in  which  we  look  upon  symptomatic  glycosuria 
as  compared  to  true  diabetes,  so,  in  our  opinion,  must  we  regard  the  symptoms 
of  Addison's  disease  developing  in  other  diseases  of  the  suprarenal  bodies  as 
a  secondary  symptom-complex,  in  comparison  with  primary  suprarenal  atrophy 
with  the  fully  developed  clinical  picture  of  Addison's  disease.  Only  these 
latter  cases  do  we  regard  as  true  primary  Addison's  disease.  To  be  sure,  we 
know  nothing  regarding  the  causes  of  this  apparently  primary  suprarenal  dis- 
ease. Impaired  nutrition,  psychic  influences,  traumatism,  possibly  sometimes 
play  a  certain  role.  In  the  main,  however,  the  disease  is  probably  due  to 
direct  exogenous  or  endogenous  harmful  influences  acting  upon  the  specific 
tissue  of  the  organ.  The  disease  itself  is  rare,  and  occurs  somewhat  more  fre- 
quently in  males  than  in  females.  Although  usually  a  disease  of  middle  life, 
we  ourselves  have  even  seen  a  case  in  a  ten-year-old  child. 

Of  the  lesions  in  other  organs  we  must  also  mention  that  Peyer's  patches 
and  the  solitary  follicles  of  the  intestine  are,  as  a  rule,  swollen.  The  spleen  is 
somewhat  enlarged  in  some  cases,  but  not  in  others.  There  is  no  striking 
pigmentation  of  the  internal  organs.  Still,  in  one  very  characteristic  fatal 
case  we  saw  marked  pigmentation  in  the  internal  lymph-glands  and  in  the 
liver,  and  once,  besides,  in  the  retina,  during  the  lifetime  of  the  ten-year-old 
male  patient.  The  changes  in  the  skin  and  in  certain  mucous  membranes  will 
be  mentioned  below. 

Symptomatology. — The  purest  type  of  Addison's  disease  appears  in  those 
cases  mentioned  above  where  the  symptoms  are  apparently  primary  in  their 
development,  and  do  not  come  on  in  the  course  of  some  other  disease,  such  as 
phthisis  or  cancer. 

The  first  symptoms  of  the  disease  are  usually  of  a  general  nature,  and  are 
referable  to  a  gradually  increasing  ansemia  and  to  general  weakness  and 
physical  lassitude.  The  ansemia  shows  itself  objectively  through  the  pallor  of 
the  skin  and  the  diminution  in  the  number  of  red  blood  corpuscles,  but  without 
other  definite  anomalies  of  the  blood  that  can  be  made  out.  A  relative  lympho- 
cytoses is  often  present,  and  perhaps  deserves  mention.  There  is  no  increase 
of  the  leucocytes.  The  general  muscular  weakness  (asthenia)  is  one  of  the 
most  regular  symptoms  of  the  disease.  This  is  shown  less  in  inability  to  make 
a  few  vigorous  contractions  than  in  extremely  rapid  exhaustion  of  the  separate 
muscles.  As  a  consequence,  any  long-continued  muscular  exertion,  such  as 
walking  for  any  length  of  time,  standing,  continuous  labor,  becomes  very  diffi- 
cult.   Not  infrequently  the  patients  complain  of  rheumatoid  joint  and  muscle 


804  DISEASES   OF   THE   URINARY   ORGANS 

pains.  To  these  are  added  numerous  other  so-called  nervous  symptoms. 
Among  these  are  the  mental  torpor  and  lack  of  energy,  the  headache  and 
tendency  to  syncope,  the  tinnitus  aurium,  the  insomnia  or  constant  sleepiness, 
etc.  Sometimes  there  are  marked  psychical  disturbances,  such  as  impairment 
of  memory,  feebleness  of  mind,  or  exaltation.  The  patient's  general  nutrition 
often  suffers  very  considerably ;  but  it  must  be  added  that  in  Addison's  disease, 
as  in  other  anaemias,  the  fatty  layer,  especially  over  the  abdomen,  often  re- 
mains remarkably  well  developed. 

In  women  persistent  amenorrhea  often  develops.  Besides  the  symptoms 
which  have  been  enumerated,  there  is  often  gastric  disturbance.  The  secretion 
of  the  gastric  juice  is  interfered  with,  and  frequently  free  hydrochloric  acid  and 
pepsin  are  absent.  The  appetite  is  poor,  and  there  is  very  often  vomiting. 
The  latter  may  sometimes  be  almost  uncontrollable,  and  then  it  is  one  of  the 
most  distressing  symptoms  of  the  disease.  It  is  usually  due  not  to  an  anatom- 
ical change  in  the  stomach,  but  probably  to  nervous  or  toxic  influences.  In 
one  severe  case  we  saw  a  constant  and  distressing  hiccough.  Cardialgic  symp- 
toms are  also  frequent.  The  bowels  are  sluggish,  as  a  rule,  but  there  is  some- 
times diarrhea.  We  sometimes  hear  functional  murmurs  in  the  heart,  but,  as 
a,  rule,  its  sounds  are  pure,  though  feeble.  The  pulse  is  usually  moderately 
accelerated. 

Eecently,  in  view  of  the  physiological  action  of  adrenalin,  special  attention 
has  been  devoted  to  the  state  of  the  blood  pressure.  In  general,  it  may  be  said 
that  the  blood  pressure  is  abnormally  low,  and  that  the  pulse  is  therefore 
small,  soft,  and  easily  compressible.  The  liver  appears  to  remain  normal. 
The  spleen  is  often  somewhat  enlarged.  We  have  already  referred  to  the  fre- 
quent swelling  of  the  abdominal  lymph-glands,  which,"  however,  is  not  clin- 
ically prominent.  The  liver  and  spleen  do  not  show  any  special  changes. 
Albuminuria  is  exceptional,  and  depends  upon  complications,  such  as  amyloid 
kidney.  Occasionally,  large  amounts  of  indican,  urobilin,  etc.,  appear  in  the 
urine  without  their  being  any  special  significance  to  these  findings.  The  bodily 
temperature  is  not  elevated,  and  not  infrequently,  indeed,  it  is  decidedly  sub- 
normal. 

The  special  characteristic  symptom,  which  alone  renders  the  diagnosis  pos- 
sible, is  the  gradual  onset  of  a  peculiar  pigmentation  of  the  skin.  This  usually 
shows  itself  first  in  the  face  and  on  the  backs  of  the  hands,  and  also  in  those 
parts  which  normally  present  a  greater  pigmentation  (the  areola  of  the  nip- 
ples, the  axillae,  and  the  genitals),  or  which  are  exposed  to  greater  pressure  by 
the  clothing,  as  the  hips  and  shoulders.  The  white  palms  of  the  hands  not 
infrequently  form  a  marked  contrast  with  their  darkly  pigmented  dorsal  sur- 
faces. There  is,  however,  also  a  marked  pigment  deposit  in  the  flexion  folds  of 
the  fingers.  After  numerous  personal  observations,  we  have  come  to  regard 
this  early  peculiar  dark  pigmentation  of  the  folds  of  skin  on  the  flexor  side 
of  the  fingers  and  palms  as  having  a  certain  diagnostic  significance.  It  is 
especially  noteworthy  that  dark  pigmented  spots  and  stripes  usually  develop 
on  the  mucous  membrane  of  the  lips,  particularly  at  the  corners  of  the  mouth, 
on  the  gums,  the  palate,  and  inside  the  cheeks.  We  also  consider  the  brown 
pigmentation  of  the  edges  of  the  conjunctivae  of  the  lower  lids  quite  charac- 
teristic. The  intensity  of  the  coloring  differs  in  different  cases.  It  usually 
increases  as  the  general  condition  grows  worse.     In  the  most  intense  cases 


DISEASES  OF  SUPRARENAL  CAPSULES  AND  ADDISON'S   DISEASE 

almost  the  whole  skin  may  become  dark  brown  or  black,  like  that  of  a  mula 
or  negro.  Sometimes,  however,  the  pigmentation  remains  Limited  to  separate 
large  or  small  spots,  and  in  other  pari-  of  the  skin  there  may  then  be  even  a 
marked  loss  of  pigment.  The  hair  is  usually  not  changed.  The  pigmentation 
of  the  skin  usually  increases  during  the  whole  disease;  only  exceptionally  does 
the  skin  become  light  again  in  the  later  stages.  Other  changes  in  the  skin  are 
usually  absent. 

The  real  cause  of  the  accumulation  of  pigment  in  the  skin  is  wholly  un- 
known. We  find  on  microscopic  examination  of  the  skin  that  the  pigment  lies 
not  only  in  the  cells  of  the  rete  Malpighii,  but  also  in  the  corium,  especially 
along  its  blood  vessels.  It  is  probably  formed  from  the  blood  pigment,  and  is 
carried  by  wandering  cells  from  the  cutis  into  the  epithelial  layers  of  the  skin 
(Demieville,  Nothnagel).  The  pigment  in  Addison's  disease  does  not  contain 
iron.  It  must  furthermore  be  mentioned  that  the  skin  pigmentation  in  Addi- 
son's disease,  although  of  great  diagnostic  significance,  must  not  be  regarded 
per  se  as  an  absolutely  essential  symptom.  The  variation  of  the  relationship 
between  the  degree  of  the  skin  pigmentation  and  the  severity  of  the  other 
symptoms  is  in  itself  worthy  of  note.  It  is  quite  possible  also  that  cases  of 
Addison's  disease  (i.  e.,  suprarenal  disease)  may  exist  without  skin  changes. 
These  cases  as  yet  are  not  capable  of  diagnosis. 

The  course  of  Addison's  disease  is  almost  always  chronic,  and  may  last  for 
years,  but  cases  have  been  described  with  a  rather  acute  course.  The  disease 
sometimes  begins  with  violent  initial  febrile  symptoms,  vomiting,  and  diar- 
rhea. The  disease  then  has  a  comparatively  rapid  termination  after  a  few 
months,  or  a  second  chronic  stage  may  follow  the  first  acute  one. 

The  final  termination  of  Addison's  disease  is  always  unfavorable.  Tem- 
porary remissions  are  often  observed,  but  the  disease  always  becomes  worse 
again  after  them.  Death  usually  ensues  gradually  amidst  the  signs  of  increas- 
ing general  uraemia  and  weakness.  In  some  cases  severe  nervous  symptoms 
also  come  on  toward  the  end  of  the  disease — coma,  delirium,  or  epileptiform 
attacks.  Conditions  of  this  sort  may  develop  comparatively  suddenly  and  un- 
expectedly ;  indeed,  they  can  be  explained  only  on  the  hypothesis  of  toxic  influ- 
ences, and  remind  us  of  diabetic  or  uraemic  coma. 

The  clinical  picture  of  secondary  Addison's  disease  is  composed  of  the 
same  symptoms,  only  they  are  added  to  those  of  an  already  existing  affection. 
This  complication  is  most  frequently  observed  in  tuberculosis,  where,  as  has 
been  mentioned,  it  is  usually  traceable  to  a  tuberculous  disease  of  the  supra- 
renals.  It  may  also  occur  in  carcinoma.  The  development  of  symptoms  of 
Addison's  disease  in  hypernephroma  has  already  been  mentioned  (page  795). 
Finally,  it  is  very  interesting  to  note  that  symptoms  of  Addison's  disease  oc- 
casionally occur  in  association  with  exophthalmic  goiter,  as  well  as  with 
scleroderma,  etc.  In  all  these  cases,  it  is  probably  always  the  abnormal  pig- 
mentation of  the  skin  that  first  calls  attention  to  the  remarkable  complication. 

Treatment. — Organotherapy  has  been  repeatedly  tried  in  Addison's  dis- 
ease, on  the  same  lines  as  the  treatment  of  diseases  of  the  thyroid  gland.  The 
adrenals  of  the  sheep  have  been  administered,  either  as  fresh  glands,  finely 
minced  and  eaten  with  bread,  or  as  an  extract,  or  in  the  form  of  tablets  of  the 
dried  glands.  In  some  cases  good  results  seem  to  have  been  obtained  in  this 
manner,  even  to  diminution  in  pigmentation,  but  in  many  other  cases  this 
51 


806  DISEASES   OF  THE   URINARY   ORGANS 

prescription  has  no  beneficial  effect.  We  ourselves  administered  adrenal  tablets- 
in  one  case  for  a  long  time  without  any  advantage.  Still,  it  would  be  proper 
to  continue  these  trials.  Whether  treatment  with  Koch's  tuberculin  might 
cause  permanent  benefit  in  those  cases  of  symptomatic  Addison's  disease  which 
are  due  to  tuberculosis  is  as  yet  doubtful.  A  cautious  trial  might  be  made 
under  proper  circumstances.  As  to  other  remedies,  tonics  are  generally  em- 
ployed— nourishing  food,  iron,  quinin,  and  arsenic;  iodid  of  potassium, 
bromid  of  potassium,  and  electricity  have  also  been  tried,  but  without  suc- 
cess. Symptomatic  treatment  is  needed  for  the  vomiting,  diarrhea,  and 
nervous  attacks.  Experience  has  shown  that  great  caution  should  be  exer- 
cised in  prescribing  laxatives,  because  in  repeated  instances  such  remedies, 
have  had  decidedly  unfavorable  results. 


SECTION   II 
Diseases  of  the  Pelvis,  of  the  Kidney,  and  of  the  Bladder 

CHAPTER   I 

INFLAMMATION    OF    THE    PELVIS    OF    THE    KIDNEY— PYELITIS 

etiology. — Isolated  primary  pyelitis  does  not  often  occur  as  an  inde- 
pendent disease.  It  is,  however,  more  common  than  was  formerly  believed,, 
and  acute  primary  pyelitis,  as  well  as  acute  pyelocystitis,  has  been  repeatedly 
observed,  not  only  in  adults,  but  also,  and  especially,  in  children.  In  the 
majority  of  cases  the  exciting  cause  is  an  infection  of  the  urinary  passages 
with  the  colon  bacillus,  and  it  is  not  improbable  that  the  infection  originates 
from  the  intestine.  It  has  not,  however,  been  definitely  decided  whether  the 
bacilli  pass  directly  from  the  intestine  into  the  urinary  passages,  or  whether 
they  first  enter  the  blood  stream,  and  thence  gain  entrance  to  the  urinary 
organs.  Secondary  pyelitis  is  more  common  than  the  primary  form.  It  is 
either  a  complication  or  a  result  of  other  diseases,  and  in  such  cases  often 
attracts  but  little  clinical  attention. 

We  sometimes  find  a  rather  moderate  pyelitis  in  the  bodies  of  persons- 
who  have  died  of  severe  general  infectious  diseases — tj^phoid  fever,  small- 
pox, diphtheria,  or  pygemia.  It  has  not  been  positively  determined  in  these 
cases  how  far  chemico-toxic  influences  play  a  role,  and  how  far  the  organized 
infectious  agent  itself  must  be  taken  into  consideration.  In  typhoid  pyelitis,, 
the  typhoid  bacilli,  which  are  often  excreted  in  great  numbers  with  the  urine, 
probably  have  a  directly  harmful  action  upon  the  mucous  membrane  of  the 
urinary  passages.  It  is  worthy  of  mention,  too,  that  in  secondary  pyelitis 
colon  bacilli  have  often  been  found  in  the  urine.  Of  the  special  poisons  which 
may  produce  a  pyelitis,  cantharides  and  certain  balsamic  substances,  such  as. 
copaiba  balsam,  are,  above  all,  to  be  mentioned. 

Pyelitis  very  often  rises  from  a  direct  extension  of  inflammation  from  the 
neighboring  organs.  In  many  cases  of  acute  and  chronic  nephritis  the  pelvis 
of  the  kidney  takes  part  in  the  inflammation  to  a  greater  or  less  degree;  but 


INFLAMMATION   OF  THE  PELVIS  OF  THE   KIDNEY— PYELITIS     807 

an  ascending  extension  of  the  inflammation  from  primary  diseases  of  the 
urethra  or  bladder  is  still  more  common.  Any  case  of  urethritis  or  cystitis 
may,  if  it  lasts  long,  advance  upward  to  the  ureters  and  the  pelvis  of  the  kid- 
ney, so  that  in  severe  cases  we  often  find  an  inflammation  of  the  whole  uri- 
nary tract,  a  pyelocystitis,  and  even  a  "ureteritis."  It  has  been  already  men- 
tioned (page  789)  that  the  inflammation  may  extend  still  farther  to  the 
kidneys  themselves  (pyelonephritis),  and  we  shall  refer  to  this  repeatedly. 
Of  all  these  varieties  of  ascending  inflammation  in  the  urinary  passages,  none 
is  so  frequent  or  of  so  great  practical  importance  as  that  which  results  from 
persistent  narrowing  of  the  urethra  (stricture,  hypertrophy  of  the  prostate), 
and  the  consequent  obstruction  to  the  flow  of  urine.  We  shall  revert  to  this 
important  variety  when  discussing  hydronephrosis.  Very  frequently  the  as- 
cending pyelitis  is  a  sequel  to  cystitis  in  disease  of  the  spinal  cord,  with 
paralysis  of  the  bladder. 

Another  form  of  pyelitis  is  that  caused  by  the  presence  of  foreign  bodies 
in  the  pelvis  of  the  kidneys — e.  g.,  calculous  pyelitis  due  to  the  mechanical 
irritation  of  renal  calculi.  This  also  will  have  a  special  consideration  below. 
Much  less  frequent  causes  are  retained  blood  clots,  parasites  (vide  supra),  and 
genuine  foreign  bodies. 

Pathological  Anatomy. — In  simple  catarrhal  inflammation  the  mucous 
membrane  of  the  pelvis  of  the  kidney  is  reddened,  swollen,  and  covered  with 
an  abundant  secretion,  which  contains  varying  amounts  of  pus  corpuscles  and 
epithelium.  In  severer  inflammations  we  often  find  quite  numerous  little 
hemorrhages  in  the  mucous  membrane,  and  sometimes  little  gray  nodules, 
corresponding  to  swollen  lymph-follicles. 

In  severe  cases,  which  are  seen  almost  solely  as  a  complication  of  a  more 
extensive  affection  of  the  urinary  passages,  such  as  pyelocystitis,  we  have  a 
purulent,  ulcerative  inflammation,  which  may  even  assume  a  diphtheritic 
character.  In  these  cases  the  kidneys  are  almost  always  coincidently  involved 
— pyelonephritis.  If  the  nephritic  abscesses  break  into  the  pelvis  of  the 
kidney,  there  arises  an  ulcerative  destruction  of  the  renal  tissue,  so  that  the 
pelvis  of  the  kidney  is  filled  with  pus  and  bounded  by  extensive  ulcers,  which 
often  penetrate  deeply  into  the  substance  of  the  kidney — pyonephrosis.  The 
pyelonephritic  abscesses  reaching  to  the  outer  surface  of  the  kidney,  and  usu- 
ally giving  a  striated  appearance  to  a  section  of  the  organ,  have  already  been 
described  (see  last  section)  and  their  bacterial  origin  mentioned. 

The  condition  differs  when  the  kidney  is  involved,  as  in  many  cases  of 
chronic  pyelitis.  This  appears  most  frequently  as  a  result  of  retention  of 
urine,  and  hence  it  is  usually  associated  with  a  dilatation  of  the  pelvis  of  the 
kidnejr.  In  these  cases  we  sometimes  find  pronounced  processes  of  contraction 
in  the  kidneys — that  is,  a  partial  atrophy  of  the  renal  tissue,  increase  of  the 
interstitial  connective  tissue,  and  evident  cicatricial  depressions  on  the  sur- 
face— in  a  word,  a  secondary  contracted  kidney,  arising  as  a  result  of  pye- 
litis, which  differs  from  genuine  contraction  of  the  kidney  only  in  its  aetiology. 

Clinical  Symptoms. — Since  in  most  cases  pyelitis  develops  only  as  one 
symptom  of  a  more  extensive  morbid  process,  its  clinical  symptoms  are  usu- 
ally but  slightly  prominent  in  the  general  course  of  the  illness.  In  what 
follows,  therefore,  we  cannot  give  any  complete  description  of  the  clinical 
course  of  pyelitis,  but  we  must  mention  only  those  symptoms  from  which, 


808  DISEASES   OF   THE   URINARY   ORGANS 

when  there  is  an  affection  of  the  urinary  passages,  we  may  conclude  that  the 
pelvis  of  the  kidney  takes  part  in  the  morbid  process. 

The  most  essential  sign  which  the  urine  presents  in  all  inflammatory  af- 
fections of  the  urinary  passages,  the  presence  of  mucus  and  pus,  will  be 
described  more  fully  in  the  chapter  on  cystitis  (vide  infra).  In  pyelitis,  also, 
the  mucopurulent  secretion  of  the  pelvic  mucous  membrane  must  mix  with 
the  urine,  and  in  every  severe  purulent  inflammation  the  amount  of  pus  in  the 
urine  must  be  considerable.  We  can  never  decide  with  certainty,  from  the 
mere  presence  of  pus  in  the  urine,  as  to  the  place  where  the  pus  mixes  with 
the  urine,  whether  in  the  pelvis  of  the  kidney  or  in  the  bladder,  or  even  in  the 
urethra.  If  only  we  were  able  to  demonstrate  other  morphological  elements 
besides  the  pus  corpuscles,  so  characteristic  that  their  origin  might  be  af- 
firmed with  certainty  to  be  the  pelvis  of  the  kidney,  we  might,  by  means  of 
them,  make  our  diagnosis  of  pyelitis  absolute.  Unfortunately,  however,  the 
microscopic  sediment  of  the  urine  leaves  much  in  this  regard  to  be  desired. 
The  greatest  weight  was  formerly  ascribed  to  the  discovery  of  pelvic  epi- 
thelium; especially  the  triangular,  long-tailed  epithelial  cells,  sometimes  ar- 
ranged one  upon  the  other,  like  the  tiles  of  a  roof    (see   Fig.   101),  were 

regarded  as  an  indication  that  the  pelvis 
of  the  kidney  was  involved  in  the  inflam- 
mation; but  the  diagnostic  significance  of 
these  cells  is  very  slight,  for,  on  the  one 
hand,  they  may  be  absent  in  a  severe  case 
of  p3^elitis,  and,  on  the  other  hand,  pre- 
cisely similar  epithelium  comes  from  the 
Fig.   101. — Epithelium  from  the  pelvis  t  p  ,,      ,,     -,  -,  n  '      x 

of  the  kidney  mucous  membrane  ot  the  bladder.     Greater 

value  is  given  of  late  to  the  discovery  of 
certain  casts  from  the  mouths  of  the  urinary  canaliculi  (ductus  papillares) 
— structures  which  are  almost  invariably  involved  in  all  but  the  milder  cases 
of  pyelitis.  Tubuliform  epithelial  casts,  cylindrical  formations  composed  of 
pus  corpuscles,  and,  above  all,  casts  composed  of  micrococci,  have  been  repeat- 
edly found  in  the  urinary  sediment  in  cases  of  pyelitis,  and  possess  some 
diagnostic  importance  (Furbringer  and  others). 

With  regard  to  the  other  characteristics  of  the  urine,  it  should  be  men- 
tioned that  it  is  often  remarkably  abundant  in  pyelitis,  and  that  it  then  of 
course  is  pale  and  has  a  comparatively  low  specific  gravity.  The  reaction 
of  the  urine  is  usually  acid,  despite  the  admixture  of  pus.  That  this  acid 
reaction  is  an  effectual  distinction  from  the  urine  of  cystitis  cannot  be  main- 
tained (vide  infra).  We  may,  however,  say  that  the  tendency  of  the  urine 
to  ammoniacal  fermentation  is  decidedly  greater  in  cases  of  cystitis  than  in 
cases  of  pj^elitis.  The  amount  of  albumen  in  the  urine  corresponds  to  the 
amount  of  pus.  If  there  is  a  very  large  amount  of  albumen,  it  arouses  sus- 
picion of  a  coincident  nephritis.  The  only  decisive  proof  of  such  a  complica- 
tion lies  in  the  finding  of  genuine  urinary  casts.  In  cases  of  simple  pyelitis 
it  is  exceptional  for  the  urine  to  be  bloody,  while  in  calculous  pyelitis  (q.  v.) 
blood  is  often  present. 

Besides  the  quality  of  the  urine,  another  symptom  is  pain  in  the  region 
of  the  kidneys,  occurring  either  spontaneously  or  through  pressure.  This 
symptom  is  present  in  many  cases  of  pyelitis,  and  is  therefore  of  diagnostic 


INFLAMMATION   OF  THE   PELVIS  OF   THE   KIDNEY— PYELITIS      809 

importance  The  pain  is  often  very  severe,  and  radiates  along  the  ureters  to 
the  bladder.  In  some  cases,  however,  there  may  be  no  pain  at  all,  so  tbat 
while  its  presence  is  one  symptom  of  pyelitis,  its  absence  does  not  weigh 
against  the  disease. 

All  the  other  symptoms  may  be  directly  dependent  upon  the  pyelitis,  but 
they  may  usually  be  referred  in  great  degree  to  the  other  coexisting  affections. 
First  among  these  is  fever,  that  either  shows  an  irregularly  remitting  course, 
or  appears  in  single  high  elevations  of  temperature,  usually  associated  with 
rigors.  The  fever,  however,  seldom  shows  this  latter  pyaemic  character  ex- 
cept in  the  severe  purulent  forms,  where  we  usually  also  have  the  formation 
of  renal  abscesses — that  is,  a  pyelonephritis.  Besides  the  fever  there  are  often, 
in  severe  cases,  general  nervous  symptoms,  such  as  headache,  delirium,  and 
sopor.  These  symptoms  are  to  be  referred  partly  to  the  general  pyaemic  in- 
fection of  the  body  and  partly,  as  well,  to  the  absorption  of  ammonia  from 
the  decomposing  urine  into  the  blood — the  "  amnionisemia "  of  Treitz  and 
Jaksch. 

The  whole  course  of  pyelitis  differs  so  much  according  to  the  primary  dis- 
ease present  that  nothing  of  general  application  can  be  said  about  it.  The 
milder  forms,  which  often  pass  off  rapidly,  are  found  most  commonly  in  child- 
bed, and  sometimes  in  acute  infectious  diseases,  poisonings,  and  as  a  result 
of  mild  cystitis.  The  severe  forms  are  chiefly,  as  we  have  said,  pyelo- 
cystitis  and  pyelonephritis,  as  a  result  of  strictures  of  the  urinary  tract  (vide 
infra),  of  severe  cystitis  in  diseases  of  the  spinal  cord,  and  in  other  severe 
diseases  of  the  kidney  and  of  the  pelvis  of  the  kidney,  such  as  new  growths 
and  parasites.  They  usually  constitute  a  very  tedious  and  incurable  affec- 
tion, which  lasts  until  the  patient's  death. 

What  appears  to  be  a  primary  pyelitis  occurs  chiefly  in  children  and 
young  persons,  and  often  begins  with  the  general  manifestations  of  an  acute 
febrile  infection.  At  first  the  diagnosis  of  the  true  condition  is  difficult,  but 
is  made  possible  by  pains  in  the  region  of  the  kidneys,  and,  above  all,  by  the 
presence  of  pus  in  the  urine.  The  absence  of  bladder  tenesmus  and  of  fre- 
quent micturition  is  to  be  noted  in  contradistinction  to  the  prominence  of 
these  symptoms  in  every  case  of  severe  cystitis.  Coincident  gastrointestinal 
symptoms  are  often  observed.  "With  proper  care  and  treatment,  a  cure  gen- 
erally results  in  from  eight  to  fourteen  days. 

The  implication  of  the  kidneys  is  shown  by  the  presence  of  casts  in  the 
urine  in  addition  to  the  pus  corpuscles.  In  the  cases  above  mentioned,  in 
which  a  chronic  pyelonephritis  is  complicated  with  the  contracted  kidney,  the 
condition  of  the  urine  is  the  same  in  many  respects  as  in  genuine  contracted 
kidney.  It  is  abundant,  usually  has  a  low  specific  gravity,  and  contains,  be- 
sides the  pus  corpuscles,  a  few  short  hyaline  casts.  In  such  cases  there  may 
be  developed  a  secondary  hypertrophy  of  the  left  ventricle,  unless  the  general 
nutrition  of  the  patient  is  too  much  impaired. 

Great  progress  in  the  more  exact  diagnosis  of  diseases  in  connection  with 
which  pyuria  occurs,  is  due  to  cystoscopy  and  to  separate  examination  of  the 
urine  from  each  kidney,  made  possible  by  the  catheterization  of  the  ureters, 
and  by  other  methods  of  segregation.  Detailed  information  in  regard  to 
these  important  methods  of  examination  will  be  found  in  special  works  upon 
the  subject. 


810  DISEASES   OF   THE   URINARY   ORGANS 

Treatment. — The  treatment  of  pyelitis  coincides  mainly  with  the  treat- 
ment of  the  primary  disease — for  example,  renal  calculi — and  to  that  extent 
it  needs  no  detailed  description  here.  In  regard  to  the  general  dietary,  the 
copious  drinking  of  fluids  (mineral  waters  of  Wildungen,  Fachingen,  Ober- 
salzbrunnen,  etc.)  will  usually  be  found  useful.  A  diet  in  which  milk  pre- 
dominates is,  therefore,  frequently  prescribed  with  success.  Spices  and  stimu- 
lating foods  are  to  be  avoided.  Among  the  internal  remedies  to  which  a 
favorable  influence  is  ascribed  in  connection  with  affections  of  the  urinary 
tract,  we  have,  first  of  all,  the  astringents  (tannin,  tannigen,  etc.).  Their 
therapeutic  effects,  however,  are  usually  very  slight,  and  often  they  are  ill 
borne.  Certain  antiseptic  remedies  are  preferable,  particularly  salol  in  cap- 
sules of  8  gr.  (gm.  0.5)  three  to  five  times  a  day;  also  boric  acid,  5  to  8 
gr.  (gm.  0.3  to  0.5)  three  times  daily,  camphoric  acid  and  chlorate  of  po- 
tassium. Urotropin,  8  to  15  gr.  (gm.  0.5  to  1)  several  times  daily,  is  the 
remedy  at  present  most  frequently  employed,  particularly  in  cystopyelitis  com- 
bined with  bacteriuria  or  with  fermentation  of  the  urine.  Judging  from 
personal  experience,  the  results  are  most  praiseworthy.  Helmitol  is  another 
drug  with  a  similar  action. 

Local  applications  to  the  region  of  the  kidneys,  warm  poultices,  or  ex- 
ceptionally local  bloodletting,  are  indicated  only  when  there  is  severe  pain, 
and  then,  of  course,  narcotics  must  also  be  used  under  some  circumstances. 
In  this  respect  warm  baths  also  do  good  service  at  times. 


CHAPTEE    II 

NEPHROLITHIASIS 

(Renal  Calculus.     Renal  Gravel.     Pyelitis  Calculosa) 

Occurrence,  Chemical  Composition,  and  ./Etiology  of  Renal  Concretions. — 

The  precipitated  concretions  of  the  urinary  constituents  which  form  in  the 
pelvis  of  the  kidney,  and  which,  under  some  circumstances,  may  be  passed  from 
it- with  the  urine,  are  designated,  according  to  their  size  and  nature,  as  renal 
sand,  a  fine,  pulverized  precipitate;  renal  gravel,  gravel-like,  granular  concre- 
tions about  the  size  of  the  ordina^  coarse  grains  of  sand,  which  can  usually 
pass  through  the  ureters  without  special  difficulty ;  or  renal  calculi,  the  larger 
concretions.  The  last  are  about  the  size  of  a  millet  seed  or  a  pea,  but  larger 
stones  are  occasionally  seen  which  may  even  resemble  actual  casts  of  the  pelvis 
of  the  kidney.  We  usually  find  a  calculus  in  only  one  kidney,  although  both 
kidneys  may  be  affected. 

In  regard  to  the  chemical  nature  of  renal  concretions,  they  consist  most 
frequently  of  uric  acid  and  urates.  The  uric-acid  stones  are  hard,  have  a 
brown-red  or  blackish  color,  and  a  crystalline  fracture,  which  in  large  stones 
is  usually  plainly  laminated ;  and,  on  the  whole,  a  smooth  although  irregularly 
shaped  surface.  If  a  small  portion  of  the  stone  is  pulverized  and  the  powder 
evaporated  to  dryness  with  a  little  concentrated  nitric  acid,  a  red  spot  arises, 
the  color  of  which  changes  to  violet  on  the  addition  of  caustic  soda  (the 
so-called  murexid  test  for  uric  acid.)     More  rarely  the  renal  concretions  con- 


NEPHROLITHIASIS  811 

sist  of  calcic  oxalate.  The  oxalate  calculi  are  extremely  hard,  have  a  dark- 
brown,  almost  blackish,  color  and  a  rough  surface,  often  furnished  with  many 
prickles,  from  which  reason  they  are  often  called  "  mulberry  calculi."  Their 
fracture  sometimes  shows  a  radiated  but  never  a  laminated  arrangement. 
Stones  are  also  frequently  seen,  which  consist  of  alternating  layers  of  uric  acid 
and  calcic  oxalate,  or  which  have  a  nucleus  of  uric  acid  and  a  coating  of  calcic 
oxalate.  The  phosphatic  calculi  are  another  variety  of  renal  concretion-.  We 
only  rarely  have  to  do,  however,  with  stones  which  consist  exclusively  of  basic 
calcic  phosphate  or  ammonio-magnesic  phosphate,  but  we  oftener  have  sec- 
ondary deposits  of  layers  of  phosphate  which  are  precipitated  on  uric  acid  or 
mulberry  calculi  in  urine  which  has  become  alkaline.  The  pure  phosphatic 
calculi,  of  course,  generally  with  a  slight  admixture  of  calcic  carbonate,  are 
grayish-white  and  rather  soft,  so  that  they  can  be  crushed  with  the  finger.  The 
largest  specimens  of  this  kind  are  not  found  usually  in  the  pelvis  of  the  kidney, 
but  in  the  bladder;  still,  as  we  have  ourselves  observed,  large  and  pure  phos- 
phatic calculi  do  occur  in  the  pelvis  of  the  kidney,  without  any  uric-acid 
nucleus.  All  the  other  calculous  formations  are  so  rare  that  they  scarcely 
possess  clinical  interest.  We  may  mention  the  light-yellow  cystin  *  calculi 
with  a  surface  of  waxy  luster,  the  xanthin  calculi,  and  the  indigo  calculi. 

As  to  the  precise  causes  of  all  these  concretions  we  have  as  yet  no  certain 
knowledge.  The  uric  acid  originates  from  the  albuminous  substances  of  the 
nuclei  of  the  cells,  the  so-called  nucleins.  An  increase  in  the  destruction  of 
leucocytes  seems  to  be  associated  with  an  increased  excretion  of  uric  acid. 
The  formation  of  a  solid  deposit  of  uric  acid  is  usually  associated  with  marked 
acidity  of  the  urine.  Yet,  we  do  not  know  at  all  in  what  way  these  circum- 
stances bring  about  the  development  of  renal  calculi.  There  is  much  prob- 
ability in  the  assumption  that  some  solid  substance  or  other  usually  forms  the 
nucleus,  and  gives  the  impulse  to  the  formation  of  at  least  the  larger  renal 
■calculi.  Such  nuclei  may  be  coagulated  mucus,  bits  of  epithelium,  and  perhaps 
bacteria.  It  is  an  interesting  fact,  although  we  cannot  completely  explain  it 
that,  as  Meckel,  Ebstein,  and  others  have  shown,  the  microscopic  examination 
of  minute  scales  of  calculi  disclose  the  crystalline  uric  acid  deposited  in  a  sup- 
porting structure  of  an  albuminous  character.  With  regard  to  the  formation 
•of  oxalate  calculi,  likewise,  we  possess  no  exact  knowledge.  Oxalic  acid  in  the 
urine  probably  is  due  in  part  to  the  oxalic  acid  which  is  introduced  into  the 
system  in  vegetables,  and  in  part  is  perhaps  formed  from  the  decomposition  of 
albuminous  substances.  The  deposits  of  crystals  of  calcic  oxalate,  as  well  as 
uric-acid  crystals,  from  acid  urine  is  well  known  to  be  a  very  frequent  occur- 
rence, while  the  actual  formation  of  calculi  is,  as  has  been  said,  comparatively 
rare.  The  cause  of  the  deposit  of  phosphatic  concretions  must  lie  in  the  urine 
becoming  alkaline.  In  such  cases,  therefore,  the  development  of  concretions 
is  probably  preceded  by  disease  of  the  pelvis  of  the  kidney  and  the  ingress  of 
bacteria  capable  of  exciting  an  alkaline  fermentation  of  the  urine. 

In  regard  to  the  predisposing  causes  of  calculous  formation  we  must  men- 
tion, first  of  all,  that  stones  are  often  found  in  children,  and  next  in  frequency 
in  advanced  life.    Men  show  a  greater  disposition  to  renal  calculi  than  women. 

1  Cystin  is  a  product  of  the  splitting  up  of  albuminous  substances,  and  is  usually  further 
■decomposed  in  the  body.  .  In  some  families,  cystinuria  occurs  as  a  peculiar  anomaly  of  tissue 
metabolism. 


812  DISEASES   OF   THE   URINARY   ORGANS 

Heredity  also  seems  to  play  a  certain  part,  since  the  disease  has  been  repeatedly 
observed  in  different  members  of  the  same  family.  The  many  relations  which 
have  been  imagined  between  the  formation  of  calculi  and  certain  conditions  in 
the  manner  of  life  and  in  the  food  taken,  all  lack  definite  proof.  As  to  mode  of 
life,  the  chief  blame  is  laid  upon  an  excessive  meat  diet,  drinking  copiously 
of  new  sour  wines,  and  drinking  water  containing  lime.  It  is  remarkable  that 
calculi  are  much  more  frequent  in  some  countries  (England,  interior  Eussia) 
and  regions  than  in  others.  In  regard  to  the  interesting  but  still  entirely  incom- 
prehensible relations  between  the  formation  of  renal  calculi  and  other  anomalies 
of  tissue  metabolism,  especially  gout,  compare  the  chapter  on  Gout. 

The  Anatomical  Changes  Caused  by  Renal  Calculi. — The  presence  of  con- 
cretions in  the  pelvis  of  the  kidney  very  frequently,  but  not  always,  excites 
pyelitis.  This  may  exhibit  all  degrees,  from  a  simple  catarrhal  inflammation 
to  a  diphtheritic  or  severe  purulent  inflammation  of  the  pelvic  mucous  mem- 
brane. As  a  result  of  the  mechanical  irritation,  there  are  quite  frequently 
large  or  small  hemorrhages. 

If  a  severe  purulent  pyelitis  has  developed,  this  may  bring  with  it  all  the 
sequela?  with  which  we  have  previously  become  acquainted.  In  severe  cases 
the  process  may  involve  the  kidneys,  when  there  arises  a  pyelonephritis,  with 
a  purulent  breaking  down  of  the  renal  tissue,  and,  under  some  circumstances, 
even  a  perinephritis,  with  extensive  suppuration  in  the  vicinity  of  the  kidney, 
and  with  occasional  perforation  into  the  neighboring  organs.  If  the  renal 
calculi  have  previously  passed  outward,  they  are  not  found  at  the  autopsy, 
although  they  form  the  special  starting  point  of  the  disease.  Sometimes,  how- 
ever, the  pus  cavity  is  entirely  filled  with  calculi. 

A  second  important  sequel  of  a  renal  calculus,  which  sometimes  develops, 
is  hydronephrosis  (vide  infra).  It  arises  when  a  large  stone  blocks  the  passage 
from  the  pelvis  of  the  kidney  into  the  ureter,  or  when  a  smaller  stone  remains 
fast  in  the  ureter  and  completely  shuts  off  the  passage  of  the  urine.  In  the 
latter  case  there  may  also  arise  a  pressure  necrosis  and  perforation  of  the  ureter. 
It  goes  without  saying  that  inflammation  and  hydronephrosis  or  pyonephrosis 
may  be  combined. 

Clinical  Symptoms. — If  there  is  merely  the  formation  of  renal  sand  or 
renal  gravel  in  the  urinary  tract,  this  condition  is  sometimes  associated  with 
no  symptoms  at  all.  The  little  granules  are  washed  away  by  the  urine  and 
evacuated,  and  at  most  they  may  give  rise  to  slight  pain  in  the  region  of  the 
kidney  and  in  the  abdomen.  Larger  stones,  however,  may  sometimes  be  wholly, 
or  almost  wholly,  without  symptoms,  if  their  position  and  their  smooth  surface 
are  such  that  they  are  comparatively  harmless. 

The  characteristic  clinical  symptoms  of  nephrolithiasis  do  not  appear  until 
the  results  of  mechanical  irritation  of  the  pelvis  of  the  kidney  arise,  or  until 
there  is  an  incarceration  of  a  calculus  in  the  ureter.  It  is  the  latter  circum- 
stance which,  after  the  analogy  of  gallstones,  causes  the  most  important  symp- 
tom in  the  diagnosis  of  renal  calculi — the  pain,  the  so-called  renal  colic.  Such 
an  attack  of  colic  sometimes  comes  on  quite  suddenly  and  unexpectedly;  in 
other  cases  it  is  produced  by  some  exciting  cause — jumping,  running,  walking, 
or  riding.  The  pain  often  becomes  frightful;  it  radiates  from  the  back  and 
the  lateral  portions  of  the  abdomen  along  the  course  of  the  ureters  downward, 
and  often  upward,  spreading  particularly  toward  the  bladder,  testicles,  and 


NEPHROLITHIASIS  813 

thighs,  and  also  up  the  back.  A  place  in  the  abdomen  which  corresponds  with 
the  bend  of  the  ureter,  and  on  the  right  side  almost  with  McBurney's  point 
(page  594),  is  particularly  often  sensitive  to  pressure.  Noteworthy  also  is 
the  frequent  sensibility  to  pressure  of  the  testicle  on  the  corresponding  .-ide. 
Nausea  and  repeated  vomiting  often  occur.  The  bowels  are  constipated,  the 
intestinal  gases  cannot  be  passed,  and  consequently  the  intestines  become 
slightly  distended  and  sensitive.  The  pulse  is  accelerated  and  often  abnormally 
tense,  and  the  temperature  usually  slightly  elevated.  Chills  are  rarely  observed. 
In  severe  attacks  there  may  be  a  general  state  of  collapse  with  a  small,  rapid 
pulse,  cold  sweat,  and  attacks  of  fainting.  The  urine,  as  a  rule,  is  scanty,  but 
frequently  evacuated  with  painful  tenesmus.  Sometimes  it  is  almost  entirely 
normal  in  quantity  and  composition,  if  it  comes  exclusively  from  the  other 
free  kidney.  Oliguria,  or  even  complete  anuria,  with  its  fatal  consequences,, 
invariably  sets  in  if  both  ureters  be  occluded.  Still,  even  with  a  unilateral 
calculous  obstruction,  the  passage  of  urine  may  be  scant  or  cease  almost  entirely 
as  a  result  of  a  reflex  inhibitory  influence  in  some  unknown  way  affecting  the 
secretion  of  urine  in  the  other  kidney.  Almost  complete  anuria  has  frequently 
been  observed  as  long  as  eight  days  in  cases  of  unilateral  obstruction  due  to 
renal  calculus.  In  such  cases  there  is  danger  of  uraemia,  though  it  is  astonish- 
ing how  rarely  this  sets  in  in  obstruction  by  stone.  If,  at  the  same  time,  there 
is  a  mechanical  irritation  or  an  inflammatory  process,  the  urine  often  contains 
blood  and  pus.  Even  if  the  urine  appears  macroscopically  to  be  normal,  micro- 
scopic examination  of  the  centrifugalized  specimen  often  shows  some  leuco- 
cytes, red  blood  corpuscles,  isolated  hyaline  casts,  and  particularly  often,  crys- 
tals of  uric  acid.  The  duration  of  the  renal  colic  depends  on  the  duration  of 
the  incarceration ;  it  may  last  for  a  few  hours  or  for  several  days.  The  attack 
often  ends  with  the  expulsion  of  the  stone. 

In  the  intervals  between  the  several  attacks  some  patients  feel  quite  well, 
while  others  have  slight  pains  in  the  loins  and  back,  at  times  also  distinctly 
localized  in  the  region  of  the  one  kidney,  as  well  as  gastrointestinal  disturb- 
ances; frequently  urinary  tenesmus  exists.  More  serious  symptoms  set  in 
as  a  result  of  severe  mechanical  irritation  of  the  pelvis  of  the  kidneys  and 
of  inflammatory  complications.  The  pains  in  the  regions  of  the  kidneys  then 
increase.  The  urine  shows  an  admixture  of  pus,  and  contains  pelvic  epithelium 
and  often  blood.  The  frequent  appearance  of  blood  in  the  urine,  in  consequence 
of  mechanical  lesions  of  the  mucous  membrane  of  the  pelvis  of  the  kidneys,  is 
a  characteristic  symptom  of  pyelitis  calculosa.  If  we  find,  as  sometimes  hap- 
pens, the  urine  at  many  times  perfectly  clear  and  normal,  but  at  other  times 
purulent,  we  may  suspect  an  occasional  blocking  of  the  ureter  coming  from 
the  diseased  kidney  by  a  renal  calculus. 

The  symptoms  are  much  more  severe  if  the  trouble  goes  on  to  a  severe 
purulent  pyelitis  and  pyelonephritis.  We  need  not  describe  the  details  again 
here — the  pain,  fever,  swelling,  and  perforation  internally  or  externally — 
since  they  agree  completely  with  what  has  been  said  before  (see  the  previous 
chapter  and  Chapter  VI  in  the  previous  section).  A  special  chapter  will  be 
devoted  to  the  symptomatology  of  hydronephrosis. 

The  course  of  nephrolithiasis  is,  as  a  rule,  very  tedious.  Since  the  disposi- 
tion to  the  formation  of  calculi  usually  persists,  and  since  also  the  sequela? 
which  have  once  developed  may  last  for  a  long  time,  a  very  chronic  state  often 


814  DISEASES   OF   THE   URINARY  ORGANS 

develops,  which,  in  varying  ways  and  with  manifold  exacerbations  and  remis- 
sions, is  composed  of  attacks  of  colic,  hemorrhages,  and  symptoms  of  pyelo- 
cystitis. 

In  many  cases,  of  course,  complete  recovery  may  finally  ensue.  The  calculi 
present  are  passed,  new  ones  are  not  formed,  the  pyelitis  that  has  arisen  dis- 
appears, and  all  the  morbid  symptoms  cease;  but,  on  the  other  hand,  nephro- 
lithiasis entails  a  number  of  dangers  which  seriously  threaten  life.  These  are, 
besides  the  rare  occurrence  of  ursemia,  first  of  all  the  development  of  pyelo- 
nephritis and  of  still  more  extensive  suppurations,  and  a  general  decline  in 
strength,  pysemic  states,  etc.  There  is  also  a  possible  danger  in  such  chronic 
suppurations  that  a  general  amyloid  degeneration  of  the  internal  organs  may 
ensue.  With  regard  to  complications  on  the  part  of  other  organs,  there  is 
•one  point  of  special  interest — viz.,  that  sometimes  gallstones  and  renal  calculi 
are  found  in  one  and  the  same  patient.  Attention  is  again  to  be  called  to  the 
combination  of  renal  calculi  with  other  gouty  affections  (vide  chapter  on  Gout) 
as  well  as  other  constitutional  diseases  (diabetes,  arteriosclerosis). 

Diagnosis. — If  typical  attacks  of  renal  colic  with  the  passage  of  stones 
have  repeatedly  appeared,  or  if  the  attacks  of  colic  are  combined  with  the 
pronounced  appearance  of  blood  and  pus  in  the  urine,  the  diagnosis  of  nephro- 
lithiasis presents  no  difficulties.  It  is  different  in  the  cases  in  which  stones 
have  never  passed,  and  the  patient  complains  only  of  pains,  gastrointestinal 
disturbances,  etc.  In  such  cases,  it  is  important  that  in  addition  to  the  other 
affections  to  be  taken  into  consideration,  the  possibility  of  renal  calculi  be 
kept  in  view  from  the  first,  and  the  history  taking  and  physical  examination 
he  directed  accordingly.  It  is  particularly  difficult  to  distinguish  renal  colic 
from  gallstone  colic,  recurring  appendicitis,  intestinal  colic,  purely  nervous 
disturbances,  floating  kidney,  lumbago,  etc.  The  assumption  of  nephrolithiasis 
is  based  above  all  on  a  careful  consideration  of  the  character  of  the  pains  (ra- 
diation to  the  bladder  and  genital  organs),  sensitiveness  to  pressure  in  the 
region  of  the  kidney  and  along  the  ureters,  the  frequent  desire  to  urinate,  with 
oliguria,  increased  tension  of  the  pulse,  and,  above  all,  on  the  careful  micro- 
scopic analysis  of  the  urine  (blood  and  pus  cells,  a  few  hyaline  casts,  uric-acid 
crystals).  Very  often,  of  course,  a  positive  diagnosis  demands  continued 
•observation  of  the  case. 

It  is  of  great  importance,  particularly  with  regard  to  any  operative  treat- 
ment, to  determine  which  kidney  is  the  seat  of  the  trouble,  and  whether  one 
kidney,  at  any  rate,  is  perfectly  healthy  or  not.  In  considering  these  questions 
we  must  be  guided  by  the  chief  seat  of  the  pain ;  the  appearance  of  the  urine — 
for  instance,  observing  whether  there  is  an  increase  in  the  amount  of  pus  if 
pressure  is  made  upon  the  diseased  kidney,  and  whether  from  time  to  time 
normal  urine  is  evacuated  as  a  result  of  occlusion  of  the  ureter  upon  the  dis- 
eased side ;  and  by  the  results  of  external  examination  with  regard  to  tender- 
ness, or  the  discovery  of  a  tumor  due  to  hydronephrosis.  In  all  difficult  cases 
a  special  examination  with  the  assistance  of  the  newer  methods  of  examina- 
tion (cystoscopy,  separate  examination  of  the  urine  secreted  by  each  kidney, 
etc.)  is  necessary.  Admirable  diagnostic  results  are  also  obtained  in  cases 
of  renal  calculi  by  examination  with  the  Eontgen  rays.  With  the  aid  of  the 
new  and  improved  methods  of  technic,  not  only  phosphatic  calculi,  but  also 
uratic  calculi,  can  be  determined  in  this  manner.     In  all  suspicious  cases 


PLATE    IV 


Radiogram  of  a  Stone  in  the  Right  Kidney.  (Patient  in  the  dorsal  position,  the  tube 
being  in  front  and  the  photographic  plate  behind  him.)  a,  shadow  of  the  twelfth 
rib;  b,  the  renal  stone  (later  removed  by  operation);  c,  shadow  of  the  lumbar  vertebrae. 


NEPHROLITHIASIS  815 

of  any  severity,  Rontgen  photography  is  therefore  urgently  to  be  recom- 
mended. 

Treatment. — Since  the  uric-acid  concretions  arc  by  far  the  commonest,  the 
methods  of  treatment  most  in  use  for  nephrolithiasis  rci'fr  especially  to  these. 

If  the  tendency  to  the  formal  ion  of  urinary  gravel  be  confirmed  in  a  pa- 
tient, or  if  the  severer  symptoms  of  nephrolithiasis  have  already  appeared,  we 
must  first  give  a  number  of  general  dietetic  directions,  in  order  to  check  the 
formation  of  uric  acid  in  general,  and  promote  the  solution  of  the  uric  acid 
already  formed  as  far  as  possible.  Without  entering  too  much  on  theoretical 
reasoning,  we  will  give  in  what  follows  the  measures  which  have  won  general 
approval.  In  the  first  place,  the  patient  must  avoid  immoderate  indulgence 
in  any  sort  of  food,  and  particularly  in  meat.  Articles  of  diet,  such  as  liver, 
sweetbread,  and  calf's  kidneys,  which  contain  an  abundance  of  nuclei n,  should 
be  forbidden.  The  patient  should  be  advised  to  choose  a  chiefly  vegetable  diet, 
with  milk  and  a  moderate  amount  of  meat;  spirituous  beverages  are  to  be  used 
little,  if  at  all,  and  acid  viands  and  liquids  are  inadmissible.  It  is  advantage- 
ous to  weigh  the  patient  regularly  in  order  to  keep  wateh  on  the  nutrition, 
and  to  avoid  any  further  increase  of  weight  in  such  individual-;  a>  are  well 
nourished;  and  in  the  obese,  to  bring  about  a  diminution  of  weight.  Moreover, 
so  far  as  the  genercl  condition  of  the  patient  allows,  he  should  have  regular 
exercise  in  the  gymnasium,  or  at  sawing  wood,  or  gardening.  He  should  also 
promote  the  assimilation  of  his  food  by  the  frequent  use  of  warm  baths  or 
salt  baths;  and  an  abundance  of  liquid  must  be  ingested,  so  as  to  dilute  the 
urine,  and  thus  increase  its  solvent  power. 

This  last  indication  is  usually  met,  in  conjunction  with  that  of  diminishing 
the  acid  reaction  of  the  urine,  by  the  ingestion  of  alkalies,  so  as  to  prevent,  as 
far  as  possible,  the  deposit  of  uric  acid;  consequently,  alkalies  and  alkaline 
mineral  waters  are  very  extensively  employed  in  nephrolithiasis.  Pfeiffer  and 
others  have  been  able  to  demonstrate  by  direct  experiment  that  the  urine  se- 
creted after  the  use  of  such  waters  and  drugs  does  possess  an  increased  power 
to  dissolve  uric  acid.  The  simplest  way  is  to  have  the  patient  use  phosphate 
of  soda  in  a  daily  dose  of  1  to  4  drachms  (gm.  5  to  15)  ;  or,  better,  carbonate 
of  soda,  1  to  2.5  drachms  (gm.  5  to  10)  ;  or,  finally,  the  specially  recommended 
carbonate  of  lithia,  2  to  8  gr.  (gm.  0.1  to  0.5),  several  times  a  day,  dissolved 
in  a  large  amount  of  simple  water,  or  carbonated  water,  or  lemonade.  Also 
mixtures  of  these  remedies  are  often  used  with  good  results;  thus  Cantani 
recommends  bicarbonate  of  soda,  8  gr.  (gm.  0.5)  ;  effervescing  carbonate  of 
lithia,  4  gr.  (gm.  0.25)  ;  citrate  of  potassium,  15  gr.  (gm.  1)  ;  also  the  so-called 
uricedin,  which  is  composed  of  the  citrates  of  sodium  and  lithium,  sulphate  of 
sodium,  and  chlorid  of  sodium.  Of  this,  15  gr.  are  to  be  given  several  times 
a  day.  Another  remedy  is  borocitrate  of  magnesium,  of  which  a  teaspoonful 
may  be  taken  in  soda  water  with  sirup,  three  times  a  day.  Of  the  natural 
mineral  waters,  the  springs  of  Fachingen,  Vichy,  Carlsbad,  Wildungen, 
Briickenau,  Salzbrunn,  and  Neuenahr  are  chiefly  used.  The  natural  lithia 
waters  of  Assmanshausen  and  Salzschlirf  contain  such  minute  amounts  of 
lithia  salts  that,  in  general,  the  artificial  waters  are  to  be  preferred  to  them. 

The  attempt  has  been  often  made  to  promote  the  solution  of  uric  acid  by 
administering  certain  chemical  substances,  but  unfortunately  the  results  have 
not  been  brilliant.     The  conditions  which  obtain  in  the  human  organism  are 


816  DISEASES   OF   THE   URINARY   ORGANS 

essentially  different  from  those  in  a  test-tube.  Piperazin,  15  to  45  gr.  (gm. 
1  to  3)  daily,  has  been  much  recommended,  but  has  not  proved  at  all  efficient, 
and  the  same  may  be  said  of  lysidin,  15  to  60  gr.  (gm.  1  to  4)  a  day,  and 
urotropin,  15  to  25  gr.  (gm.  1  to  1.5)  daily,  in  water.  Still,  further  trial  of 
these  remedies,  above  all  urotropin,  would  not  be  unjustifiable. 

The  symptomatic  treatment  is  very  important.  In  so  far  as  this  relates  to 
the  accompanying  pelvic  and  vesical  catarrh,  we  may  refer  to  the  appropriate 
chapters  in  this  book.  For  renal  hemorrhages  some  internal  remedies,  such 
as  ergotin,  hydrastis  canadensis,  etc.,  have  been  recommended,  but  their  action 
is  quite  doubtful.  Subcutaneous  injections  of  adrenalin  (one  s}^ringeful  of  a 
0.1  per  cent  solution)  deserve  somewhat  greater  confidence.  The  effectiveness, 
of  gelatin  injections  (^iij  to  v  [gm.  100  to  150]  of  a  sterilized  one-  or  two- 
per-cent  solution)  recommended  for  various  internal  hemorrhages,  is  extremely 
doubtful.  The  internal  administration  of  a  decoction  of  gelatin  (about  five- 
per  cent)  is  more  convenient  and,  therefore,  preferable.  The  treatment  of  the 
attacks  of  colic  is  of  great  practical  significance.  The  chief  remedies  are  the 
narcotics,  opium,  and  morphin,  internally,  or  with  very  severe  pains,  better 
subcutaneously.  In  severe  cases  chloral  and  inhalations  of  chloroform  may  be 
employed.  Warm  baths,  warm  poultices,  or  narcotic  embrocations,  such  as- 
chloroform  liniment,  also  frequently  give  relief.  Sometimes  patients  expe- 
rience an  alleviation  of  their  pains  if  the  pelvis  is  raised  and  the  trunk  placed 
in  a  low  position.  Some  physicians  recommend  vibratory  massage  in  the 
region  of  the  kidneys,  and  cautious  downward  massage  along  the  course  of 
the  ureter,  but  this  does  not  always  agree  with  the  patient.  The  administra- 
tion of  glycerin  (a  tablespoonful  in  tea  or  milk  two  or  three  times),  which  is. 
claimed  to  stimulate  the  contractions  of  the  ureter,  must  be  mainly  regarded 
as  a  placebo.  An  abundant  supply  of  fluid  is  always  advisable,  in  order  to- 
aid  the  washing  out  of  the  incarcerated  stone  by  an  increased  secretion  of  urine. 

Since  the  initiative  of  Simon  in  1871  the  operative  treatment  of  renal  dis- 
ease has  made  continuous  progress,  and  it  has  been  eminently  successful  in 
many  cases  of  renal  calculi.  It  is,  therefore,  most  important  in  all  instances- 
of  nephrolithiasis  with  severe  symptoms,  and  particularly  with  secondary  puru- 
lent inflammation,  to  consider  the  possibility  of  surgical  interference  by  ne- 
phrotomy or  nephrectomy.  In  the  dangerous  cases  of  nephrolithiasis,  in  which 
persistent  and  almost  complete  anuria  occurs,  timely  surgical  interference  is 
of  the  greatest  importance.  Particulars  in  these  matters  must  be  sought  in 
special  treatises  on  renal  surgery. 

What  has  been  said  thus  far  refers,  as  we  have  stated,  chiefly  to  the  treat- 
ment of  uric-acid  calculi.  If  there  are  calculi  made  up  of  oxalate,  the  amount 
of  vegetables  eaten  must  be  limited,  but  the  use  of  alkaline  waters  is  advisable. 
We  do  not  know  any  special  directions  to  give  in  case  there  were  cystin  calculi.. 
On  the  other  hand,  when  phosphatic  stones  are  present,  inasmuch  as  these  can- 
not be  deposited  unless  the  urine  is  alkaline,  we  should  recommend  the  employ- 
ment of  acids,  particularly  lactic  acid,  8  to  15  gr.  (gm.  0.5  to  1),  and  salicylic 
acid;  also,  hydrochloric  acid  and  phosphoric  acid.  Of  course,  in  most  cases, 
there  is  some  disease  of  the  urinary  passages  which  has  occasioned  the  forma- 
tion of  the  calculi,  and  if  such  disease  is  discovered  its  treatment  is  of  para- 
mount importance. 


TUBERCULOSIS   OF   THE   GENITO-URINARY   APPARATUS         817 

CHAPTER    III 
TUBERCULOSIS    OF    THE    GENITO-URINARY    APPARAH 

etiology  and  Pathological  Anatomy. — It  does  not  seem  remarkable  that, 
with  the  presence  of  many  tubercular  processes  in  the  body,  tubercle  bacilli 
should  quite  easily  reach  the  kidneys  by  way  of  the  blood  current,  and  there 
give  rise  to  an  eruption  of  tubercle.  Accordingly,  we  quite  frequently  find  a 
few  or  many  miliary  tubercles  in  the  kidneys  in  acute  miliary  tuberculosis,  in 
pulmonary  tuberculosis,  etc.,  which  are  distributed  over  the  whole  kidney,  or 
sometimes  only  in  the  territory  of  one  arterial  branch. 

While  miliary  tuberculosis  of  the  kidney,  however,  is  without  any  clinical 
significance,  there  is  also  an  extensive  local  tuberculosis  of  the  kidney,  as  well 
as  of  the  urinary  tract  and  the  sexual  organs.  Such  affections  sometimes 
occur  as  a  result  of  pronounced  preexisting  tuberculosis  of  other  organs,  espe- 
cially the  lungs,  or  they  arise  as  an  apparently  independent  disease,  which  is 
termed  genito-urinary  tuberculosis.  In  such  cases  the  infection  with  the 
tubercle  bacilli  often  seems  to  take  place  by  means  of  the  blood  from  some 
previously  existing — perhaps  concealed — tuberculous  focus  in  the  body,  such 
as  a  gland,  tuberculous  bone  or  joint  disease,  etc.  In  a  few  cases,  the  tubercle 
bacilli  perhaps  enter  the  urinary  or  the  genital  tract  from  without.  How- 
ever, a  hematogenous  infection  seems  to  be  the  rule  in  genito-urinary  tuber- 
culosis, especially  as  the  results  of  more  recent  surgical  experience  have  shown 
that  tuberculous  foci  generally  appear  in  the  kidneys  first,  and,  in  fact,  almost 
regularly  in  only  one  kidney.  The  bladder  becomes  affected  only  later  (excep- 
tionally, in  the  early  stages)  ;  the  prostate,  apparently  with  particular  fre- 
quency, and  the  seminal  vesicles  and  the  testicles  as  well.  From  the  organ 
first  involved,  the  process  then  extends  continuously  or  by  leaps  to  the  neigh- 
boring parts.  If  the  cases  come  to  autopsy,  the  tuberculosis  is  often  so  exten- 
sive that  we  can  no  longer  make  out  with  certainty  the  place  where  it  first 
began.  In  women,  tuberculosis  is  at  times  predominantly  localized  in  the 
genital  apparatus  (uterine  and  ovarian  tuberculosis). 

As  in  all  tuberculous  affections,  individual  predisposition  plays  a  part  in 
genito-urinary  tuberculosis,  which  should  not  be  overlooked.  This  predispo- 
sition may  be  congenital  (hereditary  or  family  tendency)  or  acquired.  In 
regard  to  the  latter,  it  is  to  be  observed  that  previous  gonorrheal  affections 
(gonorrheal  epididymitis,  gonorrheal  cystopyelitis)  and  in  women,  occasion- 
ally puerperal  pyelitis,  prepare  the  ground  for  tuberculous  infection.  In  the 
kidneys  the  tuberculous  infiltration  develops  either  chiefly  from  the  pelvis  of 
the  kidney  or  in  the  renal  substance  itself.  Yellow  cheesy  nodules  arise, 
which  finally  break  down  and  thus  lead  to  an  actual  "nephrophthisis."  If 
the  disease  arise  from  the  pelvis,  the  infiltrated  renal  papilla?  are  usually  first 
affected.  Ulcerative  recesses  are  formed  in  the  pelvis  of  the  kidney,  and  finally 
the  entire  lining  of  the  pelvis  is  transformed  into  a  raw  surface  covered  with 
necrotic  tissue  and  cheesy  detritus.  In  very  advanced  cases  almost  the  whole 
kidney  is  destroyed.  As  already  mentioned,  the  process  is  at  first  one-sided, 
afterwards  usually  bilateral,  but  it  is  often  more  advanced  on  one  side  than 
on  the  other. 


818  DISEASES   OF   THE   URINARY  ORGANS 

If  the  process  invade  the  ureters,  their  walls  also  are  infiltrated  with  tuber- 
cular deposits,  and  hence  they  are  thickened,  while  the  mucous  membrane  is 
often  changed  in  great  part  to  a  necrotic  ulcerating  surface.  Precisely  analo- 
gous conditions  are  found  in  the  bladder,  and  in  some  cases  even  in  the 
urethra;  while  in  the  prostate,  the  vesiculse  seminales,  and  the  testicles  there 
is  more  frequently  the  formation  of  cheesy  tubercular  nodules,  and  rarely 
disintegration  and  perforation  of  the  tubercular  formations. 

Clinical  Symptoms. — The  picture  of  genito-urinary  tuberculosis  corre- 
sponds in  most  of  its  details  completely  to  that  of  a  severe  chronic  pyelo- 
cystitis.  The  occasional  local  symptom  is  pain  in  the  region  of  the  kidneys 
and  bladder.  This  may  sometimes  assume  great  severity,  like  colic,  if  the 
ureter  become  plugged  by  a  broken-down,  crumbling  mass.  If  the  bladder  is 
also  affected,  frequent  pressure  and  pain  in  urinating  arise.  In  other  cases, 
however,  the  pain  is  but  slight  during  the  whole  disease. 

The  urine  shows  the  most  important  diagnostic  changes.  It  almost  inva- 
riably contains  an  abundant  sediment,  consisting  of  pus  corpuscles  and 
detritus.  Its  amount  usually  remains  normal  for  a  long  time;  its  reaction 
is  faintly  acid,  but  in  severe  cases  it  may  become  alkaline  through  complica- 
tion with  an  alkaline  fermentation  of  the  urine.  The  discovery  of  shreds  of 
tissue  in  the  urine,  elastic  fibers  and  connective  tissue,  is  sometimes  possible, 
and  is  of  diagnostic  value  because  it  is  direct  evidence  of  an  ulcerative  process. 
The  discovery  of  tubercle  bacilli  in  the  purulent  urinary  sediment  (Eosen- 
stein  and  others)  is,  however,  far  more  important.  This  is  possible  in  almost 
all  cases,  and  is  a  reliable  and  absolutely  decisive  factor  in  diagnosis.  There 
is,  however,  one  unfortunate  circumstance  about  the  demonstration  of  tubercle 
bacilli  in  the  urine,  for  not  infrequently  other  bacilli  (smegma  bacilli)  are 
stained  by  the  ordinary  method  of  staining,  which  is  that  employed  for 
sputum,  and  are  thus  mistaken  for  tubercle  bacilli.  As  yet,  no  easy  and  cer- 
tain method  of  distinguishing  these  two  varieties  of  bacilli  has  been  discov- 
ered, and  hence  in  doubtful  cases  it  is  necessary  to  resort  to  pure  cultures  and 
to  inoculation,  in  order  to  reach  a  decision.  Still,  if  the  urine  is  taken  by 
the  catheter,  and,  at  the  same  time,  all  other  phenomena  considered,  we  may, 
as  a  rule,  manage  with  the  ordinary  staining  method.  [Stain  with  carbol- 
f uchsin ;  decolorize  with  twenty-per-cent  nitric  acid  ;  wash  in  water ;  and  still 
further  decolorize  in  seventy-per-cent  alcohol  for  at  least  ten  minutes.  This 
will  bleach  the  smegma  bacilli.]  Other  bacilli  are  usually  entirely  absent  in 
tuberculous  pyuria.  Admixtures  of  blood  in  the  urine  are  also  seen  in  genito- 
urinary tuberculosis,  but  they  may  often  be  entirely  absent.  In  several  of  our 
cases  a  slight  hgematuria  was  the  first  symptom  which  called  the  patient's 
attention  to  the  trouble  with  the  bladder.  Pyuria,  however,  ordinarily  pre- 
cedes hematuria.  The  more  profuse  renal  hemorrhages  generally  occur  only 
in  the  earlier  stages  of  the  disease.  On  the  other  hand,  the  microscope  will 
frequently  demonstrate  a  slight  admixture  of  blood.  In  some  cases  the  urine 
is  entirely  free  from  blood. 

The  local  objective  examination  of  the  kidneys  usually  gives  a  negative 
result.  Only  in  a  few  cases  have  we  been  able  to  feel  the  diseased  kidney  as 
a  tumor  through  the  abdominal  walls.  This  is  usually  due  less  to  the  tuber- 
culous infiltration  of  the  kidney  itself  than  to  the  dilatation  of  the  pelvis  of 
the  kidney  from  hydronephrosis.    We  can  sometimes  feel  the  thickened  walls 


TUBERCULOSIS  OF  THE  GENITfMJBINARY  APPARAI  8L9 

of  the  bladder.  The  local  examination  of  the  prostate  and  the  testicles  is  far 
more  important  in  diagnosis.  Especially  in  the  latter  we  often  feel  the  hard- 
ening corresponding  to  the  tuberculous  infiltration,  and  manifesting  itself 
chiefly  in  the  epididymis,  while  the  hardening  and  enlargemeni  of  the  prostate 
and  seminal  vesicles  can  usually  be  easily  detected  by  rectal  palpation. 

.Among  the  general  symptoms  we  musl  mention,  first  of  all,  fever,  which  is 
only  exceptionally  absent,  and  usually,  in  the  severe  cases,  shows  a  pronounced 
remitting,  hectic  character.  The  other  general  symptoms  arc  the  Bame  as  in 
most  of  the  other  tubercular  diseases — anaemia,  persistently  rapid  pulse,  ema- 
ciation, loss  of  appetite,  increasing  bodily  weakness,  etc.  We  must  be  alert 
to  detect  the  occasional  coexistence  of  other  tubercular  diseases  in  the  body, 
the  lungs,  the  intestines,  the  bones,  etc.,  but  these  may  also  be  wholly  absent, 
so  that  we  may  have  to  do  with  a  purely  local  genito-urinary  tuberculosis. 

The  course  of  the  disease  is  steadily  progressive.  Eecovery  does  not  occur, 
at  least  not  in  any  cases  where  the  disease  has  attained  any  extent.  The  disease 
lasts  from  a  few  months  to  a  year  or  two,  but  sometimes  much  longer.  The 
fatal  termination  usually  ensues  from  the  increasing  general  weakness,  more 
rarely  under  the  symptoms  of  ammoniaemia,  or  sometimes  from  a  miliary 
tuberculosis  or  some  other  tuberculous  disease,  such  as  pulmonary  tuberculosis, 
tuberculous  meningitis,  etc.,  or  general  amyloidal  affection. 

Diagnosis. — The  diagnosis  of  genito-urinary  tuberculosis  is  now  seldom 
difficult  in  fully  developed  cases,  since  it  can  be  made  with  complete  certainty 
by,  the  discovery  of  the  tubercle  bacilli  joined  to  the  presence  of  pus  in  the 
urine.  Of  course  this  gives  no  information  as  to  the  exact  local  distribution 
of  the  process.  In  order  to  judge  of  this,  we  must  add  the  local  symptoms  and 
the  physical  examination  of  the  different  organs.  Cystoscopy  and  catheteri- 
zation of  the  ureters  have  become  of  great  diagnostic  importance.  Further 
details  will  be  found  in  the  special  monographs.  We  are  aided  in  the  confir- 
mation of  our  firsT  suspicion  of  a  tuberculous  disease  chiefly  by  the  considera- 
tion of  the  general  condition  and  the  habit  of  the  patient ;  the  discovery  of  an 
hereditary  taint,  or  at  least  the  probability  of  tuberculous  infection;  and  also 
the  discovery  of  other  tuberculous  affections,  especially  the  examination  of  the 
bladder,  the  testicles,  the  prostate  and  the  seminal  vesicles,  the  hectic  fever, 
and  the  tedious  course,  upon  which  nothing  has  a  favorable  influence.  At  any 
rate  we  must  make  it  a  rule,  in  every  case  of  apparently  spontaneous  hsema- 
turia  and  especially  of  persistent  pyuria  which  cannot  be  otherwise  explained, 
to  examine  the  purulent  urinary  sediment  for  tubercle  bacilli  (vide  supra). 
We  may  then  often  be  able  to  recognize  with  certainty  the  milder  and  incipient 
cases  of  this  not  very  rare  affection.  [Another  valuable  diagnostic  method, 
briefly  referred  to  by  the  author,  is  by  inoculation  of  8  to  15  minims  of  the 
urinary  sediment  into  the  peritoneal  cavity  of  a  guinea  pig.  If  tubercle 
bacilli  are  present,  the  animal  will  develop  tuberculosis  in  six  to  eight 
weeks.] 

Treatment. — Whether  specific  treatment  of  genito-urinary  tuberculosis 
with  Koch's  tuberculin  is  likely  to  have  permanent  success  cannot  yet  be  de- 
termined, as  so  few  trials  have  been  made.  Nevertheless,  it  would  be  justifiable 
to  make  a  cautious  trial  of  the  remedy,  although  we  can  hardly  cherish  the 
hope  that  it  would  prove  very  beneficial.  Beyond  this  we  must  resort,  in  the 
treatment  of  tuberculosis  of  the  urinary  passages,  io  the  same  remedies  as  in 
52 


820  DISEASES  OF  THE  URINARY  ORGANS 

ordinary  chronic  pyelitis  and  cystitis.  Of  internal  remedies  we  have  most 
frequently  used  chlorate  of  potassium,  turpentine,  creosote,  and  guaiacol  prepa- 
rations, and  have  sometimes  seen  good  results,  especially  from  the  latter.  In 
vesical  tuberculosis  it  is  well  to  wash  out  the  bladder.  Surgical  treatment  of 
renal  tuberculosis  has  become  of  greater  importance  than  the  internal.  If,  by 
means  of  an  exact  examination  it  can  be  shown  that  only  one  side  is  affected, 
the  extirpation  of  the  diseased  kidney  is  advisable,  and  has  frequently  been 
accomplished  with  beneficial  results  and  even  permanent  cure.  Therefore,  an 
early  diagnosis  is  of  the  greatest  importance.  Tuberculosis  of  the  testicle  is 
also  frequently  the  subject  of  surgical  treatment. 


CHAPTEE    IV 

HYDRONEPHROSIS 

(Dilatation  of  the  Pelvis  of  the  Kidney) 

iEtiology. — If  a  contraction  arises  in  any  part  of  the  urinary  tract  and 
checks  the  flow  of  urine,  there  is  a  stasis  of  the  urine  in  the  portion  behind 
the  stenosis  which  gradually  leads  to  a  constantly  increasing  dilatation  of 
the  tract  as  a  result  of  the  pressure  of  the  retained  fluid. 

In  general,  it  is  evident  that  gradual  constrictions  of  the  urinary  tract  and 
periodic  obstructions,  as  from  calculi,  interrupted  by  free  intervals,  lead  to 
more  marked  degrees  of  hydronephrosis  than  rapid  and  complete  obstructions. 
Under  the  first-named  circumstances  the  renal  secretion  persists  much  longer 
and  is  more  abundant  than  in  the  latter  case,  when  it  usually  soon  ceases. 
Nevertheless,  there  may  be  even  then  a  very  slow  distention  of  the  pelvis  of 
the  kidney,  particularly  if  its  mucous  membrane  continues  to  secrete.  If  the 
obstruction  is  located  in  the  ureter,  the  proximal  portion  of  that  canal  di- 
lates, and  still  more  the  pelvis  of  the  kidney,  giving  rise  to  what  is  called 
hydronephrosis;  but  if  the  obstruction  is  located  in  the  urethra  there  is  a 
gradual  dilatation  of  the  bladder  and  both  ureters,  and  finally  there  develops 
a  bilateral  hydronephrosis. 

A  closure  of  the  ureter  arises  most  frequently  in  adults  from  impacted 
renal  calculi,  and  also  from  new  growths  in  the  vicinity,  in  the  uterus  or 
ovaries,  which  compress  the  ureter  from  without.  So  great  a  pressure  may 
also  be  exerted  on  the  ureters  by  the  gravid  uterus  as  to  be  followed  by  a 
hydronephrosis,  which  is  usually  bilateral.  Cicatricial  strictures,  valve-for- 
mations and  bends,  also  are  found  in  the  ureter,  and  form  an  obstacle  to  the 
flow  of  urine.  Finally,  in  cancer  of  the  bladder  the  lower  opening  of  the 
ureter  may  be  contracted  or  entirely  closed.  Constrictions  of  the  urethra, 
which  finally  lead  to  a  bilateral  hydronephrosis,  arise  most  frequently  from 
strictures  as  a  result  of  gonorrhea,  and  also  from  enlargements  of  the  pros- 
tate.   In  rare  cases  phimosis  may  form  the  obstacle. 

It  is  worthy  of  note  that  hydronephrosis  may  also  be  congenital,  and  then 
it  is  usually  due  to  congenital  defects  of  development  in  the  ureters  or  other 
urinary  passages.  In  later  life  hydronephrosis  is  in  general  more  frequently 
observed  in  women  than  in  men. 


HYDRONEPHROSIS  821 

Pathological  Anatomy. — The  pathological   anatomy  of  hydronephrosi 
on  the  whole,  very  simple     We  have  a  dilatation  of  the  pelvis  of  the  kidney, 

which  is  associated  with  a  pressure  atrophy  of  the  renal  tissue.  The  papillae 
are  flattened,  the  uriniferous  tubules  and  the  glomeruli  are  gradually  more 
and  more  obliterated,  and  finally  the  whole  kidney  may  be  changed  to  a 
connective-tissue  sac  filled  with  fluid,  and  displaying  in  its  walls  a  few  ves- 
tiges of  the  renal  parenchyma.  The  size  of  such  a  hydronephrotic  sac  may 
sometimes  be  sufficient  to  contain  10  or  15  quarts  (liters)  of  fluid.  The 
latter  consists,  of  course,  at  first  of  urine,  but  the  farther  the  atrophy  of  the 
kidney  advances,  the  more  it  merely  represents  the  secretion  of  the  mucous 
membrane.  Inflammatory  conditions  are  found  in  hydronephrosis  only  when 
they  have  existed  previously,  as  in  pyelitis  calculosa,  or  when  excitants  of 
inflammation  in  addition  have  readied  the  pelvis  of  the  kidney.  We  then 
have  a  pyonephrosis. 

Clinical  Symptoms. — Since  the  whole  type  of  the  disease  is,  of  course,  de- 
pendent in  many  respects  upon  the  nature  of  the  primary  disease,  we  have 
here  to  describe  only  those  symptoms  which  point  to  the  development  of 
hydronephrosis.  Such  a  condition  often  causes  no  special  clinical  symptoms 
at  all,  so  that  we  can  at  most  suspect  its  existence  from  the  presence  of  an 
etiological  factor. 

The  appearance  of  a  visible  and  palpable  tumor  is  the  first  definite  point  in 
the  diagnosis  of  hydronephrosis.  This  first  shows  itself  in  the  region  of  the 
affected  kidney,  but  then  it  gradually  enlarges  toward  the  hypochondrium 
and  the  median  line  of  the  body,  and  it  may  finally  reach  very  considerable 
dimensions.  Hydronephrosis  on  the  left  side  does  not  usually  move  with 
respiration.  On  the  right  side,  however,  there  may  be  a  distinct  downward 
motion  upon  deep  inspiration.  The  resistance  of  the  hydronephrotic  tumor  is 
usually  quite  considerable,  but  there  may  sometimes  be  a  distinct  sense  of  fluc- 
tuation. On  percussion,  the  tumor  gives  a  dull  note,  from  which  the  tym- 
panitic note  of  the  colon  in  front  of  the  tumor  "is  sometimes  distinct  (see 
page  794).  It  is  an  important  diagnostic  sign  if  the  tumor  show  variations 
in  its  size  at  times — decreasing  in  size  with  a  simultaneous  increase  in  diu- 
resis, and  increasing  again  when  the  amount  of  urine  becomes  smaller  ("in- 
termittent hydronephrosis").  In  such  cases  there  is  usually  a  very  peculiar 
alternation  in  the  other  clinical  symptoms.  At  the  time  of  the  scanty  secre- 
tion of  urine  the  patient  suffers  from  violent  pain,  vomiting,  chills,  and 
similar  symptoms,  while  upon  the  appearance  of  an  abundant  urinary  secre- 
tion all  these  symptoms  quickly  vanish.  In  doubtful  cases  an  exploratory 
puncture  of  the  tumor  may  also  be  of  significance  in  diagnosis.  It  of  course 
favors  the  assumption  of  hydronephrosis  if  urinary  constituents,  especially 
urea,  can  be  found  in  the  fluid  evacuated ;  but  if  the  hydronephrosis  be  of  long 
standing,  its  contents,  as  we  have  said,  will  be  simply  seromucous,  and  then 
chemical  examination  gives  no  definite  data  for  distinguishing  hydrone- 
phrosis from  ovarian  tumors  or  other  cystic  tumors  of  the  kidney. 

The  secretion  of  urine  in  unilateral  hydronephrosis  may  be  completely 
normal  if  the  other,  healthy,  kidney  acts  vicariously.  In  stricture  of  the 
urethra,  and  also  in  bilateral  constrictions  of  the  ureters,  however,  there  is, 
of  course,  an  obstacle  to  the  passage  of  urine,  so  that  the  amount  of  urine  may 
be  abnormally  small.     There  may  be  at  times  complete  anuria,  and  even 


822  DISEASES   OF   THE   URINARY   ORGANS 

uraemic  symptoms.  The  composition  of  the  urine  depends  entirely  upon  the 
form  of  the  primary  disease.  If  the  healthy  kidney  alone  secretes,  the  urine 
passed  is  normal.  If  there  be  at  the  same  time  pyelitis  or  cystitis,  the  urine 
contains  pus  or  blood.  If  the  urine  can  also  come  from  the  diseased  kidney 
at  one  time  and  not  at  another,  the  urine,  as  we  have  said  before,  also  ex- 
hibits a  varying  composition. 

In  many  cases  of  hydronephrosis  quite  severe  local  symptoms  are  con- 
stantly present;  there  are  frequently  severe  pains  in  the  tumor,  which  shoot 
chiefly  toward  the  thigh.  Still,  these  local  symptoms  are  sometimes  surpris- 
ingly slight.  In  regard  to  the  symptoms  on  the  part  of  other  organs,  gastric 
disturbances  appear  to  be  of  the  most  frequent  occurrence;  among  them  are 
nausea,  loss  of  appetite,  vomiting,  and  eructations.  In  some  cases  the  bowels 
are  constipated,  in  others  there  is  obstinate  diarrhea.  It  is  a  very  interesting 
fact  that,  particularly  in  case  of  bilateral  hydronephrosis,  there  may  be  de- 
veloped a  distinct  hypertrophy  of  the  left  ventricle,  with  all  its  sequelae.  The 
explanation  of  its  occurrence,  in  our  opinion,  is  precisely  the  same  in  this 
case  as  in  chronic  nephritis  (vide  supra,  page  741) — viz.,  the  toxic  effect  of 
the  urinary  constituents  retained  in  the  blood. 

The  whole  course  of  the  disease  is  always  chronic.  There  are  often  varia- 
tions in  its  course,  but  no  general  statements  can  be  given,  because  the  condi- 
tions vary  in  the  different  cases  according  to  the  form  of  the  primary  disease. 
Most  cases  of  hydronephrosis  end  fatally,  either  in  consequence  of  the  primary 
disease  or  in  consequence  of  secondary  pyelonephritic  or  perinephritic  in- 
flammations, of  uraemia,  etc.  Eecovery  takes  place  in  rare  cases,  especially 
if  one  kidney  be  perfectly  normal,  and  there  be  no  incurable  primary  disease. 
Eecovery  may  ensue  spontaneously  from  perforation  or  obliteration,  or  it 
may  be  brought  about  artificially  from  operative  procedures. 

Diagnosis. — In  the  diagnosis  of  hydronephrosis,  the  points  especially  to  be 
considered  have  already  been  mentioned.  The  diagnosis  is  usually  not  easy, 
especially  if  the  aetiological  factors  be  unknown ;  and  the  disease  is  often  con- 
fused with  other  renal  tumors  and  echinococci  of  the  kidneys,  with  ovarian 
tumors,  and  even  with  splenic  and  hepatic  tumors. 

Treatment. — Except  for  the  symptomatic  treatment  of  the  pain  and  any 
accompanying  pyelocystitis,  an  efficient  treatment  of  hydronephrosis  can  be 
attempted  only  by  surgical  means,  the  details  of  which  are  to  be  found  in  the 
special  surgical  treatises. 


CHAPTEE    V 

CYSTITIS 
(Vesical  Catarrh)1 

Etiology. — In  most  cases  of  vesical  catarrh  the  agents  of  inflammation 
reach  the  bladder  from  without  through  the  urethra.  The  most  unequivocal 
demonstration  in  this  regard  is,  unfortunately,  often  made  by  the  physician 
himself,  when  he  excites  a  cystitis  by  the  use  of  an  insufficiently  purified  and 
disinfected  catheter  or  bougie.  The  development  of  the  vesical  catarrh  is 
generally  aided  in  such  cases  by  the  fact  that  there  is  usually  a  defective 


CYSTITIS  823 

evacuation  of  urine,  from  stricture  of  the  urethra  or  paralysis  oi  the  detrusor, 
with  a  consequent  retention  of  urine,  in  which  the  bacteria  can  develop  un- 
disturbed. The  agents  of  inflammation  may  also  enter  from  the  urethra 
into  the  bladder  in  incontinence  of  urine.  On  accouni  of  the  Lmperfed 
closure  of  the  sphincter,  a  stagnating  column  of  urine,  directly  connected 
with  the  contents  of  the  bladder,  tonus  in  the  urethra,  and  to  this  column 
the  air  and  the  bacteria  that  excite  decomposition  of  the  urine  have  direct 
access.  In  this  way  many  cases  of  cystitis  arise  in  patients  with  nervous  dis- 
ease who  have  paralysis  of  the  bladder,  and  also  in  persons  who  are  severely 
ill  and  stupid  from  some  other  disease,  such  as  typhoid  fever. 

Cystitis  often  follows  diseases  of  the  neighboring  portions  of  the  urinary 
tract.  Among  these,  gonorrheal  urethritis  is  the  most  common,  and  this  in- 
vades the  bladder  directly  and  leads  to  a  gonorrheal  cystitis.  In  this  case, 
is  has  not  yet  been  absolutely  determined  whether  the  gonococci  themselves 
invade  the  bladder  and  occasion  cystitis,  or  whether  the  inflammation  is  due 
to  the  secondary  introduction  and  dissemination  of  other  pyogenic  cocci, 
such  as  staphylococci  (vide  infra).  It  is,  moreover,  a  fact  of  great  importance 
that  the  development  of  cystitis  is  decidedly  promoted  by  the  unskillful  em- 
ployment of  urethral  injections.  In  women,  the  agents  of  inflammation 
may  quite  easily  enter  the  bladder  from  the  vagina  through  the  short  female 
urethra.  Thus  arise  especially  the  frequent  cases  of  cystitis  in  childbed.  In 
some  cases  communication  may  develop  between  the  bladder  and  certain 
neighboring  organs,  as  in  vesicorectal  or  vesicovaginal  fistula?,  by  which  again 
access  to  the  bladder  is  opened  to  the  agents  of  inflammation. 

Another  group  of  cases  is  due  to  the  presence  of  foreign  bodies,  which  irri- 
tate the  vesical  mucous  membrane  mechanically.  Among  these  is,  first  of  all, 
the  cystitis  which  so  often  accompanies  stone  in  the  bladder.  It  must  be 
stated,  however,  that  probably  these  cases  of  vesical  catarrh  are  not  directly 
dependent  upon  the  calculi,  but  are  first  excited  by  examination  with  catheters 
and  sounds,  and  in  brief  are  due  to  secondary  infection. 

In  distinction  from  the  methods  of  origin  of  cystitis  so  far  described,  the 
production  of  inflammation  by  way  of  the  blood  supply  is  much  rarer.  Cer- 
tain chemical  substances,  already  mentioned  (page  806)  which  are  eliminated 
by  the  kidneys  and  provoke  an  inflammation  of  the  urinary  tract,  are  the 
most  important  in  this  respect.  Cantharides  shows  the  most  intense  action 
of  this  sort,  and  it  may  cause  an  actual  croupous  cystitis.  Slight  irritative 
states  of  the  bladder  also  frequently  appear  after  taking  certain  foods  and 
drinks,  as  after  drinking  new  beer.  In  the  infectious  diseases  many  possi- 
bilities have  to  be  taken  into  consideration.  As  many  bacilli  (e.g.,  typhoid 
bacilli)  are  passed  with  the  urine,  the  possibility  of  a  hematogenous  origin  of 
a  secondary  cystitis  is  present.  On  the  other  hand,  the  severe  illness  often 
occasions  an  infection  by  way  of  the  urethra  (vide  infra).  It  cannot  be 
doubted  that  in  some  cases  an  apparently  idiopathic  primary  cystitis  appears 
after  exposure  to  cold,  but  it  is  very  rare.  In  such  cases,  naturally,  the  ex- 
posure to  cold  is  to  be  regarded  merely  as  the  predisposing  cause  of  the  in- 
fection or  auto-intoxication.  Often  such  cases  are  but  acute  exacerbations  of 
an  old  chronic  cystitis — for  example,  of  gonorrheal  origin. 

As  to  the  special  variety  of  inflammatory  germs  in  cystitis,  our  knowledge 
is  as  yet  incomplete.    In  many  cases,  particularly  in  the  cystitis  of  puerperal 


824  DISEASES  OF  THE   URINARY   ORGANS 

women,  the  germs  are  perhaps  the  ordinary  pyogenic  cocci  (streptococcus  and 
staphylococcus  pyogenes).  In  gonorrheal  cystitis  the  invasion  of  the  gono- 
coccus  into  the  bladder  has  been  absolutely  demonstrated  in  some  cases. 
Moreover,  the  bacterium  coli  commune  seems  to  play  a  great  role  in  cystitis. 
In  some  apparently  primary  cases  of  cystitis  (as,  for  example,  in  children) 
we  must  consider  the  possibility  of  an  infection  with  the  colon  bacillus  pro- 
ceeding from  the  intestine.  Moreover,  we  would  state  that  occasionally  colon 
bacilli  appear  abundantly  in  the  urine  without  simultaneous  indications  of  a 
catarrh  of  the  mucous  membrane  (pyuria).  Such,  frequently  very  obstinate, 
conditions,  termed  bacteriuria,  have  been  observed  particularly  in  children. 
The  development  of  ammoniacal  fermentation  of  the  urine  (vide  infra)  is, 
nevertheless,  not  due  to  the  bacterium  coli,  but  in  most  instances  to  special 
microorganisms.  We  already  know  a  whole  series  of  organisms  which  decom- 
pose urea  (micrococcus  ureae,  bacillus  urese,  micrococcus  urese  liquefaciens). 
In  some  cases  the  proteus  type  is  also  present. 

All  these  agents  of  ammoniacal  fermentation  of  the  urine  probably  always 
get  into  the  bladder  from  without.  They  are,  therefore,  not  excitants  of  in- 
flammation of  mucous  membranes,  although  the  ammonia  formed  through 
their  influence  certainly  does  serious  damage  to  the  mucous  membrane  of  the 
bladder. 

It  has  been  stated  in  the  previous  chapters  how  frequently  cystitis  is  only 
one  symptom  of  a  more  extensive  disease  of  the  urinary  tract.  As  cystitis 
may  invade  the  pelvis  of  the  kidney  through  the  ureters,  so,  on  the  other 
hand,  any  pyelitis  of  primary  origin  may  extend  downward  and  involve  the 
bladder. 

Pathological  Anatomy. — The  pathological  anatomy  of  cystitis  presents  the 
same  conditions  as  the  inflammation  of  any  other  mucous  membrane.  In 
simple  catarrhal  cystitis  the  mucous  membrane  is  swollen  and  covered  with 
pus,  and  is  often  studded  with  hemorrhages.  In  chronic  cystitis  the  mucous 
membrane  sometimes  takes  on  a  granulated  appearance,  because  of  the  swell- 
ing of  numerous  follicles,  and  in  other  cases  assumes  a  slaty,  grayish-black 
color,  because  of  the  pigmentation  resulting  from  numerous  small  hemor- 
rhages. 

The  severer  forms  of  cystitis,  such  as  are  often  observed  in  diseases  of  the 
spinal  cord,  are  termed  vesical  diphtheria.  These  cases  come  to  a  necrotic 
destruction  of  the  superficial  layers  of  the  mucous  membrane,  ulcerations, 
etc.  In  such  severe  cases  submucous  and  pericystitic  abscesses  sometimes  de- 
velop, which  may  perforate  into  the  surrounding  parts  in  various  ways.  The 
incrustation  of  the  mucous  membrane  with  urinary  salts,  especially  with 
ammonio-magnesic  phosphate,  is  also  frequently  found  in  chronic  cystitis, 
and  is  worthy  of  mention.  If  the  disease  of  the  bladder  is  associated  with  a 
stricture  of  the  urethra,  the  bladder  is  usually  much  dilated,  and  the  mus- 
cular layer  is  hypertrophied  and  stands  out  in  ridges  on  the  inner  surface  of 
the  bladder. 

Clinical  Symptoms. — The  local  symptoms  are  sometimes  quite  severe  in 
cystitis,  but  in  other  cases  they  are  only  slight.  In  general,  they  show  a 
greater  intensity  in  acute  cases  than  in  chronic  cystitis.  The  pain  in  the 
region  of  the  bladder  is  rarely  continuous;  it  usually  occurs  only  on  micturi- 
tion, but  it  is  often  very  distressing  then,  and  shoots  to  the  opening  of  the 


CYSTITIS 


825 


urethra.  Since  the  inflamed  vesical  mucous  membrane  shows  an  increased 
irritability,  and  since  the  morbidly  altered  urine  (vide  infra)  also  exerts  an 
abnormal  irritation  on  the  mucous  membrane,  there  is  very  often  an  increased 
desire  to  micturate.  The  patient  lias  to  empty  the  bladder  much  oftener  than 
normal,  and  in  severe  cases  there  is  an  almost  constant,  painful  "  vesical 
tenesmus,"  and  at  every  attempt  to  micturate  only  a  very  small  amount  of 
urine  is  passed,  with  severe  burning.  As  a  result  of  the  increased  irritability 
of  the  vesical  mucous  membrane,  there  sometimes  comes  on  a  very  trouble- 
some reflex  spasm  of  the  sphincter,  by  which  the  symptoms  are  increased. 

The  character  of  the  urine  is  alone  decisive  in  the  diagnosis.  This  is 
secreted  in  a  perfectly  normal  amount  and  quality,  in  case  there  is  no  com- 
plication on  the  part  of  the  kidneys;  but  in  the  bladder  it  is  mixed  with  the 
products  of  the  diseased  mucous  membrane,  and  it  is  here  exposed  to  the 
action  of  the  bacteria  in  a  way  that  will  presently  be  described.  The  abnor- 
mal constituents  of  the  urine  are  chiefly  pus  corpuscles,  bladder  epithelium, 
and  mucus  secreted  by  the  mucous  membrane.  As  a  rule,  the  urine  of  cys- 
titis contains  innumerable  bacteria,  under  the  influence  of  which  (vide  supra) 
develops  that  important  chemical  transformation  of  urea  into  carbonate  of 
ammonia,  which  is  characteristic  of  all  severe  cases  of  cystitis,  and  which  has 
been  termed  the  alkaline  (ammoniacal)  fermentation.  This  formation  of 
carbonate  of  ammonia  decidedly  aggravates  the  inflammation.  As  Lepine 
and  Roux  have  shown,  we  can  produce  a  severe  cystitis,  and  even  nephritis, 
by  injecting  very  small  amounts  of  a  pure  culture  of  micrococcus  ureas  into 
the  bladder  of  a  guinea  pig.  The  stagnation  is  a  factor  which  greatly  aids 
the  whole  process,  since  the  activity  of  the  bacteria,  as  we  have  said,  can  de- 
velop much  better  than  if  the  bladder 
were  to  a  certain  degree  constantly  puri- 
fied and  washed  out  by  the  urine;  but 
cystitis  cannot  be  produced  by  mere  re- 
tention of  urine. 

As  soon  as  a  part  of  the  urea  is 
changed  to  carbonate  of  ammonia,  the 
urine  must  be  less  acid  in  reaction. 
The  urine  has  a  faintly  acid  or  neutral 
reaction,  and  sometimes  it  is  decidedly 
alkaline  when  passed.  The  latter,  how- 
ever, is  only  rarely  the  case,  but  it  is 
often  simulated  by  the  fact  that  the 
urine  is  not  examined  until  it  has  stood 
for  some  time.  Since  during  this  time 
the  alkaline  fermentation  makes  rapid 
progress,  the  urine  that  has  stood  is  very 
often  alkaline.  Many  crystals  of  ammonio-magnesic  phosphate  and  urate 
of  ammonium  then  form  in  it;  the  former  are  easily  recognized  by  their 
"  coffin-lid  shape,"  and  the  latter  by  their  "  thorn-apple  shape "  (see  Fig. 
102).    There  is  also  a  deposit  of  amorphous  phosphates. 

If  we  then  briefly  sum  up  what  has  been  said,  the  urine  is  passed  in  about 
the  normal  amount  in  cystitis.  It  usually  looks  yellow,  and  has  an  abundant 
sediment,  which  can  often  be  recognized  as  purulent  with  the  naked  eye, 


Fig.  102. — Crystals  of  triple  phosphate  and 
ammonium  urate.     (From  Funke.) 


826  DISEASES   OF   THE   URINARY   ORGANS 

and  in  which,  microscopically,  Ave  can  find  pns  corpuscles,  often  bladder  epi- 
thelium, and  constantly  innumerable  bacteria — usually  short  rods  in  vigorous 
motion.  The  alkaline  fermentation  may  usually  be  recognized  by  the  strong 
ammoniacal  odor,  and  also,  as  we  have  said,  by  the  reaction  of  the  urine.  In 
the  severe  diphtheritic  forms  of  cystitis  we  find  shreds  of  necrotic  tissue  in  the 
urine.  If  there  are  hemorrhages  in  the  bladder,  the  urine  often  contains  red 
blood  corpuscles  and  sometimes  even  large  blood  clots.  The  mucus  in  the 
urine  appears  in  milder  cases  as  a  cloudy  opacity — "  nubecula."  The  viscid 
masses  which  can  be  drawn  out  into  threads,  and  which  are  usually  abundant 
in  the  urine  in  severe  cystitis,  and  sometimes  form  gelatinous  casts  corre- 
sponding in  shape  to  the  bottom  of  the  vessel  containing  the  urine,  are  not 
mucin,  but  they  arise  from  the  pus  corpuscles  and  the  epithelium,  changed 
and  dissolved  in  the  alkaline  urine,  and  hence  give  the  reactions  for  albumen. 
It  goes  without  saying  (compare  page  727)  that  cystitic  urine  is  always  albu- 
minous from  its  mixture  with  pus  serum.  The  presence  of  slimy  threads  in 
the  urine — the  so-called  "clap-threads"  (Tripperfaden) — is  characteristic  of 
gonorrheal  cystitis. 

There  can  be  no  doubt  that,  as  already  stated,  the  decomposing  alkaline 
urine  acts  as  a  chemical  irritant  on  the  vesical  mucous  membrane.  Hence 
cystitis  often  arises  perhaps  in  this  way,  that  the  bacteria  which  have  entered 
the  bladder  first  excite  only  an  alkaline  fermentation,  and  that  then  the 
mucous  membrane  is  affected  by  the  irritation  of  the  ammonia  salts  that  are 
formed.  Sometimes,  however,  the  mucous  membrane  endures  this  irritation 
for  a  long  time,  and  this  explains  the  fact  that  alkaline  fermentation  may  be 
observed  in  cases  which,  upon  autopsy,  present  an  almost  normal  condition 
of  the  vesical  mucous  membrane.  In  addition  to  the  alkaline  fermentation  of 
the  urine,  it  seems  probable  that  many  other  processes  of  disorganization  may 
develop  in  the  urine,  as  is  indicated  by  the  various  sorts  of  bad  odors  which 
the  urine  of  severe  cystitis  may  have.  In  a  few  cases  there  is  even  a  forma- 
tion of  gas  (carbonic  dioxid,  nitrogen,  hydrogen),  giving  rise  to  pneu- 
maturia.  This  phenomenon  indicates  the  development  of  special  bacteria 
which  generate  gas.  If  the  patient  is  also  suffering  from  diabetes  mellitus, 
the  pneumaturia  may  be  due  to  the  fermentation  of  the  sugar  in  the  bladder. 

The  other  morbid  symptoms  associated  with  cystitis  usually  depend  only 
in  part  upon  the  disease  itself  and  in  part  upon  some  existing  primary  dis- 
ease. The  most  important  symptom  is  the  fever,  which  is  often  to  be  referred 
directly  to  the  cystitis.  In  severe  cases  it  may  be  very  intense,  and  often 
assumes  a  pyaemic  intermittent  character,  especially  if  there  have  arisen  peri- 
cystitic  suppurations  or  if  the  cystitis  has  extended  to  the  pelvis  and  paren- 
chyma of  the  kidney  (see  page  788).  An  acute  cystitis  also  may  begin  with 
a  chill  and  high  fever.  If  the  escape  of  the  purulent  urine,  however,  is  abso- 
lutely free,  fever  may  be  entirely  absent  in  spite  of  the  existence  of  cystitis. 

Sometimes  in  severe  cystitis,  with  a  marked  alkaline  fermentation,  certain 
nervous  symptoms  appear,  such  as  headache,  vertigo,  stupor,  and  nausea.  The 
idea  has  been  advanced  that  in  these  cases  we  have  to  do  with  an  auto-intoxi- 
cation of  the  body,  since  ammonia  and  perhaps  other  products  of  decomposi- 
tion, such  as  sulphureted  hydrogen  (?),  are  absorbed  from  the  bladder  into 
the  blood  (ammonigemia),  and  in  this  way  excite  the  symptoms  of  poisoning 
mentioned. 


CYSTITIS  827 

According  to  the  course  of  the  disease  we  distinguish  an  acute  and  a 
chronic  cystitis.  The  former,  which  may  come  on,  \'<>v  example,  after  catheter- 
ization, in  gonorrhea,  etc.,  often  terminates  favorably  after  a  few  days  or 
weeks.  The  amount  of  mucus  and  pus  in  the  mine  is  never  great.  Chronic 
cystitis  is  observed  especially  as  a  complication  in  other  diseases  of  the  urinary 
tract,  such  as  stricture,  chronic  diseases  of  the  spinal  cord  with  paralysis  of 
the  bladder,  etc.  It  is  very  ol'len  incurable  because  the  primary  disease  is  in- 
capable of  improvement  and  the  cause  of  the  disease  therefore  persists.  The 
longer  a  cystitis  lasts,  the  greater  is  the  possibility  of  the  development  of 
severe  and  dangerous  complications,  especially  the  development  of  a  pyelo- 
nephritis, and  the  formation  of  pericystitic  suppurations.  In  this  way  cys- 
titis, especially  in  chronic  nervous  diseases,  may  become  the  immediate  cause 
of  death. 

Treatment. — The  dangers  last  mentioned  must  urgently  impress  upon  us 
the  prophylaxis  of  cystitis.  .  Fortunately,  a  good  deal  can  be  done  in  this 
respect,  in  the  first  place,  by  the  avoidance  of  all  unnecessary  use  of  bougies 
and  catheters,  by  the  greatest  cleanliness  in  the  use  of  all  instruments  of  this 
sort,  and  by  the  timely  treatment  of  all  those  conditions  which  may  lead  to 
cystitis. 

The  treatment  of  cystitis  is,  in  the  milder  and  acute  eases,  hygienic  and 
medicinal,  but  the  severer  cases  demand  careful  local  treatment.  . 

In  any  severe,  and  especially  in  any  acute,  cystitis,  the  greatest  bodily  rest 
(if  possible  rest  in  bed)  is  urgently  desirable,  since  otherwise  an  increase  of 
the  symptoms  and  a  prolongation  of  the  course  of  the  disease  is  the  almost 
inevitable  result.  The  diet  must  be  mild  and  unirritating.  Spiced  food  and 
alcoholic  drinks  are  to  be  avoided,  but  we  should  recommend  an -abundant 
supply  of  fluid,  by  which  the  urine  is  diluted  and  the  bladder  washed  out. 

We  have  the  patient  drink  plenty  of  ordinary  water,  tea  (made  from  uva 
ursi,  etc.),  or  a  suitable  mineral  water,  like  Wildungen,  Fachingen,  "Wer- 
narzer,  etc.  A  diet  mainly  of  milk  is  very  good;  under  it,  improvement  is 
often  surprisingly  rapid. 

Among  internal  remedies  those  are  to  be  considered  which  are  eliminated 
with  the  urine,  and  are  thus  able  to  act  on  the  diseased  mucous  membrane, 
or  directly  upon  the  agents  of  inflammation  and  the  ammoniacal  fermenta- 
tion. One  of  the  most  efficient  drugs,  which  never  does  harm  if  proper  cau- 
tion is  exercised,  is  chlorate  of  potassium,  of  whose  favorable  influence  on 
vesical  catarrh  we  have  often  convinced  ourselves.  It  is  prescribed  in  an 
aqueous  solution,  40  to  75  gr.  (gm.  3  to  5)  a  day,  and  it  should  never  be 
taken  on  an  empty  stomach.  Far  less  efficient  than  chlorate  of  potassium 
are  the  astringents,  such  as  tannin,  tannigen,  tannalbin,  and  uva  ursi.  The 
latter  drug  is  said  by  Lewin  to  contain  a  glucosid,  arbutin,  which  is  itself 
recommended  in  doses  of  45  to  60  gr.  (gm.  3  to  3)  a  day,  but  its  efficacy 
is  doubtful.  Of  metallic  astringents,  acetate  of  lead  in  powders  of  0.5  to  1.5 
gr.  (gm.  0.03  to  0.1),  repeated  several  times  a  day,  is  at  present  seldom 
employed.  In  cases  with  a  decided  purulent  secretion,  if  the  initial  symp- 
toms of  irritation  have  abated,  we  may  often  prescribe  with  good  results 
resinous  drugs,  of  which  the  best  are  oil  of  turpentine,  in  capsules  or  in  milk, 
or  balsam  of  copaiba, 

All  of  these,  however,  have  latterly  been  displaced  by  urotropin,  which 


828  DISEASES   OF   THE   URINARY   ORGANS 

is  best  prescribed  in  powders  of  7.5  gr.  (gm.  0.5)  three  to  four  times  daily, 
or  even  in  solution  (5  parts  in  150),  three  tablespoonfuls  daily.  Helmitol, 
though  very  similar,  is  less  effective.  Urotropin  is  the  best  remedy  in  every 
bacteriuria.  In  addition,  salicylic  preparations,  especially  salol,  in  powders 
of  8  gr.  (gm.  0.5),  repeated  several  times  a  day,  are  specially  to  be  recom- 
mended; naphthalin,  1.5  to  5  gr.  (gm.  0.1  to  0.3),  repeated  several  times 
a  day,  has  also  been  recommended,  but  it  may  produce  decidedly  disagree- 
able symptoms. 

If  there  are  severe  local  symptoms,  we  prescribe  warm  compresses  and 
poultices  to  the  region  of  the  bladder.  In  other  respects  narcotics,  especially 
subcutaneous  injections  of  morphin,  are  the  best  remedy  when  there  is  severe 
pain  and  tenesmus.  Morphin,  as  well  as  opium  and  belladonna  extract,  are 
also  employed  to  good  advantage  in  the  form  of  suppositories.  Finally,  the 
frequent  use  of  protracted  warm  baths  may  be  greatly  recommended. 

In  chronic  cystitis  all  the  remedies  previously  mentioned  are  also  to  be 
considered;  but  they  are  usually  not  sufficient  alone,  and  at  any  rate  they  are 
far  less  effective  than  a  methodical  local  treatment.  This  consists  in  a  regu- 
lar daily  washing  of  the  bladder  by  means  of  an  elastic  catheter.  A  rather 
long  rubber  tube  is  attached  to  the  catheter  at  one  end,  and  to  a  funnel  at 
the  other,  and  by  raising  or  lowering  this  funnel  the  bladder  can  be  filled  or 
emptied.  We  allow  a  moderate  amount,  say  3  to  7  ounces  (100  to  200  c.c), 
of  the  warm  fluid  to  run  into  the  bladder  and  escape,  repeating  the  process 
until  the  wash  water  is  clean.  For  this,  perhaps,  we  employ  either  a  simple 
one-half  to  one-per-cent  solution  of  common  salt,  or  preferably  a  warm  and 
weak  solution  of  acetate  of  lead,  1  to  1,000;  permanganate  of  potassium,  1 
to  1,000 ;  or  a  combination  of  boric  and  salicylic  acids.  By  treatment  of 
this  sort  many  cases  of  chronic  vesical  catarrh  may  be  cured,  while  the  most 
obstinate  may,  at  any  rate,  be  kept  within  bounds.  In  rebellious  cases  of  puru- 
lent cystitis  it  is  advantageous  to  employ  lunar  caustic.  The  bladder  is  rinsed 
out,  and  then  about  5  ounces  (gm.  150)  of  a  weak  solution  of  nitrate  of  sil- 
ver, at  first  1  to  3,000,  later  as  strong  as  1  to  1,000  or  1  to  500,  are  injected 
through  a  catheter.  The  solution  is  allowed  to  remain  two  or  three  minutes 
in  the  bladder  and  then  withdrawn.  What  is  called  the  Janet  method  of 
irrigating  the  bladder  is  also  very  useful.  The  fluid  is  placed  in  a  fountain 
syringe,  and  made  to  enter  the  bladder  from  the  urethra,  by  raising  the  reser- 
voir high  enough  to  give  a  pressure  which  overcomes  the  sphincter  of  the 
bladder.  The  advantage  of  this  method  lies  in  the  coincident  dilatation  and 
lavage  of  the  posterior  portion  of  the  urethra.  [An  excellent  remedy  is 
argyrol.  Wash  out  with  a  solution  1  to  1,000,  then  leave  an  ounce  of  five-  to 
twenty-per-cent  solution  in  the  bladder.] 

It  is  very  important,  in  treating  chronic  catarrh  of  the  bladder,  to  con- 
sider the  possible  cause  of  the  condition — for  instance,  stricture,  or  vesical 
calculi,  or  paralysis  of  the  bladder. 

In  pericystitic  suppuration  surgical  treatment  is  only  rarely  possible.  We 
must,  therefore,  confine  ourselves  to  purely  symptomatic  procedures. 


NEW   GROWTHS  IN  THE   BLADDER  829 

CHAPTER    VI 
NEW    GROWTHS    IN    THE    BLADDEB 

1.  Cancer  of  the  Bladder. — Primary  carcinoma  of  the  bladder  is  rare.     It 

forms  localized  tumors,  sometimes  with  a  pedicle;  or  it  extends  diffusely  over 
the  wall  of  the  bladder,  and  in  that  case  leads  to  such  thickening  thai  tho 
bladder  can  sometimes  be  felt  through  the  abdominal  walls  as  a  firm  tumor. 
Secondary  carcinoma  of  the  bladder  is  not  infrequently  due  to  direct  involve- 
ment by  extension  from  neighboring  parts,  such  as  the  uterus,  prostate,  or 
rectum. 

The  early  symptoms  of  primary  cancer  of  the  bladder  consist  of  disturb- 
ances of  micturition,  which  are  often  difficult  to  explain.  Usually  the  first 
indication  of  the  special  local  disease  consists  of  a  change  in  the  character 
of  the  urine,  which  is  probably  coincident  with  the  beginning  of  ulceration  in 
the  tumor.  Then  the  complete  picture  of  severe  chronic  cystitis  is  rapidly 
developed,  a  particularly  characteristic  symptom  being  the  frequent,  though 
irregular,  appearance  of  blood  in  the  urine.  The  condition  becomes  most  dis- 
tressing if  the  vesical  termination  of  the  urethra  is  occluded  by  the  new  growth. 
In  the  cases  which  we  have  seen,  cancerous  cachexia  did  not  develop  until 
rather  late.  One  case  was  in  the  person  of  a  quite  young  man.  In  general, 
the  entire  course  of  the  disease  seldom  occupies  more  than  one  or  two  years. 

The  diagnosis  of  vesical  cancer  is  not  always  easy,  particularly  at  first. 
The  main  point  is,  that  when  there  is  a  chronic  disease  of  the  bladder  and 
no  other  sufficient  reason  for  it  is  discovered,  we  should  think  of  the  possibility 
of  tuberculosis  or  cancer,  and  make  a  careful,  examination  with  these  severe 
conditions  in  mind.  It  is  sometimes  possible  to  confirm  the  diagnosis  by 
finding  bits  of  tumor  in  the  urine,  but  this  is  not  invariably  possible;  conse- 
quently a  number  of  methods  have  been  elaborated  to  facilitate  early  recog- 
nition of  vesical  tumors  by  means  of  a  direct  and  careful  examination  of  the 
bladder — thus  we  have:  cystoscopy  (N/itze)  ;  exploratory  cystotomy;  and  in 
women  dilatation  of  the  urethra  and  digital  examination  of  the  bladder. 

Particulars  with  regard  to  these  procedures  and  their  value  are  to  be  found 
in  monographs,  and  in  them  the  reader  can  also  inform  himself  as  to  the 
results  of  the  attempts  which  have  thus  far  been  made  to  remove  vesical  tumors 
by  operation. 

2.  Papilloma.— Papilloma  of  the  bladder  is  usually  a  very  soft  fibroma, 
which  is  located  in  the  trigonum  or  fundus  and  has  delicate  waving  papillae, 
which  are  covered  with  several  layers  of  cylindrical  epithelium.  The  local 
discomfort  which  this  not  very  rare  form  of  tumor  occasions  is  often  slight, 
but  the  hemorrhage  it  causes  may  be  very  important,  being  chronic  and  obsti- 
nate; for  months  and  years  the  hematuria  may  be  more  or  less  continuous. 
The  clotted  blood  as  it  passes  through  the  urethra  often  assumes  the  shape 
of  a  worm.  There  is  not  much  disturbance  of  micturition  unless  portions  of 
the  tumor  obstruct  the  inner  end  of  the  urethra.  Anyone  who  has  had  the 
experience  which  we  have  had  of  seeing  an  otherwise  healthy  and  vigorous 
man  die  because  of  persistent  hemorrhage  from  a  papilloma  hardly  as  big 
as  a  walnut,  cannot  insist  enough  upon  the  value  of  an  early  and  certain  diag- 


830  DISEASES.  OF  THE   URINARY  ORGANS 

nosis  (reached  by  examining  portions  of  the  tumor,  or,  still  better,  by  cystos- 
copy) and  of  surgical  treatment. 


CHAPTER    YII 

ENURESIS    NOCTURNA 

{Nocturnal  Incontinence  of  Urine) 

Enueesis  nocturna  is  a  nervous  affection  of  the  bladder  by  no  means  rare 
in  children  of  both  sexes,  and  therefore  quite  important  in  its  practical  rela- 
tions. Of  course,  in  small  children  there  is  no  sharp  boundary  to  be  drawn 
between  normal  and  pathological  conditions;  but  it  is  decidedly  pathological 
if  larger  children,  from  four  to  ten  years  of  age  and  even  older,  pass  their 
urine  in  bed  more  or  less  frequently  during  sleep,  in  spite  of  well-developed 
reasoning  powers  and  professedly  the  best  intentions.  This  may  extend  to 
the  years  of  puberty  and  even  beyond,  and  then  it  frequently  produces  a  very 
depressing  mental  influence  upon  the  patient.  Special  causes  for  it  are  not 
to  be  discovered  in  most  cases.  We  are  compelled  to  assume  either  an  abnor- 
mal weakness  of  the  sphincter,  which  is  probably  sometimes  congenital,  or 
an  abnormal  irritability  of  the  detrusor.  Most  frequently,  but  not  invariably, 
the  child  has  a  neurotic  constitution.  At  any  rate,  in  wetting  the  bed  at 
night  the  process  of  micturition  comes  on  in  a  purely  reflex  way,  but  it  is 
often  accompanied  by  certain  ideas  in  dreams  referable  to  micturition.  It 
does  not  hold  in  all  cases  that  the  sleep  is  especially  deep.  Many  patients, 
of  course,  do  not  notice  the  mishap  till  morning,  but  others  almost  always 
wake  directly  after.  The  involuntary  micturition  usually  occurs  in  the  first 
hours  after  going  to  sleep,  but  sometimes  it  is  later,  and  even  toward  morn- 
ing. By  day  micturition  is  often  perfectly  normal;  but  in  many  cases  there 
is  even  then  a  noticeable  weakness  of  the  bladder,  so  that  the  child  has  to 
make  water  oftener  than  usual,  and  sometimes  even  wets  its  clothes. 

Although,  as  we  have  said,  we  can  usually  find  no  special  cause  for  the 
trouble,  still,  in  some  cases,  certain  morbid  changes  in  the  urinary  organs  may 
give  rise  to  the  incontinence.  We  should,  therefore,  in  every  case  at  least  think 
of  the  possibility  of  stone  in  the  bladder,  of  congenital  phimosis  and  adhe- 
sions of  the  prepuce  to  the  glans  penis,  of  ascarides,  of  inflammatory  condi- 
tions, and  foreign  bodies  in  the  vagina,  and  make  a  special  examination  into 
these  points.  We  must  also  bear  in  mind  polyuria  caused  by  diabetes  or  renal 
disease,  and  finally,  of  course,  in  the  diagnosis  of  a  purely  nervous  nocturnal 
incontinence  of  urine,  we  must  exclude  the  existence  of  any  actual  anatomical 
spinal  affection. 

In  all  the  cases  just  mentioned,  the  treatment  must  be  directed  first  to  the 
primary  disease;  but  in  the  ordinary  nocturnal  incontinence  the  treatment 
must  be  aimed  at  the  symptom  of  nocturnal  micturition  as  far  as  possible. 
The  child  must  take  only  a  very  little  fluid  in  the  evening,  and  he  should  be 
made  to  empty  his  bladder  immediately  before  going  to  sleep,  and  perhaps1  once 
again  later.  He  should  not  be  covered  up  too  warmly,  and,  if  possible,  he 
should  not  lie  on  his  back  during  sleep.     Tying  a  brush  to  the  back  is  there- 


ENURESIS   NOCTURNA  831 

fore  a  well-known  domestic  remedy.  It  is  strongly  recommended  that  the 
child  should  be  made  to  Lie  in  bed  with  the  hips  elevated  and  the  head  low. 
A  somewhat  strict  mental  treatment  is  often  effective,  since  thue  the  attention 
to  the  process  is  increased,  although  unconsciously,  and  the  child  often  learns 
to  wake  up  at  the  right  time.  We  have  seen  many  eases  of  enuresis,  which  did 
not  recover  when  treated  at  home,  get  well  quite  rapidly  when  the  children 
were  isolated  in  the  hospital.  The  employment  of  the  rod  is  rarely  allowable; 
on  the  other  hand,  we  often  must  shield  the  child  from  injudicious  parents. 

Internal  remedies,  such  as  belladonna  and  tincture  of  nux  vomica,  were 
formerly  recommended,  but  they  seldom  do  good.  Lately  the  tincture  of  rhus 
aromatica  has  been  employed  again;  of  this,  15  drops  are  given  in  the  after- 
noon and  in  the  evening  before  going  to  bed.  In  anaemic  children  preparations 
of  iron  are  indicated.  It  is  often  useful  to  employ  electricity,  although  it  may 
be  that  the  only  influence  it  has  is  psychical.  We  put  the  broad  anode  over  the 
lumbar  cord,  and  the  smaller  cathode  over  the  region  of  the  bladder  or  on 
the  perineum,  and  let  quite  a  strong  constant  current  pass  through  for  two 
or  three  minutes.  The  current  may  also  be  interrupted  and  closed  a  few  times. 
Then  we  pass  the  wire  end  of  one  conducting  cord,  which  we  make  the  cathode, 
into  the  mouth  of  the  urethra  for  1  or  2  cm.,  while  we  place  the  other  broad 
electrode  on  the  perineum  or  above  the  symphysis,  and  let  quite  a  strong  and 
somewhat  painful  faradic  current  act  for  one  or  two  minutes  (Seeligmuller). 
The  sittings  must  at  first  be  repeated  daily.  It  is  also  a  very  good  plan  to  let 
the  whole  body  be  Avell  rubbed  with  cold  water  before  going  to  sleep.  It  is 
said  that  in  obstinate  cases  the  introduction  of  large  bougies  and  the  conse- 
quent distention  of  the  posterior  portion  of  the  urethra  are  often  attended  with 
rapid  improvement. 

Even  in  cases  in  which,  despite  careful  treatment,  no  permanent  success  is 
attained,  we  have  this  consolation  with  regard  to  the  prognosis,  that  in  simple 
enuresis  the  abnormal  condition  usually  undergoes  gradual  and  spontaneous 
improvement  as  the  patient  grows  older. 

[Belladonna,  strychnin,  or  nux  vomica,  or  a  combination  of  the  two,  are 
often  of  unquestionable  service.  If  the  enuresis  is  only  nocturnal,  belladonna 
alone  may  be  used,  either  in  a  single  dose  at  bedtime  or  three  times  a  day.  If 
the  enuresis  is  diurnal  also,  the  two  drugs  should  be  combined  and  given  three 
or  four  times  a  day.] 


(18) 


^    0     /D      .  , 


